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Seems like the eighth? Yes, the eighth article in the series. Let's sit down, brew some tea/coffee/cocoa, and start dissecting another steroid that is actively used as a doping agent in sports.
Today's focus is Nandrolone, and let's start with the most pressing issue.
What's up with neurotransmitters, eh? Let's go!
The first study, "
Sub-chronic Nandrolone Treatment Modifies Neurochemical and Behavioral Effects of Amphetamine and 3,4-Methylenedioxymethamphetamine (MDMA) in Rats," reveals:
Preliminary exposure to nandrolone altered the ability of amphetamine to increase LMA, as shown in Fig. 7 (p < 0.001; ANOVA). The effects of prior nandrolone treatment on behavioral patterns induced by amphetamine were similar to those observed in the LMA results (p < 0.001 AUC; Kruskall-Wallis). There was less stereotypical behavior; the frequency and duration of rapid and repetitive aimless behaviors and intense sniffing were reduced, head and body trembling were not as pronounced, and head swaying was no longer observed.
Preliminary exposure to nandrolone also changed the ability of MDMA to increase LMA, as evident in Fig. 7 (p = 0.008; ANOVA). After MDMA injection, the behavioral scores in rats pre-treated with nandrolone were lower than in rats that received a vehicle…
We'll take the second study - "
The Impact of Nandrolone Decanoate on the Central Nervous System"
- Dopamine and Dopamine Receptors:
In young Syrian hamsters treated with AAS (anabolic androgenic steroids), increased levels of dopamine (DA) and the expression of dopamine D2 receptor (DA D2R) in the anterior hypothalamus were observed [108, 109]. D2 receptors are sensitive to androgens, and AAS treatment significantly increases the expression of D2 mRNA in the brain [110]. An increase in D2R immunoreactivity in the hypothalamus (AH) was noted following AAS treatment in young hamsters in the study by Ricci et al. [111]. Since D2R activation enhances neuronal suppression, the increase in DA and D2R expression in the AH suggests that hypothalamic DA augments aggression. Another theory proposes a disinhibitory mechanism for the enhanced expression of aggressiveness. Thus, blocking D2R would allow for increased GABAergic suppression of excitatory neurons in the AH. It is hypothesized that these D2-GABA neurons are synaptically connected to vasopressin (VP) neurons within the AH. Additionally, GABA was previously thought to be capable of modulating VP activity in the AH [112]. It has been demonstrated that hypothalamic VP activity plays a significant role in the control of aggression.
Nandrolone Decanoate (ND) is capable of inducing several psychological effects, a graphical representation of which is presented in the figure. Many of these effects and their associated mechanisms are thoroughly explained in this review.
Alright guys, anyone who wanted to argue with me about whether nandrolone affects the CNS and all neurotransmitters – you're free to go.
We've dissected the topic that was of great concern to me.
Anyone who wants to argue this point should go and write scientific articles, and we'll move on.
Nandrolone, also known as 19-nortestosterone, exists in two well-known esters: decanoate and phenylpropionate, both of which are used in the treatment of various diseases.
To not just make empty claims, as many self-proclaimed gurus do today – a title I will never claim for myself – let's consider the following studies.
Nandrolone decanoate (ND) increases bone mineral density (BMD), hemoglobin levels, and muscle mass, as well as reduces the frequency of vertebral fractures in elderly women with osteoporosis.
We conclude that treatment with nandrolone decanoate indeed increases bone mineral content; however, this may not be related to a direct increase in bone formation. The mechanism may theoretically involve a combination of reduced bone resorption and increased muscle mass, both of which have a beneficial effect on the preservation of bone tissue.
Treatment of 10 cases of aplastic anemia using nandrolone decanoate at a dose of 50 mg/week was conducted.
The mortality rate in the anabolic group was 20% compared to 50% in the other group. Of the six surviving patients in the non-anabolic treatment group, two showed no change in condition. The condition of each of the eight surviving patients in the anabolic group improved.
The increase in hemoglobin and hematocrit levels was progressive in the ND group, with significant differences (p < 0.003) evident after six months (9.6 +/- 1.0 vs 11.0 +/- 1.4 and 28.9 +/- 4.7 vs 33.0 +/- 4.7 respectively), which remained unchanged in group E. Group A showed a significant increase in serum creatinine, total protein, transferrin, and anthropometric parameters. These indicators remained stable or even tended to decrease in group E. In group A, there was a significant increase in triglyceride concentration and a significant decrease in both HDL cholesterol and apolipoprotein A-1. However, lipoprotein (a) decreased significantly. No significant changes were found in group E.
