As this is ridiculously long. Here is a summary and conclusion of part two of the research with the full complete study below.
EDIT: From conversation with DfromPhilly where we discussed ambiguity around the use of terms: TRT, HRT, AT, HT etc. For the purpose of understanding, pls note the term therapy applies to nandrolone or test etc. given as a form of therapy for a particular ailment, not just for low testosterone issues, although there are 2 cases of deca being used in combination with testo discussed/referenced in recent times up to the point Organon pulled the Deca Brand (by MD Grossman, quoted below) and beyond in the case of a TRT experts' (Nelson Vergel) personal use of deca over 10 years.
:

Abstract/Summary

Part two set out to answer the following questions. The answers have been included below each question:

The big question(s) / research problem(s)
1. Do 19-nor's cause an increase in prolactin in vivo?
a. 19-nor nandrolone does not directly impact prolactin but can impact prolactin through conversion to estrogen via aromatase at a fraction of the level of testosterone.
2. Are 19-nors more suppressive than testosterone?
a. 19-nor nandrolone is NOT significantly more suppressive than testosterone E/Cyp
3. Does testosterone cause increases in prolactin?
a. Testosterone can increase prolactin significantly via conversion to estrogen
4. Is testosterone essential for a 19-nor cycle?
a. It is proven that it is not needed for a 19-nor cycle of nandrolone decanoate/NPP and it has been recently/is currently in use as a form of Androgen/Hormone Therapy (alongside Test) and as a therapy for cachexia respectively, without adverse effects concerning prolactin and/orusing ai's.

Say What Now?!?!

Due to limited 19-nor human studies in oral and injectable trenbolone, we need to initially focus on the 19-nor Nandrolone which is currently and has been a HRT and hormone therapy since the 1950’s. This study has concluded that 19-nor Nandrolone is not a direct influencer of prolactin and in combined test/Nandrolone cycles, is able to indirectly influence prolactin via conversion to estrogen, but only at .2 the amount of testosterone. Further Nandrolone has a stronger binding affinity to the androgen receptor than testosterone, leaving the spotlight firmly on testosterone as the culprit, via its huge rate of conversion to estrogen (78).

To be clear: 19-nor Nandrolone does not directly impact prolactin.

Testosterone is the primary culprit. However, it should be noted that ANYTHING that stimulates the estrogen or prolactin receptors can raise prolactin as does HGH, for example. Therefore it is technically true to say that Nandrolone could impact prolactin indirectly via being converted to estrogen. However, in a Nandrolone only cycle, the body would require an amount of Nandrolone at 5 times the amount of testosterone taken to cause increased prolactin levels. E.g. if a 750mg dose of testosterone causes a prolactin raise, you would require a dose of 3750mg of solo - nandrolone to achieve a similar raise! In a combined cycle, a combination of testosterone and nandrolone will result in the nandrolone binding more strongly to the androgen receptor than testosterone resulting in elevated levels of unbound testosterone to convert to estrogen and impact prolactin (78).
Nandrolone (only) has been studied on bodybuilders at doses to 600mg of nandrolone decanoate, for 12 weeks with shutdown the same as testosterone and no libido/water/erectile dysfunction. 19-nor Nandrolone or NPP does not shut you down significantly more than test E/Cyp. Bloods in community forum show trends in high estro correlate with high prolactin cases, general forum search shows correlations between fear and needing caber, between cookie-cutter advice and caber inclusion on-cycle – However, there has been no evidence found in this study of 19-nor induced high prolactin at all.

***This study found no edivence on eroids, whatsoever, that 19-nor’s cause prolactin to raise

The study results and research findings refutes the Nandrolone/Prolactin controversy and shows it unlikely that solo nandrolone runs will cause ED or estrogen issues -When estrogen is managed carefully. Low estrogen SHOULD be monitored in such runs. A barometer should be the testosterone-estrogen aromatase conversion rate. Furthermore, the results of this study firmly point the finger at testosterone and it's capacity to aromatise to estrogen.
As a next step Solo Nandrolone cycles must be studied at supraphysiological doses that keep estrogen within a range that does not need an ai. Nandrolone may be a better option than testosterone in cycles with compounds that have significant binding affinity to the androgen receptor (78) and may be a significant alternative for TRT users. Future research should focus on trenbolone, and possible links between UGL testosterone and phytoestrogens in terms of the manufacturing process - how filtered are the products etc, are all phytoestrogens removed? And so on.

