Anabolic Steroids And Liver Death?

By: Author L Rea

As a researcher, consultant and writer I find myself fortunate enough to be in contact with some truly wonderful people and very bright minds. On occasion these contacts bring a sense of sadness and other times merely a need for urgency. The following is a question I received from a very intelligent individual, whose words needed that possible issue of urgency.

A Loaded Question

In reality I need your opinion; being one of the very few people I can actually have an intelligent conversation with about health and pharmaceuticals.

I'm in my forties and certain adjustments have to be made for health as well as maturity issues.

I have been battling health anxiety since I've been on anabolics. Now I know I have an anxious, obsessive type of personality, but at times my suspicions were actuated where my blood works showed unfavorable results... mostly cholesterol and liver enzymes.

Needless to say, I resorted to more research to counteract the deleterious effects of the AS by ingesting 20 to 25 pills/day of all kinds of supplements (fish oil, vit. E, C, Selenium, Lecithin, lycopene, psyllium... bla bla bla.)

My latest results sure blew the wind out of my sails... with a twist though.

My Cholesterol is way up there (irrelevant of safeguards) as well as my Bilirubin (2.3 mg/dl) while all my other enzymes are the lowest they have been in 10 years (AST, ALT, Alk. Phos, GGT) so go figure. My doctor is stumped, I realized (according to the available medical diagnostics) that hemolysis could be at work here.

Now I'm not taking any 17-alpha alkylated compounds. All I do is Test and Deca. My only explanation is excessive erythropoesis, hence hematocrit breakdown. Could this be the cause or am I way off?

In your opinion, I want to still maintain a decent physique without indulging into a 20 year old's fantasies.

I am willing to adjust my intake of Deca (as I love that compound) as well as a bit of Testosterone to maintain a libido, without taxing my system, yet maintaining a level of acceptable anabolism going.

I'm about 195 lbs today at 5' 9", with a BF of about 6 to 7% (happy with). Have been 265 lbs in my twenties.

Now I have been on AS for most of my 25 years of lifting, what I actually need is a semblance of a recurring cycling pattern that will keep me semi-healthy as well as keep my interest in training.

In Reply

No Warning Signs Necessary

The quest for a memorable physique is a life long pursuit. Many who were in top condition in their 20's and 30's simply give up erroneously accepting that a muscular body is the domain of the young.

There are many natural and not-so-natural approaches to ones quest of perfection and neither is promised to be without potential for negative. In many cases this is due to genetic predisposition. More often it is a matter of misuse or abuse.

25 consecutive years in a row certainly is a prolonged AAS (Anabolic Androgenic Steroid) cycle to say the least. But in truth I can say that I have known of a few longer ones that had shown little in verifiable adverse side effects as well as many much shorter ones that had several reasons for concern arise.

However in the case of this individual, it is possible that he is heading for cirrhosis of the liver and likely is currently suffering from fatty liver.

	How To Properly Cycle Off Steroids While Keeping Your Gains! In this article I will outline the different drugs used for the two purposes mentioned above. Finally I will outline a few different post cycle protocols that will help you minimize side effects from your cycle, and also help you to keep your gains... [ Click here to learn more. ]

For those not aware of these conditions it seems an in depth explanation is necessary. By the way, cirrhosis of the liver can be quite deadly and the stages have few warning signs.

Fatty Liver

The term 'fatty liver' refers to the build-up of fat in liver cells. Naturally fat in the liver usually is not a cause of damage by itself. But it is obviously not a normal liver condition. Under certain conditions the build-up can be a sign of harmful events taking place. Often the result is inflammation of the liver itself.

When inflammation becomes excessive scaring and hardening of the liver occurs. When scaring becomes extensive it is called cirrhosis... and that is a very serious condition.

Sadly there is a poor association between fatty liver and abnormal findings although the commonly used biochemical tests for liver disease have some value. Often a mild increase may occur in alkaline phosphatase or transaminase. Ultrasound and especially CT may reveal excess fat.

