I found an article on this and wanted to share it with you bros. Though it isn't the one I mentioned about a week ago it states some of the same things as the other article I refered to. It is obvious that the individual in this Q/A session is somewhat apprehensive to the idea that deca is indeed one of the worst steroids on HTPA and LH production but he also states that the current lack of data is the reason for his descision to remain objective to such a claim. Here is the bulk of his interview and what he said.
" Deca's reputation as being highly suppressive to the Hypothalamic-Pituitary-Testicular Axis (HPTA) is probably deserved, but Trenbolone may be even more suppressive. Unfortunately there is not much research to rely on here so we are forced to speculate to some degree. There are several reasons that could explain Deca's ability to shut down the HPTA relatively strongly. First, the decanoate ester is very long lived. By this I mean because of its hydrophobicity (insolubility in water or plasma) it has a tendency to diffuse very slowly out of the injection site into the plasma where the ester is removed from the nandrolone molecule. I like to refer people to the study by Minto et al to see this depicted graphically in Figure 1 from the Pharmacology website.
As Fig.1 shows, it takes over a month for nandrolone plasma levels to return to zero after a single injection of Deca. Figure 3 in the same study shows that plasma levels of endogenous testosterone levels are a virtual mirror image of plasma nandrolone levels, with testosterone taking a month to return to baseline. And bear in mind this is after just one injection of Deca. The second reason Deca may be so suppressive is that besides being an androgen, it also has progestigenic properties, meaning it binds to the human progesterone receptor at relatively low concentrations where it acts as an agonist (1). As an example of the relative binding affinities of androgens to the progesterone receptor (PR), if progesterone itself is given an arbitrary relative binding affinity (RBA) of 100, testosterone's RBA is 1.1; DHT's is 0.9; nandrolone's RBA is 20; trenbolone's is 60 (2). So we see that nandrolone binds to the PR with about 20% of the strength of progesterone. The significance of this to our discussion is that progesterone, as well as synthetic progestins can act on the HPTA to reduce luteinizing hormone (LH) production (3). Most of our readers are aware that LH secreted from the pituitary is what drives testicular testosterone production. So by acting as a progesterone receptor agonist, nandrolone is contributing to the suppression of the HPTA. This is in addition to the ability of androgens in general to suppress pituitary LH production by interfering with the Gonadatropin Releasing Hormone (GnRH) signal sent from the hypothalamus to the pituitary, which drives LH secretion.
The above mentioned ability of Deca and other androgens to suppress natural testosterone production by acting to disrupt GnRH signaling is the third reason Deca is quite suppressive. The presence of androgen receptors in the GnRH secreting neurons has been demonstrated in a number of studies (see 4,5 for example) and it is believed that androgens act directly on these receptors to disrupt GnRH pulse signaling. As most readers are aware, nandrolone binds to the AR with a greater affinity than does testosterone, so this may be another factor in nandrolone being more suppressive than other steroids. However, as (4) points out, DHT could possibly be the active androgen in the hypothalamus. If this is the case, one might expect testosterone, via its conversion to DHT, to be more suppressive at the hypothalamic level. This clearly requires more research.
Deca also aromatizes to some degree, and since estrogens are quite suppressive, this certainly could contribute to Deca's ability to shut a person down compared to nonaromatizing steroids. On the other hand, testosterone aromatizes quite readily and the resulting elevated estrogen levels contribute significantly to HPTA suppression. Moreover, by suppressing testosterone production, which is a superior substrate for aromatase, Deca has been shown to either lower estrogen levels or leave them unchanged. So aromatization is the least likely mechanism for Deca's HPTA suppression. "