To shed further light on 19-nor debate we must prove the research findings by trialling supraphysiological nandrolone only cycles relevant to the AAS lifestyle/goals etc. Firstly a thorough review TRT testosterone doses that result in no estrogen issues must be carried out. From this it is expected one could formulate a solo nandrolone dosing range that will not impact estrogen negatively. This will be part 3, the experiment.

The study

Having established that there is both conflicting information and controversy when it comes to 19-nor’s vs. prolactin, a lack of clarity surrounding a possible cause and the subsequent use or misuse of ancillary medications such as prami or caber, it has become apparent that we need to understand the truth. The prevalence of gynecomastia/estrogen/prolactin/erectile dysfunction issues within the AAS community is a massive issue. It is clearly correlated with testosterone, seemingly in every case, but also with 19-nors. We need answers.
The positive benefits of steroids and 19-nors are clearly acknowledged in studies of athletes, bodybuilders and those with medical conditions, dating back to the 1950’s. There are tens of thousands of publications of peer reviewed studies printed in journals such as the Journal of Strength and Conditioning, as well as being firmly recognised by the Endorine Society from a performance enhancement perspective and adverse effects perspective (to the point of going public about it). They highlight something very interesting and relevant to the questions surrounding supraphysiological doses of AAS as seen in the bodybuilding community and related sides including those questioned in my 19-nor reports:* Is testosterone all it’s cracked up to be?(ref: recent FDA releases on TRT); *Do 19-nors spike prolactin etc? They highlight the fact that the medical society and most researchers have difficulty in what they consider an ethical issue; to have trial subjects use and take the associated risks that come with extreme steroid dosages. They acknowledge that research is limited and they NEED to do more observational work on the AAS community. This makes this study highly relevant, despite it’s blatantly obvious shortcomings/limitations (no placebo, no randomisation, limited controls, cannot be considered a true scientific approach etc.) (1,2)
Therefore, this basic study should be thought of as an observation from within the AAS community with basic relevant research in the AAS community, and not a scientific study. It’s limitations include the author’s bias, limited oral/injectable trenbolone information, a lack of controls, the lack of understanding/research within the medical/academic community with regard to the bodybuilding community and various ethical factors.

Study Selection:

Many academic publication and clinical studies were reviewed. They were comparative, randomized, and nonrandomized and reported the effects of testosterone, 19-nors, HGH and related factors such as dosing, relevant hormones, side effects and benefits on outcomes of interest. Sources included eroids/internet forums, TRT specialists sites, media personalities with youtube presence, academic sources, TRT/HRT experts/forums/publications, HIV/AIDS experts/forums/publications and others. Also reviewed were the opinions, publications and research of thought leaders such as Scally, Roberts, Llewellyn, and Rand McLain and outliers/contrarians via internet forums, as well as subjective anecdotal experiences of this author and other eroids members. Bloodwork reviews were carried out from forum members submission on www.eroids.com . It is important to note that there was significant evidence reviewed both from academic studies on bodybuilders and supraphysiological doses of 19-nor’s making the study particularly relevant to our community.

So how long are we at this?
Androgen Therapy /Hormone Therapy/ Testosterone replacement therap (TRT) has been studied since the 1950’s. Naturally testosterone has been heavily studied (3) as has Nandrolone and many other AAS’s (4). As has nandrolone for a range of medical conditions including hormone therapy / TRT for low T (79, 80, 81), Osteoporosis (5), anaemia and HIV. Lacking are; human studies of Trenbolone due to its never having been released as a product suitable for use in humans, just animals, where there are again limited relevant studies (hence the need for AAS community research and observations). 19-nor therapy, or nandrolone therapy in humans is very well documented and at non-supraphysiological doses shows a large range of benefits including muscle mass, positive treatment outcomes for bodyweight, positive perceptions of libido, sexual function, general health and wellbeing. But also importantly, these standard doses 1-300mg nandrolone decanoate, show almost no negative side effects(6)
There was a study that showed no improvement in quality of life (not a decrease but no improvement) but later studies (including a very detailed and focused study at supraphysiological doses for bodybuilders @ 600mg nandrolone decanoate) showed improved quality of life, relationship and sexual function confirming the original therapy trials and studies of the 1990’s. This has been repeated many times and a number of studies repeatedly show that there are very few risks associated with Nandrolone Therapy and it could increase quality of life of patients. (7,8,9, 10).
Solo DECA THERAPY is very real, exists since the 1960’s and is used to date, shows no prolactin issues and no negative perception of quality of life and libido. This information is a combination of: Academic lit reviews, clinical studies at 1-600mg doses of nandrolone, suprahysiological doses on bodybuilders at 5-600mg of nandrolone. This appears to be definitive, but the anecdotal debate on high prolactin issues from forums and bodybuilders must be addressed. Trenbolone research is beyond this study due to the lack of human trials and is an area of future research.