An enlarged liver as a result of inflammation can sometimes be found during a normal annual check up. This itself suggests fatty liver. However the only way to confirm this is through a liver biopsy. This is performed using a long hollow needle which is inserted into the patients liver to obtain a small tissue sample for examination under a microscope.

In reality the simple presence of excessive fat in the liver is not actually a serious problem. In fact, treatment aims at eliminating the cause or treating the underlying disorder. But, repeated liver injury from toxic substances may eventually progress from fatty liver to cirrhosis.

	Hepatoxicty: Fact Or Fiction? Will Steroids Ruin Your Liver? By: Roy Harper. We all know that the alpha alkylated steroids are hepatotoxic, right… We've been told for years that if you take 17 alpha-alkylated steroids, you will eventually run into liver problems. Learn the truth! [ Click here to learn more. ]

What Causes Fatty Liver?

I suppose that it would seem somewhat logical that eating fatty foods would be a cause of fatty liver, but this is not the case. Though the liver does play an important role in the metabolism or breakdown of fats. Something goes wrong in this process of metabolism, but it is still not known what does cause fat to build-up in the liver.

It is known that fat accumulates in the liver with a number of conditions. The most common is obesity. Fatty liver is also associated with diabetes mellitus, high blood triglycerides, and the heavy use of alcohol. It may occur with certain illnesses such as tuberculosis and malnutrition, intestinal bypass surgery for obesity, excess vitamin A in the body, or the use of certain drugs such as valproic acid.

It may also occur with the use of corticosteroids (cortisone, prednisone), estrogens and other steroids. Sometimes fatty liver can occur as a complication of pregnancy.

Known Causes: High blood triglycerides, heavy alcohol ingestion, Vitamin A toxicity, obesity, Diabetes Mellitus and several drugs have been implicated.

	What Is Vitamin A Toxicity? Excessive vitamin A intake results in a toxic syndrome known as hypervitaminosis A. Vitamin A toxicities in humans may be generally categorised as either acute or chronic. Acute toxicity occurs following ingestion of high doses of vitamin A. It may occur within hours or at most a day or two after a very large intake. Chronic toxicity occurs after consuming smaller amounts of vitamin A for a long period of time. - several weeks, months or years. Vitamin A has a long biological half-life and it tends to accumulate in the body. The tendency of vitamin A to bio-accumulate suggests that chronic exposure to excessive amounts would be unsafe.

No laboratory studies can help definitively establish a diagnosis of fatty liver or NASH.

Aminotransferases

• The only abnormality may be an elevated aspartate aminotransferase (AST) or alanine aminotransferase (ALT) level. These may be elevated as much as 10-fold. However, the AST and ALT may be normal in some patients with fatty liver or NASH.

  	What Is Nash? Non-alcoholic steatohepatitis (NASH) or Nonalcoholic Fatty Liver Disease (NAFLD) is fatty inflammation of the liver when this is not due to excessive alcohol use. It is a major cause of cryptogenic cirrhosis of the liver. It differs from the simple accumulation of fat in the liver (fatty liver, or hepatic steatosis) in that the inflammation of NASH causes damage to the liver cells while simple fatty liver probably does not.

• In the absence of cirrhosis, an AST-to-ALT ratio of greater than 2 suggests alcohol use, whereas a ratio of less than 1 may occur in patients with NASH.

Alkaline phosphatase

• This can be elevated in some patients with NASH.

• Usually, it is less than 2- to 3-times normal.

Lipids

• Hyperlipidemia may be present.

• Increased triglycerides are common in children.

Iron studies

• Elevations in serum ferritin, iron, and/or decreased transferrin saturation may occur in patients with NASH.

• Although iron overload occurs in a small proportion of patients with NASH, these patients have more severe disease.

• Viral serological markers: Before the diagnosis of NASH can be made, viral markers should be tested and viral infection excluded.

Cirrhosis Of The Liver

Cirrhosis of the liver is a life-threatening condition. It occurs when scarring damages the liver. This scarring (also called fibrosis) replaces healthy tissue and prevents the liver from functioning, as it should. Usually years of inflammation results in cirrhosis.

