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Testosterone + Nandrolone + Drostanolone is a Good Lean-Bulk Stack


#1

Hi guys, I’m new here, pharmacy student with some thoughts on AAS pharmacology to share with you.

Test:

  1. provides E2 and it’s anabolic effects
  2. reduction of SHBG (high affinity to the protein), CBG, TBG
  3. 11BHSD2 & 11-hydroxylase inhibition (excessive water retention even w/o E2)
  4. androgenic properties

Test is what I call a good compromise when we consider a bulking phase.

Nandrolone:

  1. slight E2 & estrone synthesis
  2. reduction of SHBG (however, has low affinity to the protein)
  3. increase of TBG
  4. partial agonist/antagonist to PR (slight increase of ER synthesis so elevated E2-related sides)
  5. doesn’t affect 11BHSD2 but probably inhibits 21-hydroxylase (decreased synthesis of corticosteroids) - if E2 in check, shouldn’t provide any significant water retention
  6. low androgenocity (DHN, more estrone, E2 from test and unfavorable androgenic/estrogenic ratio)

It seems that PR&ER-related sides from nandrolone comes only in an excess of E2 coming from testosterone aromatization (some amounts of estrone comes from nandrolone as well - E2 reservoir). Almost a perfect steroid with strong anabolic properties w/o much androgenocity and E2-related sides. Positive impact on joints probably comes from early peak of cortisol after a therapy is started, the effect disappear over chronic use.

Drostanolone:

  1. doesn’t convert to E2 obviously
  2. very potent affinity to SHBG (decreases this protein in a strong manner as well), lowers CBG and TBG
  3. no influence on MR and GR (no water retention) and it’s ligands related enzymes
  4. good androgen (better than on the paper)
  5. probably an aromatase inhibitor (no evidence for direct ER-antagonism)
  6. anabolic properties comes from AR stimulation and reduction of SHBG

Used instead of another ancillary drugs, in addition the drug delivers training aggression and strength which makes the process of hypertrophy phase a bit easier (and is very mild in an aspect of side effects). It helps to move retained water from wet compounds from SC space to muscle tissue.

The thing is to choose your dosages accordingly, more is not always better (remember about AR-desensitization and dimishing returns from massive AAS intake). Trenbolone would be a great addition to the cycle if you accept another sides from the compound.


#2

I really like this post!!

Many AAS do inhibit 11BHSD2 to some extent, fluoxymesteorone appears to be the most potent at doing so, which would explain why so many people develop hypertension on the drug.

Also the reduction in SHBG from testosterone (although testosterone plays a part) is more related to its 5a reduced metabolite dihydrotestosterone. DHT has a much higher binding affinity

Nandrolone is the perfect steroid in theory. However it’s effects on neurotransmitters (esp dopamine), and the effect it appears to have long term on the cardiovascular system (independent of binding to the AR in cardiac myocytes or changes in the lipid profile) is very concerning, that being said the research is done on rat models (who have different antioxidant, elimination and metabolic pathways) therefore it must be taken with a grain of salt. That being said there is a myriad of research on nandrolone in various animal models and certain in vitro studies with human cells that have made me very cautious about nandrolone. However it’s interesting what you noted about the joint pain reduction from nandrolone. I tried it once and it helped significantly, however I only tried it for a very short period of time (NPP for around 3-wks).

Drostanolone I am interested in though, I’m curious to hear you’re thoughts as to exactly just how androgenic it is, in relation to testosterone, mg for mg, is it more androgenic than straight testosterone, test has caused a lot of body hair growth for me (I’ve always been hairy for as long as I can remember, but it’s getting out of hand), and I’ve never even gone over 250mg/wk!

I can link a paper in which drostanolone was used to treat pubertal gynocomastia, I was under the opinion it didn’t directly decrease estrogen, it just decreased the effects of estrogen via competitive inhibition (similarly to SERMS, but different because it doesn’t mimick estrogen with regards to any other activities such as cholesterol metabolism)


#3

I’m glad that you’ve answered with such a valuable content.