Ok, so there is no evidence that 19-nors raise prolactin and test free cycles are nothing new, so…. what are the modern experts saying?

1. Steroids and TRT expert, thoughtleader and Muscleinsider media personality Dr. Rand McClain says that he has never once seen a case of prolactin being increased by a 19-nor steroid. (17)
2. Thoughtleader William Llewellyn’s research shows that testosterone increases prolactin within 4-5 days, likely via estrogen effects. He also notes that the clinical studies of nandrolone show no increases in prolactin, but his book Anabolics does not touch on this subject making his knowledgebase in the subject appear to be as limited as this and other similar research at best. (18)
3. Thoughtleader and psuedo Ph.D. Bill Roberts notes that some of the men using testosterone had large increases in prolactin; many had no increase, whilst some women with extremely elevated estrogen saw no prolactin increase yet some men did (with estro). Some using a combination of test with nandrolone saw increases in prl whereas others did not and importantly that there is no evidence that deca will raise prolactin in “all users”. Interestingly Bill Roberts personally trialled and found to be successful as a TRT therapy; a solo Boldenone run. (19, 20)
4. Thoughtleader Scally MD takes a different approach and looks/quotes direct evidence WRT; TRT patients and those with hyperprolactinaemia. He shows a proven link in prolactin regulation via estrogen conversion, but also states that if a compound aromatises to estrogen and interacts with the estrogen receptors “there will be an effect on prolactin secretion” but highlights that TRT patients, as stated in clinical studies, should consider the use of non-aromatizable androgens. (20)
5. Contrarian and natural remedies/AAS Personal trainer Taeian Clark on God of Hormones GH15 forum recommends solo deca cycles up to 2000mg and has himself run 3 grams of deca solo. He advocates that the level of conversion to estrogen becomes sufficient at 500mg nandrolone + with no sides. He also advocates stacking with DHT’s for the relevant compounds effects such as hardening (21, 22, 23). Solo Deca cycles at 3 grams with no deca dick and no estrogen or prolactin issues??
   But… it’s not just the TRT, Steroids and Abusers that say this is possible, a study of bodybuilders showed nandrolone doses of 500 and 600mg/wk and nandrolone 600mg/wk coupled with Anadrol at 100mg/wk caused no rise in prolactin (24). Calleja et al’s study of bodybuilders stacking nandrolone with various orals such as primobol, anadrol and dianabol showed no increases in prolactin, but a decrease in prolactin with a cycle using dianabol (25)

We still cannot ignore the negatives of AAS use. Studies in rats (rats have similar hormone systems to humans) have shown testosterone to be more damaging to the prostate, but nandrolone at super high doses 7.5mg/kg is more damaging to pelvic muscles. This sheds light that nandrolone does impact various receptors beyond the AR and Estro receptors, that higher doses correlate somewhat with higher sides and levels of damage, test vs. daca are interchangeable. Interestingly though, deca increases seminal vesicles more than test (26, 27, 28). But no mention of prolactin! None!

Bloody hell!