The use of ND will allow us to provide acceptable treatment for anemia and improve the nutritional status of elderly male patients on dialysis.
Another interesting point - "
Effect of nandrolone decanoate on Sjögren's syndrome-like disorders in NZB/NZW mice"
Injections of ND for 9 months, once every 3 weeks starting from the age of 4 weeks, reduced the number and total area of infiltrates in the submandibular glands of female and castrated male B/W mice. Since ND has relatively weak virilizing properties, this substance may be useful in the treatment of Sjögren's syndrome in humans.
Here's a relatively old study, but let's include it: "
Nandrolone decanoate added to tamoxifen in the treatment of advanced breast cancer"
Steroid receptor assays have found wide clinical application in selecting appropriate treatment for patients with advanced breast cancer (12), and they also correlate with survival (13). In our material, 55% of patients with positive estrogen and progesterone receptors responded objectively (CR + PR) to endocrine treatment, whereas only 7% of patients with negative estrogen and progesterone receptors responded to therapy. This finding underscores the prognostic value of estrogen and progesterone receptor assays for the application of endocrine treatment also in clinically selected material like this. The low response rate (55%) in patients with positive estrogen and progesterone receptor response may be related to the receptor sample site, which was the primary tumor in 88% of cases. It is reported that the status of estrogen and progesterone (dual receptor status) changes over time in 43% of cases (14). Therefore, it is important to differentiate between contemporary and previous data when reporting response rates in relation to the status of the target object.
On the same topic, but more recent: "
Hormonal treatment of advanced breast cancer. A randomized trial of tamoxifen versus nandrolone decanoate"
The median duration of remission was 24 months in the TAM group and 17 months in the NAN group (not significant). As second-line treatment, NAN after TAM resulted in one complete remission and three partial remissions, but none responded to TAM after NAN. Side effects of both drugs were rare and mild. These data show that TAM and NAN are comparable in the treatment of advanced breast cancer.
We concluded that nandrolone is superior to placebo and not significantly different from the FDA-approved regimen of rhGH in improving muscle mass in HIV-infected men with mild to moderate weight loss.
It seems we've covered the diseases and their potential fix with nandrolone. I hope you have enough material and didn't expect me to bring every study and its interpretation into the article. All of this will be necessary for our conclusions.
Moving on, we've talked about the good, let's talk about the bad. Some of the main
side effects of Nandrolone include masculinization, acne, increased hair growth, changes in voice, and decreased libido.
Again, words are just words, but it's hard to argue with numbers.
180 patients visited the AAS clinic from May 2011 to May 2016. The patients were strength athletes (99% men, average age 34 years, range 19-61 years) who started using AAS at an average age of 23 years (range 16-53 years). 95% used AAS in cycles (on average 4 cycles, average duration 10 weeks). The cycles consisted of three different AAS, most often testosterone, nandrolone, and trenbolone. Growth hormone was used by 34% in addition to AAS. Side effects occurred in 96% of patients, mainly acne (38%), gynecomastia (34%), and agitation (27%) during courses; reduced libido (34%) and erectile dysfunction (20%). The drugs regularly used by patients for self-treatment of side effects were aromatase inhibitors, clomiphene citrate, human chorionic gonadotropin, and tamoxifen.
But in the interest of truth, let's also note this about libido, since we are not the tabloid press that loves headlines like "NANDROLONE WILL MAKE YOUR DICK NOT STAND UP." No, there are studies, like "
Reversible azoospermia induced by the anabolic steroid 19-nortestosterone"
Esterified 19-nortestosterone, an anabolic steroid that has been used in clinical practice for over 20 years, was administered intramuscularly to five healthy volunteers in doses of 100 mg/week for 3 weeks, then 200 mg/week for the next 10 weeks. Azoospermia occurred 7–13 weeks after the start of treatment and persisted for 4–14 weeks after the last injection. Serum gonadotropin and testosterone levels were reduced, but androgenic effects were maintained, as indicated by unchanged libido and potency. No serious side effects were noted. 19-nortestosterone appears to be a potential means of controlling male fertility.
Just note that this study isn't very recent.
I even found this interesting image for you.
And just a bit more, above we discussed breast cancer in terms of benefits, now let's talk about the flip side.
There's this study - "
Nandrolone and stanozolol upregulate aromatase expression and further increase IGF-I-dependent effects on MCF-7 breast cancer cell proliferation".
