Nilevar

(norethandrolone)

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  • Nilevar (Anaplex brand) from Australia

Androgenic: 22-55
Anabolic 100-200
Standard Methyltestosterone (oral)
Chemical Names 17alpha-Ethyl-17beta-hydroxyestr-4-en-3-one, 17a-ethyl-19-nortestosterone
Estrogenic Activity high
Progestational Activity high

Description:

Nilevar is a trade name for norethandrolone, an anabolic steroid closely related to nortestosterone (nandrolone) in structure. The activity of this steroid is that of a mild to moderate oral anabolic steroid, which is accompanied by distinguishable androgenic and estrogenic components. Although this steroid is essentially nandrolone modified (alkylated) to make oral dosing viable, it cannot be looked at simply as an oral alternative to Deca-Durabolin®. Most notably, the greatly increased estrogenicity caused by 17-alkylation makes norethandrolone much more problematic when trying to build quality (lean) muscle mass. In administering an effective amount of steroid in terms of muscle growth, the user has to deal with much more in terms of estrogenic side effects. The muscle accumulation with norethandrolone is also going to be accompanied by a high level of water and (likely) fat retention, not the quality muscularity normally associated with nandrolone decanoate.

History:

Norethandrolone was first described in 1954.553 It was developed into a medicine by Searle, which introduced it into the U.S. prescription drug market under the Nilevar brand name during the late 1950’s. The drug was originally sold as an oral tablet, an oral solution (with dropper bottle), and an injectable solution (in 25 mg ampules). The latter form of norethandrolone has been out of commerce for so long that few remember it was once also given by injection. Nilevar was prescribed for a variety of illnesses that were benefited by a protein sparing anabolic agent, Listed indications included preparation for and recovery from surgery, severe or prolonged illness, anorexia nervosa, severe burns and trauma, decubitus ulcers, osteoporosis, bone fracture healing, gastrointestinal disease, prolonged corticosteroid administration, and various forms of malnourishment in adults and children.

Nilevar ultimately saw only limited success as a prescription anabolic agent. It did make its way to Europe and certain other markets, but not widely. The drug was an early functional anabolic, displaying more tissue-building properties than androgenic effects. But it also remained an agent with a troubling estrogenic side. This eventually led to norethandrolone being passed over clinically for more refined compounds as they became available. Searle decided to discontinue the sale of Nilevar in the U.S. during the 1960’s, and instead began focusing energies on its newer, more strongly anabolic, and non-estrogenic steroid oxandrolone (sold as Anavar). Most other markets carrying norethandrolone, either by Searle or other companies, soon began losing this compound as well. Today, this drug is available on a limited basis, most notably in Australia where it remains viable on the veterinary drug market.

How Supplied:

Nilevar is available in select veterinary drug markets. Composition and dosage may vary by country and manufacturer, but typically contain 5 or 10 mg of steroid per tablet.

nilevar norethandrolone molecule structure

Structural Characteristics:

Norethandrolone is a modified form of nandrolone. It differs by the addition of an ethyl group at carbon 17-alpha to protect the hormone during oral administration.

Side Effects (Estrogenic):

Norethandrolone is aromatized by the body, and converts to a synthetic estrogen with a high level of biological activity (17alpha-ethyl-estradiol). As a result, it is a highly estrogenic steroid. Gynecomastia is often a concern during treatment, and may present itself quite early into a cycle (particularly when higher doses are used). At the same time water retention can become a problem, causing a notable loss of muscle definition as both subcutaneous water retention and fat levels build. Sensitive individuals may want to keep the estrogen under control with the addition of an anti-estrogen such as Nolvadex®. One may alternately use an aromatase inhibitor like Arimidex® (anastrozole), which is a more effective remedy for estrogen control. Aromatase inhibitors, however, can be quite expensive in comparison to standard estrogen maintenance therapies, and may also have negative effects on blood lipids.

It is of note that norethandrolone has some additional activity as a progestin in the body.554 The side effects associated with progesterone are similar to those of estrogen, including negative feedback inhibition of testosterone production and enhanced rate of fat storage. Progestins also augment the stimulatory effect of estrogens on mammary tissue growth. There appears to be a strong synergy between these two hormones here, such that gynecomastia might even occur with the help of progestins without excessive estrogen levels being present. The use of an anti-estrogen, which inhibits the estrogenic component of this disorder, is often sufficient to mitigate gynecomastia caused by norethandrolone.

Side Effects (Androgenic):

Although classified as an anabolic steroid, androgenic side effects are still common with this substance. This may include bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic steroids may also aggravate male pattern hair loss. Individuals sensitive to the androgenic effects of this steroid may find a milder anabolic such as Deca-Durabolin® to be more comfortable. Women are additionally warned of the potential virilizing effects of anabolic/androgenic steroids. These may include a deepening of the voice, menstrual irregularities, changes in skin texture, facial hair growth, and clitoral enlargement.