So what’s happening to the eroids crew with high prolactin?
A thorough review of posted lab test images was conducted using results from a 3 page google search. Each return was reviewed; on eroids members who posted bloodwork relating to prolactin. This covered 5/6 years of bloods listed (but not discussion in forums). The search was conducted to try to find images of real test lab results. The simple search string used was: site:eroids.com inurl:pics prolactin high -inurl:caber .
There is no evidence found whatsoever of a 19-nor elevating prolactin, and only correlations between 19-nors and prolactin within high testosterone and high estrogen cycles. HCG was also correlated with high estrogen and high testosterone. All, bar 1, cases of high prolactin are correlated with high testosterone and high estrogen, with several being *testosterone only cycles. All cases of low prolactin in these results were due to the misuse of caber. There was one high prolactin case due to a pituitary tumour (26).
A second search of the entire eroids site, using the search string: “site:eroids.com ("high prolactin" OR "prolactin is") AND (tren OR trenbolone OR deca OR NPP OR nandrolone)” resulted in a mere 235 results ONLY. 74 of these results pages contained one or more of the words FEAR OR WORRIED OR SCARED. There is a clear theme within page after page of tboth sets of results where people discuss prolactin and how to control it. There is a clear presumption that tren and deca cause prolactin to raise and when an individual states the cause might be something other than a 19-nor they are rubbished.
Within both sets of results, there is no evidence whatsoever of a 19-nor elevating prolactin.

Okayyyy, well what about my beloved testosterone??

For years we have been told 19-nor’s raise prolactin and we MUST use the essential Testosterone as a base. What the hell is the truth? Well, the facts are:
(1) Testosterone aromatises to estrogen
(2) Estrogen regulates prolactin
(3) Anything that interacts with the estrogen receptor can regulate prolactin
(4) HGH interacts with the Estrogen Receptor and influences prolactin
(5) The Thyroid system regulates prolactin
(6) Deca aromatises at a rate of 20% that of testosterone and can therefore interact at a lower rate than testosterone, with the estrogen receptor, and this estrogen CAN regulate prolactin (switch from test to 19-nor and you have lower estrogen and no need for an ai or prolactin issues and then no need for caber/prami? – how much money, trouble, time and health issues would this save us??????????????)

Testing testing, 1,2… test-free??!

According to former Arnold Era professional bodybuilder Ric Drasin, bodybuilders in the 60’s used only Dianabol (D’bol aka 17α-methylated derivative of testosterone) (11). In the 80's tests using D’bol, nandrolone (19-nor) and Mepitiostane (DHT), "an orally active steroidal antiestrogen and anabolic-androgenic steroid of the dihydrotestosterone group" showed no changes to prolactin(12). However, D’bol (17α-methylated derivative of testosterone)actually is proven to lower prolactin (13). Other studies of different esters of nandrolone including decanoate and NPP show no changes with prolactin whatsoever(14, 15). In animal studies with trenbolone acetate using a 150mg dose there is no increase in prolactin (16). So, both studies and AAS Bodybuilding cycles without testosterone has been in existence for many moons.

There is no known/observed mechanism by which a 19-nor has interacted directly with prolactin based on 60 years of therapy/research/trials

Yeah testo……..but, uh oh….. guess what…… OH SNAP…Testosterone IS NOT testosterone

Synthetic testosterone is NOT the same as endogenous testo and “synthetic hormones are not created structurally the same as human endogenous hormones, which often leads uncomfortable side effects.” (29, 30, 31). Big Pharma sells both bioidentical and non-bioidentical hormones – TRT lads should get doctors to ensure they are prescribing bioidentical to reduce sides, which they mostlikely already are. So the question is; what is UGL testosterone made from? Is it bioidentical? If not, is it responsible for oh so many sides not always seen as severly? Regardless, big doses of either leads to big estro conversion. Are phytosterols/estrogens correctly removed from the precursors as done by big pharma (32, 83)

So how is this pseudo-testosterone made?

Much big pharma is synthetic yet bioidentical and behaves exactly like the real thing as far as we know (83). But, not all big pharma testo is made this way (WARNING!). Much Pharma and UGL testosterone is made from Soybean (and Yam) plant derivatives. They are made from substances derived from these plants, called Phytosterols, which are in fact Phytoestrogens: (33). Fish studies showed significant estrogenic activity of two phytosterol preparations. To confirm, several manufacturers of Androstenedione were contacted. To date only one has responded and confirmed by email: "We supply Androstenedione, its from the fermentation of phytosterol" (85).