And it's quite recent, from 2012.
Collectively, these data clearly indicate that the use of high doses of AAS, as occurs in doping practices, may increase the risk of breast cancer. This potential risk is higher when AAS are used in combination with IGF-I. To our knowledge, this is the first report directly linking AAS to this type of cancer.
It seems we are creating a very comprehensive article. Let's at least remember that nandrolone and its esters were first described and introduced
for medical use in the late 1950s. Otherwise, it's all studies and more studies, and we might end up with a meta-analysis. Let's add a few fun facts too, like
nandrolone sulfate was used as eye drops in ophthalmological medicine.
Now, let's talk about nandrolone itself. It acts as an agonist of the AR, the biological target of androgens like testosterone and DHT. Unlike testosterone and some other
AAS,
nandrolone is not potentiated in androgenic tissues such as the scalp, skin, and prostate gland, thus reducing harmful effects on these tissues.
This is because nandrolone is metabolized by 5α-reductase into the much weaker AR ligand 5α-dihydronandrolone (DHN), which has both reduced affinity to the androgen receptor (AR) compared to nandrolone in vitro and weaker AR agonistic activity in vivo.
It is noted that while the absence of 17α-alkylation greatly reduces the hepatotoxic potential of nandrolone, hepatotoxicity can still occur at sufficiently high doses.
Here's the evidence - "
Reversal of the hepatic damage induced by the supraphysiological dose of nandrolone decanoate after its withdrawal in the adult male rat"
The results showed that treatment with nandrolone led to a significant increase in body weight and levels of alanine and aspartate transaminases in serum. Moreover, liver sections of rats treated with nandrolone showed; expansion and congestion in blood vessels, inflammatory cell infiltration with liver fibrosis, severe vacuolar cytoplasmic degeneration, apoptotic hyperchromatic nuclei, and partial loss of mitochondrial cristae in hepatocytes. Furthermore, nandrolone treatment led to a significant increase in the apoptosis index and the percentage area of GFAP-positive stellate cells in liver tissues. Importantly, discontinuation of nandrolone for 4 weeks eliminated these biochemical and histological changes. In conclusion, our results demonstrated that a supraphysiological dose of nandrolone exerts hepatotoxic effects in adult rats, and showed that these toxic effects are reversible after discontinuation of treatment.
In addition to its agonistic activity, unlike many other
AAS, nandrolone is also a potent progestogen.
It binds to the progesterone receptor with approximately 22% of the affinity of progesterone.
Nandrolone has a very high anabolic to androgenic activity ratio.
In fact, nandrolone-like AAS, such as nandrolone itself and trenbolone, have the highest anabolic to androgenic activity ratio among all AAS.
When administered orally to rodents, nandrolone had about one-tenth the efficacy of subcutaneous injection of nandrolone.
Metabolites of nandrolone include 5α-dihydronandrolone, 19-norandrosterone, and 19-norethiocholanolone, and these metabolites can be detected in urine.
It has been found that single intramuscular injections of 100 mg of nandrolone phenylpropionate or nandrolone decanoate produce an anabolic effect for 10–14 days and 20–25 days, respectively.
. Nandrolone decanoate apparently has a half-life of about ~6 days.
Evidence:
First,
Second,
but we have slightly more detailed research, - "
Pharmacokinetic parameters of nandrolone (19-nortestosterone) after intramuscular administration of nandrolone decanoate (Deca-Durabolin) to healthy volunteers"
Peak serum concentrations are reached after 30 hours (for 50 and 100 mg) and 72 hours (for 150 mg), while the terminal half-life is 7–12 days.
Nandrolone phenylpropionate has an attached "PP" ester with a half-life of just 4.5 days.
Chemistry?
Nandrolone, also known as 19-nortestosterone (19-NT) estra-4-en-17β-ol-3-one or 19-norandrost-4-en-17β-ol-3-one, is a naturally occurring estrane (19-norandrostane) steroid and a derivative of testosterone (androst-4-en-17β-ol-3-one).
Specifically, it is a demethylated (nor) analog of testosterone at the C19 position.
Nandrolone is an endogenous intermediate in the production of estradiol from testosterone via the aromatase enzyme in mammals, including humans.
Complex esters of nandrolone have a complex ester, such as decanoate or phenylpropionate, attached at the C17β position.
In conclusion of this chapter, if you want to learn more about Nandrolone, you can read this study - "
Nandrolone Decanoate: Use, Abuse and Side Effects"