Yes, fluoxymesterone is a potent 11BHSD2 inhibitor, in the end it’s a cortisol-like anabolic drug (C11 -OH), thanks for the study (it was previously speculated it’s a specific 11BHSD1 inhibitor so no bloating is observed with this “cutting” compound). It’s unique androgenocity probably eliminates excessive water retention from 11BHSD2 inhibition. However, I don’t like halogenated AAS, their metabolism is peculiary painful (and Halo is faked too often).

Yes, the reduction in SHBG from testosterone (not DHT) isn’t very important, but what’s important is it’s reduced bioavailability because of SHBG - that’s why DHT derivatives should be incorporated in most stacks (in this case and many another cases, e.g. for logical and economical reasons).

Nandrolone is a partial agonist (or antagonist, probably the latter) of PR, so it’s unique psychical side effects. PR stimulation leads to hypnotic and anti-anxiety effect known from medicines taken by insomniacs (r-GABA-A1 relationship?). Many users (including me, even at this moment) suffer from sleeplessness using higher nandrolone dosages, which agrees with the theory above - the problem is assigned to trenbolone as well (which is PR agonist, so better sleep should be achieved, the reverse is due to it’s AR potency, IMO). About nandrolone and the CV system - I haven’t any reliable source to confirm your fears (the plus is that low doses of nandrolone are enough to get the best from this anabolic AND rats are given sick amounts of AAS).

DHT derivatives are known to compete with no-DHT for active site of aromatase (or/and influences it’s synthesis), so lower aromatization is achieved (literature statement). Plus two studies:

https://www.ncbi.nlm.nih.gov/pubmed/28739284 (DHT inhibited aromatase transcription in fish)
https://www.ncbi.nlm.nih.gov/pubmed/12694114 (DHT as a competitive antagonist of the enzyme in granulosa cells)

Plus I’ve found some posts from people whose E2 level dropped significantly after drostanolone’s administration (I will confirm this in a week on my own).

DHT derivatives don’t have a chemical component to affect ER anyhow (drug chemistry).

Drostanolone’s androgenocity is lower than known from DHT (on a paper), but it’s actually similiar to testosterone’s (in reality). The thing is, it’s C2 methylated and 3HSD have some problems to metabolize it as fast as DHT - by this result it should be a bit more anabolic in muscle tissue than DHT (probably as anabolic as T which works just fine before it’s 5alfa-reduced) and definitely provides more AR-mediated side effects in prostate, hair follicles, CNS, etc., it’s users experiences just confirms that (AR-sides and libido increases dramatically).


#4

God has blessed us with another Drug angel. Now can you both speak in terms I can understand without having to google search every other word.


#5

It’s interesting you mention this, as in rats nandrolone has been found to increase synaptic currents interceded by GABBA receptors. (In a specific part of the hypothalamus, I forget, increases in GABBA mediated synaptic currents is associated with anxiolysis).

Well, not exactly, the human equivilant doses to what the rats are given usually equate to around 100-1000mg/wk, that being said rats may very well be a whole lot more sensitive to AAS than humans, what concentration of T does 10mg/kg get them up to, that’s a HED of around 120mg weekly for me. The equation for conversion in rats —ARROWPOINTINGTHISWAY

(couldn’t find the arrow symbol lol)

Is to multiply the dose by you’re weight in KG then divide by 6.2
Actually I’m certain rats are more sensitive to AAS given testosterone HED doses of like 70mg/wk cause cardiac enlargement and fibrosis in rats (normal, rats, not castrated ones either), such a dose wouldn’t affect a human negatively.

As to not having seen any literature as to what I’m afraid of

Aaaaaaaaaaaaaaa (although a concentration of nine micromolar is virtually impossible to obtain from injecting nandrolone, still it appears pound for pound to be more damaging), there’s a few others I’ll link later when I can find them

That being said this recent study has shown a potentially protective effect from ridiculous, ungodly amounts of vitamin E (hmmmm it won’t let me link the study) the name of the study is

Effect of Nandrolone on Rat Cardiac Muscle and the Possible Protective Role of Vitamin E : A Light & Electron Microscopic Study

The only reason I’d use nandrolone is for the joint benefits, however if the benefits aren’t chronic then I have no use for it, is mast is as androgenic as test I’ll just stick to test. It’s interesting you mention the component of drostanolone being unable to be broken down by the 3HSD, my question is, mesterolone is C1 methylated, yet it is extensively metabolised by the 3HSD and is therefore rendered useless in skeletal muscle tissue, why is this? I couldn’t figure out why this alteration couldn’t save it from the fiery depths of the 3HSD.