Phytoestrogens, as we are all becoming aware, are very similar structurally to both testosterone and to estrogen, are estrogenic and are similar to testosterone in terms of chemical structure, and bind to estrogen receptors. They also increase SHBG. The strongest phytoestrogens are the phytosterols which are used to make many testosterones as we now know, by using microbacteria, similar to gut bacteria to ferment these estrogens into precursor materials to make testosterone from. So, future research should look to the production of some exogenous testosterones from phytosterols and whether it retains it’s estrogenic nature and/or if it is easier to convert to estrogen via enzymes/acids like (but not limited to) aromatase and 5alpha reductase or other proteins/acids etc etc. This is all speculation, but a brighter mind might be able to shed more light on this because we all know there is a big difference between how endog and exog testo behave in the body (34), particularly when we include supraphysiological doses. Furthermore, it is likely an analysis of UGL products would need to be carried out to test the level of phytoestrogen NOT filtered from the finished product to ascertain the degree to which they may or may not be affecting the body during the proccess of synthesising testosterone from precursors. It is clear that companies such as Pfizer have excellent processes in place..... but what about the UGL's sources for precursors?(83).

So, it seems it is important to understand how these things work
Androgen receptor: The hormone, or synthetic hormone that binds to a receptor does so by a lock and key method (68). Once bound through various mechanisms the combo of the receptor and hormone travel/send messages to the specific cells they are contained within. E.g. in muscle cells testo bound to the AR will message the cell to go ahead and synthesise protein and store glycogen within the cell (35, 36, 18)
This is also true to Estrogen Receptors, and Prolactin Receptors. Prolactin receptors can also be activated by Growth Hormone which can lead to gynecomastia (37, 38). But guess what… the thyroid system also stimulates prolactin (as do tumours such as prolactinoma, see bloods review below (39).
BUT who is the organ grinder, and who is the monkey?!
It is important to note that it is the bound product that causes signalling, NOT the hormone. The implication is that anything that binds to and activates the receptor can replace the natural hormone at that site/in that cell. Following this revelation we know steroids that bind to the AR can replace testosterone there, but need to account for estrogen balance, androgenic traits, anabolic traits etc. The 19-nors have the highest binding affinity to the AR’s (78) and are more potent than testosterone, but when they convert during 5alpha processes do not maintain the androgenic potency which reduces concern for things like prostate hair growth (women) etc. (40). The list of binding affinity relating to testo is as follows: methyltrienolone>nandrolone>methenolone>testosterone>mesterolone. The infamous "duchess" cocktail administered to Russian athletes at the Sochi Winter Olympics consisted of oxandrolone, metenolone, and trenbolone (41).
So it seems that there are stronger exogenous steroids that can fulfil the duty of exog testo and act as the key to the AR. However, it is not yet fully understood to what extent an anabolic steroid (including non-bioidentical testosterone) expresses in ALL cells as exogenous testosterone does (42) . Furthermore, hormones act in unison to achieve certain outcomes such as sexual desire/libido etc. (43, 44). So estrogen is also important and possibly progesterone (although 19-nors are progestins and therefore can act as weak progesterones) but not why you think. Progesterone in fact acts as an anti-estrogen and therefore can inhibit estrogen stimulated prolactin. 19-nors being progestins, could have an anti-prolactin effect. In men, low estrogen/high estrogen can lead to erectile dysfunction commonly called deca dick. So a balance is needed, perhaps not a traditional test to estro ratio, but we would need to see estrogen levels within a range to prevent ED problems. There are other hormones involved (Oxytocin and vasopressin) but they are beyond this particular study. It is also important to note that nandrolone has been used as a therapy for aids muscle wasting for years without any reports of adverse effects on libido and only positive increases in sense of wellbeing and sexual function. (44, 45, 46, 47, 48)

But what about the little general? (no homo)