Note that in androgen-responsive target tissues such as the skin, scalp, and prostate, the relative androgenicity of norethandrolone is reduced by its reduction to dihydronorethandrolone. The 5-alpha reductase enzyme is responsible for this metabolism. The concurrent use of a 5-alpha reductase inhibitor such as finasteride or dutasteride will interfere with site-specific reduction of norethandrolone action, considerably increasing the tendency of the drug to produce androgenic side effects. Reductase inhibitors should be avoided with this steroid if maintaining low relative androgenicity is desired.

Side Effects (Hepatotoxicity):

Norethandrolone is a c17-alpha alkylated compound. This alteration protects the drug from deactivation by the liver, allowing a very high percentage of the drug entry into the bloodstream following oral administration. C17-alpha alkylated anabolic/androgenic steroids can be hepatotoxic. Prolonged or high exposure may result in liver damage. In rare instances life-threatening dysfunction may develop. It is advisable to visit a physician periodically during each cycle to monitor liver function and overall health. Intake of c17-alpha alkylated steroids is commonly limited to 6-8 weeks, in an effort to avoid escalating liver strain. Severe liver complications are rare given the periodic nature in which most people use oral anabolic/androgenic steroids, although cannot be excluded with this steroid, especially with high doses and/or prolonged administration periods.

The use of a liver detoxification supplement such as Liver Stabil, Liv-52, or Essentiale Forte is advised while taking any hepatotoxic anabolic/androgenic steroids.

Side Effects (Cardiovascular):

Anabolic/androgenic steroids can have deleterious effects on serum cholesterol. This includes a tendency to reduce HDL (good) cholesterol values and increase LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a direction that favors greater risk of arteriosclerosis. The relative impact of an anabolic/androgenic steroid on serum lipids is dependant on the dose, route of administration (oral vs. injectable), type of steroid (aromatizable or non-aromatizable), and level of resistance to hepatic metabolism. Norethandrolone has a strong effect on the hepatic management of cholesterol due to its structural resistance to liver breakdown and route of administration. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.

To help reduce cardiovascular strain it is advised to maintain an active cardiovascular exercise program and minimize the intake of saturated fats, cholesterol, and simple carbohydrates at all times during active AAS administration. Supplementing with fish oils (4 grams per day) and a natural cholesterol/antioxidant formula such as Lipid Stabil or a product with comparable ingredients is also recommended.

Side Effects (Testosterone Suppression):

All anabolic/androgenic steroids when taken in doses sufficient to promote muscle gain are expected to suppress endogenous testosterone production. Without the intervention of testosterone stimulating substances, testosterone levels should return to normal within 1-4 months of drug secession. Note that prolonged hypogonadotrophic hypogonadism can develop secondary to steroid abuse, necessitating medical intervention.

The above side effects are not inclusive. For more detailed discussion of potential side effects, see the Steroid Side Effects page.

Administration (General):

Studies have shown that taking an oral anabolic steroid with food may decrease its bioavailability.555 This is caused by the fat-soluble nature of steroid hormones, which can allow some of the drug to dissolve with undigested dietary fat, reducing its absorption from the gastrointestinal tract. For maximum utilization, this steroid should be taken on an empty stomach.

Administration (Men):

The original prescribing guidelines for Nilevar called for a daily dosage of 20 to 30 mg. This was to be administered on an intermittent basis, with the drug taken for no more than 12 consecutive weeks. Thereafter, a break of at least 1 month was advised before therapy was resumed. When used for physique- or performance-enhancing purposes, the drug is also used intermittently, with cycles usually lasting between 6 and 8 weeks in length followed by 6-8 weeks off. A daily dosage of 20 to 40 mg is most common for such applications. This level is typically sufficient for rapid gains in strength and muscle mass (bulk). The high estrogenicity makes norethandrolone of little value in speed and endurance sports, causing an unwanted retention of water weight. When given by injection, the same milligram dosage is recommended as when the drug is given orally.

Administration (Women):

The original prescribing guidelines for Nilevar made no special dosing recommendations for women, although it did warn that androgenicity is likely on a high dosage. When used by women for physique- or performance-enhancing purposes, a daily dosage of 5-10 mg is most common, taken for no longer than 4 weeks. This level is quite effective for promoting new muscle growth. Note that virilizing side effects are still sometimes noticed at lower doses,and need to be carefully examined for.

Availability:

Pharmaceutical preparations containing norethandrolone remain scarce, and are rarely diverted for black market sale. The only region of note where this compound is still made is Australia.

 

References:

553. Colton F.B., Nysted L.N., Riegel B., et al. J Am Chem Soc. 79 (1954), 1123.
554. Studies of the biological activity of certain 19-nor steroids in female animals. Pincus G., Chang M., Zarrow M., Hafez E., Merrill A. December 1956.
555. Anabolic Steroids and Sports Volume II. James E. Wright. Sports Science Consultants, Natick, MA 1982.

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By | 2017-04-07T01:11:34+00:00 April 13th, 2015|Categories: Steroid Profiles|0 Comments

About the Author:

William Llewellyn is a researcher in the field of human performance enhancement. He is also author of the bestselling ANABOLICS book series, most recently the ANABOLICS 10th Edition. William is an active supporter of the harm reduction community, and currently serves as honorary lecturer at the Centre for Public Health at Liverpool John Moores University.

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