Not to mention the price, here it’s like 200 bucks for 50 10mg tabs (that may or may not be legit). Granted I pay 200$ for 3ml of pharm grade test sometimes so, it isn’t as if price is an issue for me however the price of halo would likely put many off.


#6

Yesterday I was in the supermarket and in the frozen food isle section I found these vegetable spring rolls, I can either oven bake or lightly pan fry them, given the pan frying is quicker I made myself some (along with various fruits, vegetables, duck and plain yoghurt) for dinner, and let me tell you these spring rolls were DELICIOUS!!! Theyre unhealthy but my god they’re amazing, I’m making myself like 15 for breakfast today. I just thought I’d share this because it’s so irrelevant and off topic that it’s funny that I’d share this random detail


#7

https://www.physiology.org/doi/full/10.1152/jn.2000.83.6.3299

AR stimulation in the brain by AAS in general induces r-GABA-A neurotransmission in the hypothalamus (which is a good target of the study for our needs here, because it regulates circadian rhythms). When juicing with testosterone derivatives people rarely complain about sleep disturbances. If they do, their E2 level is excessively raised, usually (increase in adrenergic & serotonin transmission).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462037/ (review of the literature)

Is this the paper you are talking about? Nandrolone as an anxiolytic agent, nothing new and nothing at all about it’s influence on sleep. However, it’s been said that ND has an inhibitory effect on preoptic area (NREM onset modulation). IMO still, ND’s negative impact on sleep is due to it’s PR partial antagonism (that agrees with PR physiology and satisfies me).

The result of Vit. E group - just LOL. It’s a pity this is the only such study.

It seems that vit. E in rats is a way to immortality.

https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2265.2006.02715.x

4 weeks in humans, no difference.

Cardiac hypertrophy, obviously.

Worsening of flow disturbances complications.


Cardiac hypertrophy, proinflammatory agent, ventricular fibrillation risk.

The thing is, obviously, that all AAS in an excess have the same negative influence on the CV system. I couldn’t find anything special about ND in this regard.

Drostanolone’s metabolism by 3HSD is difficult because of C2 -CH3 group.
Methenolone is metabolized slower than DHT as well, having additional C1 -CH3 and C1-C2 double bond.
Mesterolone, however, is very similiar in structure (C1 -CH3) to methenolone, but their A rings geometry is a bit different (slight ring bending by an electron cloud in Primo) which provides another properties of both compounds (still comparable). Provi is metabolised rather quickly.
Oxymetholone’s C2 =CH-OH specific substitution ensures high stability in 3HSD environment (T’s t1/2 is around 20 min, Anadrol’s t1/2 is about 8 h, partly because of that).

All major substrates for 3HSD are A-ring reduced without any substitution (v. quick 3HSD metabolism known from DHT or mestanolone). As you can see above, the bigger the change in the area of C2 (-CH3, double bond or =CH-OH), the bigger resistance to the enzyme.

I’m happy with you. After 6 months of cutting (1500 kcal at the end of the phase) I still just love my oatmeal with peanut butter, whole milk and huge amounts of spices, plus skyr (if you don’t know this yet, google it) with WPC in a separate bowl!


#8

Yeet, thank you, I was looking everywhere for that study but couldn’t find it!!! I’ll put it in my bookmarks now, that’s how I manage to referance all my studies, I just bookmark them so I don’t have to go searching for them lol.

Actually I’ve got more, not with nandrolone though, the one works with grape seed extract and boldenone induced cardiotoxicity.

Testosterone and garlic powder lessening cardiotoxicity (the full study is in a different language, do you speak persian? If so please translate it)

Yeah but an equivilent dose of vit E for humans would be for a 70kg human 4500mg/day, that sure as shit ain’t happening lol.

