06-28-2005, 09:23 PM #1Associate Member
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- Apr 2005
say someone takes advil everyday...
how does that compare to someone who it taking an oral steroid (liver toxicity)?
i was wondering what the comparsion was to harshness on liver
06-28-2005, 09:27 PM #2
06-28-2005, 09:27 PM #3
Well I don't know in comaprison, but the oral AS passes through your liver twice(the injectable once), and I believe that advil passes only once. Someone correct me if I'm wrong.
06-28-2005, 09:28 PM #4Associate Member
- Join Date
- Apr 2005
06-28-2005, 09:29 PM #5
I dont think advil is nearly as bad as oral AS. Again, the oral AS passes through the liver TWO times.
06-28-2005, 09:31 PM #6
anyone have any actual studies on this topic?
06-28-2005, 09:36 PM #7Originally Posted by BlInDsIdE
Doctors Aware of Acetaminophen-Related Liver Risk, Must Educate Public
ANN ARBOR, MI -- June 18, 2001 -- The message that a common pain reliever can have uncommonly bad effects on the liver under certain conditions seems to have reached most physicians, a new study finds. Now, the challenge lies in getting the word out to their patients and the public.
The newly published study surveyed physicians to assess how well they understand the potentially liver-damaging effects of acetaminophen, commonly sold as Tylenol or as an ingredient in other medications. The results are published in this month's Journal of Clinical Outcomes Management by researchers from the University of Michigan Health System (U-MHS) and School of Public Health.
Acetaminophen can lead to potentially fatal liver damage if taken in large doses - either intentionally in a suicide attempt or unintentionally in a prolonged attempt to quell pain - or if taken in conjunction with alcohol, certain other medications or fasting, or by people with existing liver problems. Intentional overdoses are the most common cause of such liver problems, but other causes are gaining notice.
The survey also looked at physicians' understanding of how to treat acetaminophen-related liver problems, their knowledge about how common such problems are, and their attitudes toward recommending liver transplants for those whose livers had been damaged by acetaminophen.
"It appears that most doctors' knowledge is good, with more than 95 percent of them aware of certain risk factors, though there's still room for improvement," says Robert Fontana, MD, assistant professor of internal medicine at UMHS and senior author of the report. "We should encourage physicians to talk with their patients about all the risk factors, while at the same time, finding more ways to educate the public about this avoidable risk."
While acetaminophen products are safe for most people when used as directed, its toxic effect on the liver can be dramatic under certain conditions. The drug can hamper the liver, or even cause it to fail, when taken in large doses or in conjunction with alcohol. Those who are fasting, and those with cirrhosis, can also suffer the effects at excessive doses. Required warning labels on many packages tell of the potential alcohol-related risk, but some organizations and scientists are calling for even stronger warnings and more public education.
Since physicians are often important educators on health risks, especially for those whose risk is heightened, the U-M team set out to test the knowledge of a sampling of primary care physicians and gastroenterology specialists.
The 28-question survey was mailed to 1,180 randomly selected Michigan physicians in 1999 and 2000, with 397 returning a response. The survey included questions on risk-factor knowledge, knowledge about the safety of acetaminophen and painkillers like ibuprofen (Advil) known as NSAIDs or non-********* anti-inflammatory drugs, and attitudes toward liver transplantation for those who had acetaminophen-related liver failure.
Overall, 96 percent of the physicians knew that people who drink more than three alcoholic drinks a day and take acetaminophen are at a higher risk for liver toxicity. The same percentage knew that the total dose of acetaminophen taken in a certain time period can also raise liver risk - for instance, exceeding the recommended 24-hour dose on a bottle of extra-strength painkiller.
And nearly 95 percent knew that those with cirrhosis of the liver have an increased risk from the drug, though 38 percent knew that acetaminophen is preferred over NSAIDS for such patients.
Meanwhile, despite recent evidence suggesting that taking the painkiller during prolonged fasting can have an effect, only about 60 percent of physicians surveyed knew of these issues. The physicians showed variation in their knowledge about the difference in the risks posed by acetaminophen and NSAIDs. For example, only 61 percent knew that more people die each year from the toxic effects of NSAIDs than die from liver toxicity caused by acetaminophen. And just under half knew that most cases of liver toxicity from acetaminophen result from intentional overdoses.
As might be expected, more gastroenterologists than primary care physicians had handled a case of acetaminophen-related liver toxicity in the past year. And slightly more gastroenterologists knew that N-acetylcysteine could be used to treat it, even after more than 12 hours had passed since the last dose of acetaminophen.
But overall, the primary care physicians showed an impressive knowledge of the issue surrounding the drug - suggesting that recent research and public attention has influenced their awareness. Now, Dr. Fontana and his colleagues say, the next frontier for decreasing incidence of the drug's harmful effects is surveying and educating the general public. Besides Dr. Fontana, the study's authors are Leonard Quallich, M.D., and Thomas Shehab, M.D., gastroenterology fellows at UMHS, and J. Winchester Brown, Ph.D., of the U-M School of Public Health.