On Sex… Do we actually NEED estrogen?
Yes. We know that low estrogen and high estrogen can cause libido issues, independent of high testo, but it has been reported that even just taking supplements to lower estro can cause a range of health issues (49). It appears that despite there being much talk of a test-estro ration, it’s merely a marker and more important is the estrogen level within range. So…. This raises the question: at baseline, what is to be considered a normal baseline?
The ratio itself, is only a marker. It appears from TRT use research, as well as youtubers like Dr. Rand McClain and TRT forums such as Peak Testosterone, that 20-40 pg/ml is a reasonable level for estrogen, regardless of normal to high testosterone level in the various so-called ranges (50). Estrogens are involved in sex drive in both women and men (45) but what about 19-nors (Deca Dick?)… Nandralone and ED ?.... No literature shows a correlation and anything in HIV/Aids research shows positive sexual function. 19nors/Deca/Tren most often used in clinical environment and in therapies when anabolic effects are desired such as with cachexia. They include the nandrolone esters and trenbolone (51). In fact, since the 1950’s 19-nors have been used in therapy for ailemts such as: Osteoperosis, then anaemia, then significantly in HIV/AIDS/Muscle wasting related diseases but also recently in HRT/Androgen Therapy (52, 79, 81) where Deca has been used in combination with very low dose testosterone for HIV/Aids patients suffering from Low Testosterone. Nelson Vergel admits to using low dose Testosterone with Nandrolone Decanoate for 10 years straight without any prolactin issues or ai.

Yeah but 19-nor’s shut you down HARRRRRD, don’t they?
Ok, so we can see that we need to focus on Nandrolone, due to the prevalence of study. Deca suppression is almost identical to that of testosterone. What? Yep. Nandrolone shutdown is the same as test give or take a couple of days. In terms of it’s esters; Slower/longest with deca, fastest/shortest with npp (53, 54). LH/FSH will rebound in the same way as with testo. But even the most learned gentlemen have not seen any evidence of the 19-nor ED concern (9).

However - it is important to note that ED is still a big concern, as an absence is not necessarily evidence of absence

In other words, more research/experiment is needed, and with both estrogen and prolactin in mind.

Let’s get real here. Has anyone actually really studied a 19-nor ALONE in BODYBUILDERS?

Yep, at supraphysiological doses and in bodybuilders. The dose was 600 mg nandrolone decanoate only for 12 weeks. They used resistance weight training with progression, reps within the hypertrophy range and end to failure. This resulted in greater LBM for nandrolone versus placebo increased fat loss and increased strength. There was no caloric surplus, total cholesterol and triglycerides reduced… BOOM! There were no reports of negatives on libido or health just improvements in feeling of well being KAPOW! The researcher also noted the strong possibility increases in connective tissues (beneficial for us as a part of LBM increases) (9). This is all aside the FACT that Nandrolone doesnt greatly convert to estro (55, 56) and will not create prolactin problems.
Yeah but….. Can a 19-nor actually REPLACE testosterone?
YES!!! In one study of 303 people they compared nandrolone decanoate with placebo and testosterone to see which is most effective for weight loss prevent in aids. Doses were nandrolone decanoate (150 mg), testosterone (250 mg) or placebo intramuscularly every 2 weeks for 12 weeks. Nandrolone won the race where the "perception of benefit was significantly greater in the nandrolone group when compared with both the placebo and the testosterone groups" and dverse effects are rare and primarily happened in the testosterone group (57). In fact it’s been done for years now; QUOTE: Howard Grossman, a New York City physician with a big HIV/AIDS oriented medical practice. "We use nandrolone extensively in patients who have testosterone deficiency and are also losing weight. We've seen better weight gain than with testosterone alone and more accumulation of muscle mass. People feel better. I haven't found any increase in side effects” (58, 79, 81, 82). Holy $4!t!!!

This is pretty serious

Nandrolone is an existing solo therapy that does not cause prolactin problems, ED, Gyno, water retention and is clearly noted to be better than HGH all while being exceptional for nitrogen retention, fat loss, strength and lbm gains, lowering cholestorol /bad lipid values and improving quality of life, increasing insulin sensitivity and glucose disposal. Wow! (59, 60, 61).

It gets better!.....

If you double the dose, you double the lean weight gains

This trend is visible across multiple independent studies. (62, 63, 64, 65). The pharmacokinetics are very similar to testosterone e. Suppression from exog steroids can be difficult to measure although there are tools to do so. Looking at FSH LH time to baseline, it is circa 10-14 days. Endogenous Test then follows. Looking at NPP it can be 10 days for test to return to normal and 14 days for Deca. Therefore, test and deca are in fact very, very similar in terms of how suppressive they are to natural testosterone production. This is significant.

Soooooooooo…….. logically…… we need an experiment to really, REALLY prove this, or otherwise…. Right?
In cinemas near you… part 3, the experiment!

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