Nandrolone Data (including joint pain relief mechanisms)
Nandrolone Data
(including joint pain relief mechanisms)
19-nortestosterone; 19-nor-4-androsten-17β-ol-3-one; 17β-hydroxyestr-4-en-3-one; Nandrolone; Deca; NPP
Removal of the methyl group at C-19 yields a product that is 20% as susceptible to aromatization as T (Vida (227)). Its C-4,5 double bond does render it susceptible to 5α-reduction, however, its 5α-reduced product, dihydronandrolone (DHN) is a weak AR ligand, thus its action in prostrate, scalp is relatively weakened. [1]
Unlike Trenbolone, Nandrolone has no effect on GR number (glucocorticoid receptor expression) in rat muscle (40). [2]
Erythropoiesis
Markedly augments erythropoiesis (>Oxymetholone) [3] (decanoate > phenylpropionate)
Bloodwork
600mg Deca only:
E2 8.1 pg/mL (low-normal)
IGF-I 327 µg/L (high)
Source: withheld; off-site reference
Potency for muscle anabolism
[4] 200mg 8 weeks ND yielded +2.6 kg FFM
[5] 300mg ND vs. 300mg TE * 6 weeks, skinfold caliper measures, insignificant between-group differences (n=8 or 9)
(consider inaccuracies inherent to caliper use and inter- subject & inter- & intra- practitioner variation in measurement technique; small group sizes & high likelihood of type II error [statistics])
Psychological effects of Nandrolone
Hannan et al. (1988) have examined plasma homovanillic acid changes following 6 weekly intramuscular injections of 100 or 300mg of testosterone enanthate or nandrolone decanoate administration in 25 males and found significant increases in homovanillic acid for both of the nandrolone but neither of the testosterone treatments. Since a large proportion of plasma homovanillic acid originates from CNS metabolism of dopamine, the demonstrated change associated with nandrolone administration confirms an anabolic-androgenic steroid-induced alteration in CNS neurotransmitter metabolism and suggests a mechanism to explain reported altered behaviour in some anabolic-androgenic steroid users. Interestingly in this regard the deletion of the 19-methyl group in nandrolone produces a more planar steroid than testosterone that thus, like 5α-dihydrotestosterone, has altered receptor binding affinities, as well as unique metabolites. It must be added that estrogens are also known to alter central nervous system neurotransmitters through inhibition of monamine oxidase activity, so aromatisation of testosterone to estrogen could also play a role (Klaiber
* Serum homovanillic acid (HVA) changed significantly in ND 100 mg weekly (+17.6 ± 7.7 pmol/L) and ND 300 mg weekly (+11.0 ± 3.3 pmol/L) but not in TE 100mg nor TE 300mg groups. That is, even therapeutic/replacement doses of nandrolone produced significant changes in dopamine metabolism.
Dopamine metabolism changed by nandrolone but not by testosterone... could have originated from both intra- and extra- cerebral sources. The difference in effect may reside in differences in the biologically active metabolites, but high TE (300mg) producing by far the greatest change in estrogen concentration while not producing any change in HVA argues against a role for estrogen alone in dopaminergic activity of androgens. [7]
- The proposed dynamic interaction of changing concentrations of estrogen metabolites with ND (half-life, 8 days) and its metabolite DHN may be implicated in changes in the number of dopamine receptors that are dependent on the timing of exposure to estrogens and on the presence of other steroid hormones (Hruska, 1980; Fernandez-Ruiz, et al., 1989) [7].
Aromatization
After 6 weeks, serum E₂ was reduced to 11 ± 9 pg/mL (100mg ND) and 14 ± 4 pg/mL (200mg ND) [7]
Molecular modeling of predicted activity
Swiss Target Prediction:
Nandrolone-SwissTargetPrediction-Table.ProM.png
Pharmacokinetics & Pharmacodynamics
Nandrolone_levels_after_a_single_100_mg_intramuscu lar_injection_of_nandrolone_esters.ProM.png
NPP (nandrolone phenylpropionate; Durabolin [sans Deca]): duration of activity of 10 days vs. Deca-Durabolin's duration of activity of 21-28 days. The phenylpropionate ester is characterized by a relative molecular weight of 1.46 & relative parent hormone content of 0.69 (comparable to cypionate & enanthate).