Thank you for the detailed response, I believe you have a lot of knowledge that you could pass down to me (yaaaaaaaaayyyyyyyyyy). You said you were a student studying pharmacy? Do you plan to go from pharmacy into medicine or work in the realm of pharmacy. I’m still in school, the reason I’m on here is complicated, but justifiable.

So, I have a question for you. AAS and heart rate, what impact should it have? I don’t fully understand the mechanism behind this one, however nervous system stimulation from androgens should theoretically increase HR right?

Recently I was having some issues with a very fast heart rate (wasn’t on anything other than a ton of dietary supps), so I stopped using the supps and two days later everything went back to normal, however yesterday I decided to do an experiment because I was curious as to get to the bottom of this once and for all. In the past (on TRT, not alone) I tried oxandrolone @25mg/day, it shot up my BP dramatically and gave me tachycardia, however I was still using a ton of dietary supps, so I took one tablet yesterday to see what impact it would have without the supps, today my HR in response to exercise and at rest post-exercise was marketedly elevated, my resting HR is typically around 55-60 however today it’s around 75! I was curious as to whether this could legitimately be from oxandrolone (and I’m just sensitive to the drug), or whether there’s a possibility my ox (which I hadn’t taken in many months, I have no use for it, I’m actually gonna throw out the remaining ox, I was originally trying it because I was curious) is tainted with a stimulant or beta 2 agonist or something. I mean it was ONE 25mg tablet, that can’t be a normal response. I’ve had an ECG done on me when I was born and about four months ago to rule out the possibility of any cardiac abnormalities, however I do think it’s strange the reaction I have to that particular drug and whatever is in some of my dietary supps. I may be ordering something to test whats in the var, but there’s no point in me really doing so as I don’t intend on using it due to the adverse affects I had the first time round. Either it’s that or natural heart rhythm variability (I have terrible anxiety, so I’m always anxious about something)

Also, in rats (male rats) small doses (however an equiv dose of nandrolone still causes detrimental changes in rat cardiac structure and function) of methenolone doesn’t appear to cause cardiac hypertrophy)

and for some (god knows what) reason, trenbolone in rats doesn’t appear to detrimentally affect cardiac function


#9

In general, because in hurry, AR stimulation upregulates beta-adrenergetic receptors (so lipolysis, increased BMR, FFA and glucose release to the blood) so HR should go up directly and indirectly, at least in the beginning of a cycle (biofeedbacks, SNS & PSNS regulation in long-term).

15-20 rise in HR isn’t so disturbing, take into account physical stimulation from AAS as well (especially in an acute manner, as mentioned). If you say you have a terrible anxiety, placebo effect can play an important role. My HR when on clen & tren (low effective doses) is elevated by 15-30 BPM for throughout the cycle, but I don’t feel any serious discomfort (LISS cardio seems to eliminate some complications).

And yes, tren is cool.


#10

Interesting, thank you for the response, I had a similar hypothesis (the beta adrenergetic receptor upregulation), I just wasn’t how much of an impact was normal, whether it was a chronic or acute thing etc. Yes, anxiety tends to control a lot of my life, it has gotten significantly worse over the past few years, as a youngster (say 12-13-14) I was very brash and impulsive, now I tend to meticulously plan out and think everything I do with great detail. My anxiety is what has curbed me from properly experimenting with AAS and really taking up bodybuilding (as in attempting to compete, using cycle doses etc, the highest dose I’ve ever used is 250mg/wk, my TRT is currently 140mg/wk but will bump to 200mg/wk as I tend to feel better on higher doses (also 200mg isn’t enough to get me above range based on my past bloods, 250mg shouldn’t get me much above 1200-1300 with free T 1.5x top of the range).

