Bodybuilding Pharmacology: Fried Liver
by Jerry Brainium
Your liver is your life. That sounds like a grandiose statement, but it’s true. The human liver is located behind the lower ribs, right below the diaphragm on the right side of the abdomen. It averages slightly more than three pounds in weight and is six inches thick. Without a functioning liver, you’d die a miserable death. Common food elements like protein would put you into a coma, since the by-products of protein metabolism, such as ammonia, would increase in the blood. In fact, many common food elements and drugs would prove fatal if you didn’t have this organ around to render them innocuous.
The liver is a potent chemical-processing plant. It quietly performs more than 500 vital functions, including the following:
•Manufactures bile, which is needed for complete fat absorption.
•Converts protein, carbohydrate and fat into other elements.
•Metabolizes drugs, including alcohol.
•Cleanses the blood of toxins.
•Produces blood-clotting factors, without which a minor cut could prove fatal.
•Stores nutrients—such as fat-soluble vitamins A,D, E, and K; vitamin B12 and carbohydrate—as glycogen.
•Maintains blood glucose levels by way of liver glycogen breakdown and release into the blood as glucose.
•Synthesizes cholesterol and protein carriers for cholesterol in the blood.
•Produces immune factors that protect against disease.
That’s just a partial list. Obviously, you want to maintain proper liver function for maximum health. Many things are known to harm the liver, including excessive alcohol intake and drug use. From an athletic standpoint, certain types of anabolic steroids are frequently mentioned as having bad effects on liver function. They’re usually oral drugs that are classified as 17-alpha ankylated drugs.
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