HPG axis suppression
- Testosterone suppression: complete suppression between 5-10 days with a single 100mg bolus:
Testosterone-suppression-single-nandrolone-bolus-time-course.ProM.png
Joint Pain Relief
Mechanisms in improved joint pain symptoms:
- increased collagen synthesis & deposition in tendon & ligament
- synovial joint fluid retention
Collagen synthesis
Supraphysiological AAS (primarily Nandrolone & T):
- ↑ serum PIIINP [dose-dependently]
- ↑ urine HP:LP
High AAS doses enhance soft tissue collagen metabolism, with no change in bone resorption [8]
Withdrawal ↓ serum ICTP [time-dependently] [8]
* procollagen Type III N-terminal propeptide (PIIINP): a marker of interstitial fibril biosynthesis in soft tissues
- highly relevant to sport; this is what is stimulated by fast movement/velocity training in tendon, where stiffness benefits velocity, whereas muscular strength adaptations must compensate for the heightened risk of muscular strain due to excessive tendon stiffness
Urinary markers:
* HP (PYD): hydroxylysylpyridinoline; reflects turnover of collagens Type I (bone), II, III & IX; present in tendon, cartilage, bone, vessel walls & dentine
* LP (DPD): lysylpyridinoline; reflects turnover of collagen Type I (bone); present in bone & dentine
- There is an age-associated decline in HP (↓), LP (↓), and HP/LP ratio (↓)
- HP:LP (urine) excludes skin metabolism (useful)
- The urinary HP and LP are potentially more useful markers of the catabolism of collagen fibres from skeletal tissues than urinary hydroxyproline. The latter has a lower specificity profile since it is found in all collagen types of all connective tissues (including skin). Moreover, it may also be released from collagen molecules prior to their incorporation into fibrils, and a large proportion of hydroxyproline is metabolized in the liver, thereby evading quantitative analysis of the resorption of mature collagen by urinary measurements (9- 12). [9]
- Lower HP:LP may reflect higher relative proportion of bone resorption vs. collagen & cartilage turnover since bone collagen is the primary LP source whereas HP reflects soft tissues generally (except skin)...suggests that resorption of Type III collagen (more HP than Type I) also decreases with age [9]
- Peak bone mass & HP:LP occurs at age 27 [9]
crosslinked telopeptide of Type I collagen (ICTP): released into circulation during the osteoclastic phase of bone modeling and remodeling (bone/collagen breakdown). ICTP constitutes pyridinoline crosslinks formed in mature collagen type I, and their concentrations in serum and urine reflect bone resorption.
RAS (fluid retention & collagen deposition in tendon)
Both mechanisms (increased collagen production in i.e. flexor tendon) and synovial joint fluid retention may be positively acted upon by the renin-angiotensin system (RAS). The RAS regulates water and electrolyte balance, connective tissue cell growth, and the metabolism of loose and dense connective tissue and sites of tissue repair [11] . Pathologically, RAS activation increases vascoconstriction, cardiac hypertrophy, and fibrosis (resulting in myocardial infarction, fibrosis of the liver) [11]. Therefore, it is important to consider the duality of the potential joint (i.e., knee extensor tendon) augmentation while on nandrolone: you may have a transient benefit in tendon remodeling (i.e., extensor tendon), but via this same mechanism, may be accruing fibrotic or cardiac/left ventricular maladaptations.
So, to the potential transient benefits: Angiotensin-I converting enzyme (ACE) is a marker positively correlated with collagen type I mRNA activity, and may reflect ECM remodeling wherein collagen synthesis outstrips degradation.
Whereas AAS generally decrease matrix metalloproteases (MMP), collagen gene expression, nandrolone increases ACE activity and increases matrix type I collagen deposition. The results of [11] showed Nand + jump training >> Nand > jump training > sedentary in ACE activity in tendon (i.e., knee extensor). Consider, however, that this same pathway is implicated in cardiac tissue remodeling and pathological action.
Npp or deca for joint relief is a key
DOSAGES
300-600mg