Trenbolone may be an amazing drug, however it’s something I intend to (this is just me personally, no judgement to anyone who thinks otherwise) stay far, faaaaaaar away from… forever. My contendors for experimentation later on are methenolone, (was thinking mast one day but ehhhh), mesterolone, mestanolone, higher dose (say 350mg/wk) testosterone. As you can see none of these (aside from test) are drugs commonly used to bulk up, they may be used in a stack to aid the lean bulking process like you mentioned earlier, as androgens (aside from mestanolone/DHT) tend to directly aid in fat burning via upregulation of adipocyte alpha 2-adrenoreceptors thus stimulating catecholamine induced lipolysis (https://www.ncbi.nlm.nih.gov/pubmed/7943287, https://www.ncbi.nlm.nih.gov/pubmed/2153523, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770848/) … also androgen receptors are present in adipose tissue, therefore a stronger androgen (in this case DHT or mestanolone) such as Fluoxymesterone should bind to them more efficiently than… a much weaker androgen like 4-chlorodehydromethyltestosterone. I’m more interested in the libido aspect and obviously gaining as much muscle mass as possible, however I’d prefer to do it in a way that is slightly safer than traditional use of high dose anabolics (although I’m willing to take some risk because bodybuilding has been a huge part of my life starting from a very young age), I don’t mind if it takes me 20-30 years to get where I want to be… as long as I’m able to get where I want to be, to me it’s a marathon, not a sprint. Granted I never intend to go above 400mg/wk (but I do intend to one day venture into that dosage territory)

I could be wrong, feel free to correct me, I’m just in the game here to learn. I think androgens also stimulate forsolkin induced lipolysis, however I’m unsure as to the mechanism on how that occurs, almost sure it’s related to androgen receptor specific binding though.

All I know is that we need to be eating entire garlics, downing a bottle of grape seed extract and ingesting over four grams of vitamin E everyday (just kidding)


#11

Hi gents, I can see some substantial chem knowledge here related to AAS. I’d be grateful if you could give your professional opinion on the use of NPP (nothig over the board) concomitantly with T by sy with a known history of depression and on long-term SSRI. (T in itself seems to be OK.)
Let’s now put aside the question what the purpose of use would be, and focus on the very question of safety in this case. Thx in advance!


#12

Well, I don’t want to talk about workouts and diet here, but while on low doses - sure, you can achieve a success in BB (even in natural federation, planning intelligently), but in a slower pace, and final effect won’t be as dramatic as on a heavy cycle. But the closer to physiology you are, the more important perfect training & diet routine would be.

Low doses are cool, but too low doses are as illogical as crazy AAS intake. AAS knowledge is power only if you still train like a beast (I mean, if your hypertrophy mesocycle comes in, mainly) and eat like a pedant. I know several idiots (and not because I’m the smartest guy, lol, but because of BS they speak with 100% confidence) who have no real idea what they’re doing, but because they do it with a real dedication for years, and even if 1/3 of their decisions are stupid as hell, it still leads to success in long term, so in competition.

I see you are an ambitious, intelligent guy, but if you want to compete in the future, you should give up your “almost risk-free” approach. I wouldn’t cycle on doses below 400 mg of TE (effective dose threshold sits at around 200-300 considering hypertrophy response) in the beginning (considering you are healthy) and I would increase doses and stack composition gradually during a career (at best during each cycle). That’s my approach I use myself with 100% satisfaction.

Forskohlii in real is useless (weak evidence & used myself several times), the mechanism is to stimulate adenylyl cyclase (more cAMP), but caffeine evidence is much better and there’s no doubt (PDE inhibition, more cAMP as well). More beta-adrenergic receptors from AAS plus more beta-agonists means more beta-adrenergic (coupled with Gs protein) stimulation what leads to increased cAMP level (PDE inhibitors & adenylyl cyclase stimulators increase final effect) = enhanced lipolysis.


#13

Given that I’m on TRT, I wouldn’t be able to make it into a natural federation (as they test for it and are against it here), I’m aware some cycle with short esters and do it in a smart way as to not get busted by figuring out when the drugs will be out of their system, however I can’t go off test, my natural T won’t recover because I have hypogonadism (seemingly a combination of primary+secondary, my LH and FSH were mid range after 6 months on TRT, but not elevated)

