All oral anabolic steroids have the same tweak, known as 17-alpha alkylation, which enables them to escape first-pass deactivation by the liver and accumulate there. Many scientists feel that the buildup leads to the eventual destruction of liver cells. Studies show various problems in the liver related to oral steroid use, including a type of hepatitis, or inflammation, that blocks the normal flow of bile through the liver, an action called cholestasis.
If people take oral steroids in large doses or for extended times, they may experience actual destruction of the liver. In some cases that involves bloody pockets of liver tissue, known as peliosis hepatis. Such cases are rare in athletes; instead they show up in hospitalized patients who took oral steroids as therapy for five consecutive years or more. That practice no longer occurs, since doctors now treat those patients with other drugs.
When most athletes use oral steroids, the stress on their livers is reflected in increased liver enzyme levels. Generally the levels don’t become critical, which has led doctors to think that the steroids cause minor damage, if any. In addition, the liver is one of the body’s tougher organs and can take a lot of abuse before it finally quits. That’s because liver enzymes rapidly return to normal when a person stops using anabolic steroids.
Even so, no one knows why or how oral anabolic steroids induce liver damage. A new animal study, using both sedentary and exercising rats as subjects, offers some plausible answers.1 The drug that the rats were on for eight weeks was stanozolol, more familiarly known by its trade name, Winstrol.
Winstrol is available in both oral and injectable forms. The injectable version gained worldwide notoriety when sprinter Ben Johnson was stripped of his ’88 Olympic gold medal after testing positive for Winstrol-V. It’s a DHT derivative, which means it can’t be converted into estrogen—so there’s no water retention or other estrogen-related side effects, like gynecomastia, or male breast formation.
Winstrol has long had a reputation among bodybuilders for promoting a harder-looking physique. It also appears to significantly increase strength levels. Some suggest that Winstrol displaces the primary androgen protein carrier in the blood, sex-hormone-binding globulin (SHBG), which would reinforce the effectiveness of any other steroids used with Winstrol. The average oral dose is about 25 milligrams daily, with up to 50 milligrams a day for the injectable version.
The drawbacks of Winstrol are similar to those of other oral steroids. Since Winstrol features the 17-alpha alkylation, it is potentially toxic to the liver. The injectable versions also feature the liver tweak, which means they, too, are possibly liver toxic. The DHT feature of the drug makes it a poor choice for those concerned about male-pattern baldness. While DHT-derived drugs also often promote acne, that’s a lesser problem with Winstrol.
The liver is subjected to a huge amount of oxidative stress, during which large amounts of cell-damaging free radicals are released. The liver has its own augmented antioxidant defense system to offset oxidative onslaught. In the rat-based study, however, the rats getting Winstrol showed a significant increase in internal liver oxidation that overwhelmed the usual defenses.
The liver has a second line of defense should its oxidative protection be overwhelmed. It involves the rapid production of antistress substances known as heat shock proteins, which potently preserve cell integrity. In the rats that exercised but didn’t get Winstrol, the heat shock proteins were upgraded. In fact, the protection lasted for 48 hours after exercise. The steroid rats, though, didn’t even produce the protein. Steroids blocked its synthesis and release, leaving the liver cells open to attack and destruction by rampant free radicals.
None of those activities shows up in normal liver-function tests. In other words, anabolic steroid users can appear to be undergoing little or no liver damage when in fact uncontrolled oxidation is destroying their liver. While the liver shows remarkable regenerative ability, it’s not difficult to see how long-term or excessive oral steroid use may promote a subtle level of liver damage that’s all the worse for not being immediately apparent.
It’s vital for anyone contemplating the use of any type of oral anabolic steroid to also use antioxidant supplements. Since glutathione is the major liver antioxidant, nutrients that boost glutathione—such as silymarin (milk thistle), NAC, lipoic acid and whey protein—may be especially useful in helping the liver deal with the extensive oxidation that results from oral steroid use.
The Molecular Key to Growth Hormone Benefits
Growth hormone is popular with athletes because of its potent anabolic effects. Most studies examining the impact of GH in athletes, however, have found that it has little or no effect in increasing muscular size and strength. On the other hand, most studies also support the fat-mobilizing effects of growth hormone. So even if GH isn’t the miraculous anabolic drug it’s reputed to be, its fat-mobilizing effects alone make it attractive.
Other attributes make GH alluring to athletes as well. Research shows that it helps maintain muscle during stringent dieting, thus enabling athletes to retain hard-earned muscle mass that they might otherwise sacrifice. In addition, scientists believe that it both protects and speeds the healing of muscle and connective-tissue injuries.
Recent studies have shown how GH promotes healing, and the implications are highly relevant to the aging process. In fact, they explain why it has acquired its reputation as a fountain-of-youth drug.
GH apparently promotes tissue healing by turning on a gene called the Forkhead Box m1B gene (Foxm1B) that is a critical component of cellular function, controlling cell regeneration and rebuilding. During youth, the gene is active, which helps explain why younger people heal more rapidly than older people do. As people age, the gene becomes less active, which causes cell disruption and eventually tissue and organ breakdown.
As GH levels decline with age, so does the Fox1mB gene, which depends on GH for its activation. Cells become less effective at repairing damage. That was illustrated by a study of liver regeneration in old and young rats.2
In the past studies showed that when the human Fox1mB gene was inserted into rat liver cells, the cells regenerated at a pace typically seen in young rats. In the new study, scientists focused on the relationship between GH and the Fox1mB gene. When they partially removed the rats’ livers and gave them GH, Fox1mB activity dramatically increased. That led to a level of cell regeneration seen in much younger rats. In older rats not given GH, the cells regenerated far more slowly and more in keeping with the rats’ age.
The scientists then disabled the Fox1mB gene in other rats. When those animals got GH, nothing happened, indicating that GH works through the Fox1mB gene. The gene is required for normal cell repair, and GH stimulates its activity. If GH declines, as it does in older people, the activity of the gene likewise declines. That results in slower cellular repair, increasing the chances of cell mutations, which, in turn, lead to a number of diseases linked to aging, such as cancer, organ failure, infections, dementia, skin wrinkling and muscle loss.
One of the scientists involved in the study suggests that GH may be useful as short-term therapy for increasing healing and promoting faster recovery from surgical procedures, especially in the aged. From an athletic perspective, the findings explain why GH seems so effective in promoting healing, particularly of injured connective tissue, which takes longer to heal because it’s not well supplied with blood. GH may overcome that deficit and speed the healing process.
References
1 Pey, A., et al. (2003). Effects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and heat shock protein HSP72 levels in the rat liver. J Steroid Biochem Mol Biol. 87:269-77.
2 Krupczak, K., et al. (2003). Growth hormone stimulates proliferation of old-aged regenerating liver through Forkhead Box m1B. Hepatology. 38:1552-1562.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