Usually, as cirrhosis develops, there is an accumulation of scar tissue that surrounds healthy liver cells. This results in tissues becoming nodular or "bumpy." Commonly the next step is that the nodular liver tissue blocks the bile ducts or makes them swollen. When this occurs bile can back up in the liver and of course the blood stream.


Cirrhosis Of The Liver
Click To Enlarge.

In many cases the situation worsens when scar tissue blocks blood flow through the liver. Obstruction of blood flow can lead to a condition called portal hypertension. Portal hypertension occurs when the veins that bring blood to the liver become larger and lead to high blood pressure in the veins that flow from the intestines to the liver.

The best known causes are: Alcoholic liver disease; Chronic Hepatitis B, C, and D; Autoimmune Hepatitis; Inherited diseases; Blocked bile ducts; Nonalcoholic steatohepatitis (NASH); Drugs, toxins, and infections.

What Does A Healthy Liver Do?

The liver is the largest organ in the body. It is found high in the right upper abdomen, behind the ribs. It is a very complex organ and has over 500 functions.
• Storing energy in the form of sugar (glucose) In fact it plays a major role in maintaining normal blood sugar levels, an important source of energy for the brain, heart and muscles.

• Storing vitamins, iron, and other minerals.

• Making proteins, including blood clotting factors, to keep the body healthy and help it grow.

• Processing worn out red blood cells.

• Making bile which is needed for food digestion .

• Metabolizing or breaking down many medications and alcohol.

• Killing germs that enter the body through the intestine.

• The liver is an "incredible chemical factory," producing many important chemical compounds needed to survive, such as bile, albumin, blood clotting factors, cholesterol, Vitamin E.

• Converts amino acids (proteins) and lipids into glucose, a complex process catalyzed by a series of enzymes.

• Performs numerous other functions such as regulating lipids or metabolizing prescribed and over the counter drugs, alcohol, and many other ingested chemicals such as caffeine, etc.

• Eliminates various harmful chemicals from the body. Treats about 1,300 ml of blood per minute, thereby acting as the body's "garbage disposal."

Liver Dysfunction Takes Some Scary Forms

• Commonly prescribed cholesterol-lowering medications such as statins (Lipitor), among many other chemical drugs, are known to be toxic to the liver.

• Cirrhosis of the liver is the eighth leading cause of death in the United States - kills 25,000 people per year.

• Widely taken OTC medications are not as safe as they seem. For example, Acetaminophen (e.g. Tylenol) can be toxic to the liver and its toxicity can be accentuated by alcohol.

• The American Journal of Emergency Medicine notes that in one year, hospitals treated over 26,765 patients for alcohol toxicity and another 16,635 for Acetaminophen (Tylenol) toxicity.

• Fatigue, aches, and pain in joints and muscles, frequent headaches, stress and appetite fluctuations may be signs of an over-worked liver.

• 4,000,000 people have Hepatitis C in the United States, causing 10,000 deaths every year.

Possible Treatments On The Horizon?

Adiponectin
According to a few studies the fat derivative hormone adiponectin has the ability to reverse both alcoholic and non-alcoholic fatty liver disease in mice. Naturally it would seem a bit difficult to find an adequate number of non-hard partying rodents but I assure you the study is for real.

In this study researchers found that recombint adiponectin administered to mice can decrease hyperglycemia, reverse insulin resistance, and cause sustained weight loss without affecting food intake.

Circulating concentrations of adiponectin decreased significantly following chronic (continuous) consumption of high-fat ethanol-containing food. (Beer and pizza possibly) Delivery of recombinant adiponectin into these mice dramatically alleviated hepatomegaly and steatosis (fatty liver) and also significantly attenuated inflammation and the elevated levels of serum alanine aminotransferase.

These therapeutic effects resulted partly from the ability of adiponectin to increase carnitine palmitoyltransferase-I activity and enhance hepatic fatty acid oxidation (burns liver fat), while it decreased the activities of two key enzymes involved in fatty acid synthesis, including acetyl-CoA carboxylase and fatty acid synthase.