SOURCE: University of Michigan Health System
06-28-2005, 09:39 PM #8
The designation “17-alpha ankylated” refers to a change made on position 17 of the basic steroid structure. Scientists developed the testosterone derivatives after noticing that orally taken testosterone is degraded in the liver in a process called first-pass metabolism. Drug developers circumvented that formidable problem by making testosterone available in an injectable form, which bypasses initial first-pass liver metabolism, and by manipulating the basic steroid chemical structure, as is the case with oral 17-alpha ankylated anabolic steroids .
While the structural change in oral anabolic steroids did result in a far slower rate of breakdown in the liver, it also led to an inordinate buildup of such drugs in the liver. Since the injectable versions of steroids don’t build up in the liver as much as oral versions, the injectables are considered less of a problem in terms of normal liver function.
The oral drugs adversely affect the liver through several mechanisms. For example, they interfere with the function of certain liver enzymes. Anabolic steroids are known to increase the activity of some liver enzymes while downgrading that of others. One enzyme that’s increased with oral anabolic steroid use is hepatic triglyceride lipase, which degrades high-density lipoprotein (HDL), a beneficial cholesterol carrier in the blood. A lowered HDL level is considered a risk factor for cardiovascular disease. Athletes who use oral anabolic steroids nearly always show depressed HDL levels. The buildup of 17-alpha ankylated oral anabolic steroids in the liver leads to a type of toxic or chemical hepatitis. Hepatitis, by the way, is a general word for an inflammation of the liver and can be caused by various factors, such as drug use and viruses. Oral steroids cause liver inflammation by promoting an increase in the size of liver cells, which leads to a congestion of bile flow through ducts in the liver that empty into the gallbladder, where bile is stored.
The interference with bile flow induced by the effects of anabolic steroids on liver cells is called cholestasis. It usually occurs only in people who use higher doses of oral steroids or who use such steroids for extended periods of time. Certain oral steroids are reputed to have more potent toxic effect in the liver and to promote the liver swelling that can lead to cholestasis. They include oxymetholone (Anadrol -50) and fluoxymesterone (Halotestin ), although it may be that those drugs cause problems because they’re often used in higher doses than other oral steroids. Both drugs are 17-alpha ankylated, as are most oral steroids.
According to existing medical research, most cases of serious liver ailments due to oral anabolic steroid use have involved hospitalized patients who were given oral steroids such as Anadrol-50 to combat rare blood anemias. Many stayed on oral steroids for three or more years. The consensus of medical reviews is that certain potentially adverse liver changes do occur with athletic use—with the extent of the changes again depending on the drugs used, the doses and the length of time—but the changes regress when the athletes stop using the steroids. The liver is known to have an amazing capacity for regeneration unless it’s irrevocably damaged, a scenario that rarely occurs with short-term steroid use.
Physicians often warn about elevated liver enzyme levels due to oral anabolic steroid use. While that could indicate an inflammation of the liver, the problem is that some of the measured liver enzymes aren’t specific to the liver and exist in other tissues. For example, two enzymes found in liver, ALT and AST, also exist in muscle. Any type of injury to muscle—including the kind that occurs with intense weight training—causes an elevation of those enzymes in the blood. A physician who’s not looking at the big picture—or measuring levels of other liver and muscle enzymes—may wrongly conclude that such liver enzyme increases are indicative of liver problems.1 Measuring enzymes such as creatine kinase and GGT would provide a more definitive picture of existing liver function, as would liver imaging tests.
One visible early sign of liver inflammation due to oral steroid use is jaundice, which is characterized by a retention of bile in the body, leading to a yellow discoloration in the skin and whites of the eyes. Anyone using oral anabolic steroids should stop using them immediately if such symptoms occur. If you ignore the symptoms, you’re at risk for a more serious liver complication.
Peliosis hepatis, as it’s called, consists of blood-filled cysts in the liver. It’s thought to be due to cholestasis; that is, the elevated pressure in liver tissue brought about by lack of proper bile flow in the liver leads to a breakdown of liver cells followed by the appearance of the cysts. The blood-filled cysts can rupture, leading to death. Most cases of peliosis have occurred in hospitalized patients on long-term steroid therapy, although the occurrence of peliosis isn’t dependent on dosage.
One published instance of peliosis involved a 27-year-old bodybuilder who was using a steroid stack consisting of oxandrolone (Anavar ), methandrostenolone (Dianabol ), nandrolone (Durabolin ) and testosterone for five weeks.2 What he took before that time wasn’t disclosed in the published report. The interesting aspect is that the drug stack he used isn’t considered highly toxic to the liver. The bodybuilder may have used more toxic oral steroids over a longer period, however, or he may have taken a drug such as Nolvadex , an estrogen blocker that few bodybuilders know can also cause peliosis if used in too high a dose for too long.