Furthermore, adiponectin treatment could suppress the hepatic production of TNF-alpha and plasma concentrations of this proinflammatory cytokine. Adiponectin was also effective in ameliorating hepatomegaly, steatosis, and alanine aminotransferase abnormality associated with nonalcoholic obese, ob/ob mice.

These results demonstrate a novel mechanism of adiponectin action and suggest a potential clinical application of adiponectin and its agonists in the treatment of liver diseases.

Translation...

Adiponectin has been shown to enhance fat burning... including by the liver, and reduce the factors that contribute to fat accumulation (such as obesity and insulin resistance) in mice. Further more, the damaging inflammation is inhibited and reduced as well.

Growth Hormone

My experience with fatty liver disease is that GH (growth hormone) has a profound effect upon even liver fat oxidation. In fact it seems that those who have shown the few "suggestive" symptoms while obese tend to not do so after employing a GH and keto diet protocol.

The reason is simplistic, but almost any drug that increases fatty acid oxidation (fat burning) also promotes a decrease in liver fat as well. Additionally there is some evidence that supports the belief that GH triggers an up-regulation (increase) in adiponectin synthesis within the body.

Click Here To Learn More About Growth Hormone.

Rosiglitazone

A common diabetic drug called Rosiglitazone (Brand name Avandia) appears to hold some key benefits for both treatment and prevention of fatty liver disease. Rosiglitazone is used by diabetics, and not surprisingly athletes to reduce insulin insensitivity.

	Insulin & Supplements: What You Need To Know! I've talked a bit about insulin in the past. I'm going to review my previous article previously published on Bodybuilding.com before delving into some new info. [ Click here to learn more. ]

The result is a sort of repartitioning effect that favors nutrient transport into lean tissue (uh, like muscle) and away from fat cells. This is due to an improved metabolic profile favoring muscle growth from supporting hormones.

Studies have validated this fact by showing an increase in lean muscle mass and a decrease in fat stores for those whom it is administered to. Oh, and Rosiglitazone use triggers an increase in (you guessed it) adiponectin and even the anti-fat hormone leptin.

So it seems that there is a key Action/Reaction Factor at play here that should be considered. (Can you see a GH/ Rosiglitazone protocol coming? No, maybe next time.)

Most AAS inhibit the normal process of steroid biosynthesis. This means that the fist step in steroidal hormone production is hindered and that cholesterol is not converted into pregnenolone. The result is cholesterol back-up. This in itself could potentially create the environment for Fatty Liver.

Another and more likely possible contributor is that many AAS aromatize (convert to estrogens) to some extent. Since estrogens can foster a significant increase in triglycerides and increase the amount of food stuffs converted into fats as a whole, it seems plausible that there is a potential back-up in fats in the liver as well that could result in Fatty Liver.

There is no doubt that some degree of liver toxicity occurs from AAS use that can differ from person to person. This can have an additive value upon the effects of estrogen and cholesterol back-up... especially after a 25 year cycle. Then again, so can Tylenol.

Editors Note: After 16 years of academia and 20 years in the field Author L. Rea has written the ultimate anabolic steroid information books "Chemical Muscle Enhancement" and "Building The Perfect Beast". Both are now available at www.anabolicbeast.com.

Reference Materials:

1. Elevated AST or ALT to nonalcoholic fatty liver disease: accurate predictor of disease prevalence? Am J Gastroenterol. 2003 May;98(5):955-6.
2. The prevalence and etiology of elevated aminotransferase levels in the United States. Am J Gastroenterol. 2003 May;98(5):960-7.
3. Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathways. Trends Endocrinol Metab. 2003 Jul;14(5):214-21.
4. The association of dehydroepiandrosterone, obesity, waist-hip ratio and insulin resistance with fatty liver in postmenopausal women--a hyperinsulinemic euglycemic insulin clamp study. Hepatogastroenterology. 2003 May-Jun;50(51):771-4.
5. Effect of hens fed dietary flaxseed with and without a fatty liver supplement on hepatic, plasma and production characteristics relevant to fatty liver haemorrhagic syndrome in laying hens. Br Poult Sci. 2003 May;44(2):234-44.
6. The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice. J Clin Invest. 2003 Jul;112(1):91-100.

Author L Rea

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