The other serious liver disease often linked to oral anabolic steroid use is liver cancer. Reviews of liver cancer in various medical journals indicate that it’s of a more benign nature than other cancers. Simply put, the liver tumors that develop with steroid use usually regress if the person stops using the drugs. That’s not always the case, however.
A few published accounts document liver cancer fatalities among athletes who have used oral anabolic steroids. In most cases, though, the athletes stayed on the drugs for extended periods. For example, one 26-year-old bodybuilder used a steroid stack consisting of Dianabol, Anavar, Winstrol , Deca -Durabolin and Primobolan for four years before being diagnosed with liver cancer.3 He refused chemotherapy to treat his cancer—probably because it had progressed to a fatal stage—and died.
Another bodybuilder who succumbed to liver cancer took Anadrol-50 for five consecutive years,4 and a 27-year-old Indian bodybuilder died after a liver tumor allegedly induced by his anabolic steroid use ruptured.5 The report documenting that case failed to list his specific steroid regimen. The most recent case of a bodybuilder who had apparent steroid-induced liver cancer involved a 31-year-old man.6 His cancer was considered benign and had not spread or metastasized; however, his liver tumors didn’t decrease in size even after he’d been off steroids for 18 months.
Several options have been suggested as methods of protecting the liver from steroid-induced damage. One obvious technique is to avoid taking oral steroids that are especially toxic to the liver, such as Anadrol, for extended times. A drug available in Japan called malotilate (Hepation) may reduce liver inflammation. A study showed that using ursodeoxycholic acid, a substance that thins bile secretions and is often used to treat gallstones, relieved the bile backup induced by androgens.7
Natural means of protecting the liver involve the use of various herbs. One example is Astralgus, which works by increasing glutathione levels in the liver. Glutathione is an antioxidant that also plays a major role in detoxifying substances in the liver, including anabolic steroids. Certain nutrients are known to increase glutathione synthesis in the liver, such as alpha-lipoic acid and N-acetyl cysteine. Milk thistle (silymarin) and a lesser known herbal substance, Picrorhiza kurroa, increase glutathione synthesis and also help regenerate liver cells. Both Astralgus and Picrorhiza kurroa are used in Europe to treat hepatitis and help maintain liver function. Increasing glutathione levels in the liver may be especially important, since one study of isolated liver cells treated with both injectable and oral anabolic steroids showed that the oral drugs depleted liver glutathione levels.8
Having sufficient amounts of chemicals called methyl groups in the liver also helps keep it healthy. Nutrient sources of methyl groups include lecithin, choline, betaine and S-adenosylmethionine (SAMe). Studies show that SAMe is especially useful for promoting increased bile flow in the liver and may help relieve the bile flow obstruction induced by oral anabolic steroids. SAMe, however, is quite expensive. An alternative method is to increase the intake of nutrients that promote SAMe synthesis in the liver, such as vitamins B12, B6 and folic acid.
Gamma-linoleic acid (GLA), which is found in evening primrose and borage oils, is often suggested as a way for those using oral anabolic steroids to help protect the liver. Ostensibly, the mechanism involved is a reduction in liver inflammation caused by oral steroids. GLA may help in that respect because it’s a precursor for anti-inflammatory prostaglandins that may be in short supply when the liver is inflamed.
Those who are concerned about liver cancer should be conscientious about avoiding contracting all forms of viral hepatitis, which is considered a direct cause of the type of liver cancer that’s more fatal than the type usually caused by steroid use. Since such forms of hepatitis are caused by blood contact, be wary of tattooing, body piercing, acupuncture and even sharing razors and toothbrushes (yech!). Sharing needles is a risk factor not only for hepatitis but also for HIV infection.
1 Dickerman, R.D., et al. (1999). Anabolic steroid-induced hepatotoxicity: is it overstated? Clinical J Sports Medicine. 9:34-39.
2 Cabasso, A. (1994). Peliosis hepatis in a young adult bodybuilder. Medicine and Science in Sports and Exercise. 26:2-4.
3 Overly, W.L., et al. (1984). Androgens and hepatocellular carcinoma in an athlete. Annals Internal Medicine. 1:158-159.
4 Goldman, B. (1985). Liver carcinoma in an athlete taking anabolic steroids. J American Osteopathic Association. 85:56.
5 Creagh, T., et al. (1988). Hepatic tumors induced by anabolic steroids in an athlete. J Clinical Pathology. 41:441-43.
6 Bagla, S., et al. (2000). Anabolic steroid-induced hepatic adenomas with spontaneous hemorrhage in a bodybuilder. Aust N Z J Surgery. 70:686-7.
7 Mork, H., et al. (1997). Successful therapy of persistent androgen-induced cholestasis with ursodeoxycholic acid. Z Gastroenterol. 35:1087-91.
8 Welder, A.A., et al. (1995). Toxic effects of anabolic-androgenic steroids in primary rat hepatic cultures. J Pharmacol Toxicol Methods. 33:187-95
06-28-2005, 09:46 PM #9
thanks bro, good read
06-28-2005, 09:55 PM #10
no problem, take care
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