I may give up my “almost risk free” approach eventually, however for the next few years I’d like to see where low doses and good work ethic can get me, as a large part of bodybuilding is built around genetics. I’m very afraid of dying in my 20’s or 30’s suddenly from a lethal arrythmia brought on by AAS use, hence my predisposition towards low doses, I am healthy with regard to my cardiovascular health, lipids etc, (hell my BP is usually around 90/60), but given my past luck with health I can’t help but think I’d just have the worst luck possible and drop dead in my 20’s. I do have chronic joint and muscle pain that has eased off significantly (exercise seems to help) over the past year to the point where I am back into the swing of things (full on bodybuilding), it’s complicated and long to talk about so that’s the shortened sum of my history, hence why I’ve used nandrolone before. This " almost risk-free" approach of mine might not last forever, I feel as if I should accomplish something that impacts society in a positive way before I go out (my family history is excellent, I have a blood relative who lived to be over 100). I don’t know if I’ll be able to compete due to my joints though, I’ve taken nand for joints before (NPP at around 90mg/wk) and it was the shit, really helped my shoulders, knees, back, ankle (one has screws in it due to bad luck). I’m still very young with hopefully a full life ahead of me, and I don’t want to put myself at serious risk at dropping before I can reach my goals, granted I’m not sure if the risk is significant or not, there isn’t enough literature on the subject, and I believe a lot of who dies and who doesn’t boils down to how much people take (abuse vs extreme abuse), and genetics.


#14

If a doctor prescribed SSRI (fluoxetine?), 5HT deficiency symptoms were observed during medical consultation.


“Nandrolone decreased the firing rate of spontaneously active serotonergic neurons in the DRN while increasing the firing rate of noradrenergic neurons in the LC.”


“AAS treatment reduced levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex, reduced the expression of low-affinity glucocorticoid receptors in the hippocampus, and increased morning trough basal plasma corticosterone levels.”

All I’ve found about ND and neurotransmission and is worth our attention. Why the results you ask me. IMO it’s related to lack of E2 (only ND or stanazolol were used). E2 is known to potentiate adrenergic and 5HT neurotransmission, an excess in male of the hormone in presence of T leads to mania (almost a “reverse depression”). Proper E2 level in addition of adequate AR stimulation should help in depression treatment. The thing is, ND is a PR partial antagonist (as mentioned previously many times), so it could lead to an anxiety (dosage is the key).


#15

Nand has also been shown to reduce mRNA content in the D 1 dopamine receptor subtype (in rats) as well as the density of the overall dopamine receptors, hence earlier I said the effect of nand on dopamine is concerning, esp considering some report feeling a profound lack of interest in life and general activity that may or may not persist after nandrolone use (wears off eventually), although unrelated to seratonin, for someone struggling with depression, I’d think depleting dopamine would be risky would it not, as it could potentially compound problems (not to mention the issues with serotonin).

I will chime in and say I took nandrolone despite being on an SSRI (not stating which one as I’m a paranoid individual), I was aware of most of the potential risks, but wanted joint pain relief really badly, and if I think (nandrolone or pain meds) I’d pick nand hands down. My SSRI use isn’t for depression per se, it’s for reactive depression related to certain events in my life and anxiety, personally I think it’s innapropriately prescribed, doesn’t do much for my anxiety.

I’ll link the literature tommorow however I’m currently working on a project while typing this response, I have like 40 tabs up on the internet lol #multitasking.

So, if you don’t mind me asking @chemania, are you planning to become a pharmacist, doctor or something within the lines of that realm?


#16

I don’t really know what to do in the future. It’s just over a year to get a MS in Pharmacy. I’m a MS in Project Management already. I can work in a pharmacy, clinical trials or in pharma industry with my experience and knowledge. At first I’ll leave the country I live in (will move to UK or USA). I love science as much as to lift heavy and dieting. The thing is I won’t give up my passion for career in pharmacy, that’s for sure - just can’t live without sport (one year of a break in the past caused that it was the worse period of my life). Currently I consult some competitive BBs basing on my knowledge. It’d be awesome to do it in the future on professional level, who knows.


#17

Firstly, thx for the prompt and scientific reply. I really appreciate it.
TBH, I did some research myself, and found, among others, the adolescent rat one you quoted. My problem is this. Although I think my insight into physiology and endocrinology somewhat exceeds that of average Joe, I don’t have a medical degree. I’m comfortable with the most relevant hormones, the concept of receptors vs agonists and antagonists, etc., but when it comes to subtle analysis of what happens with this or that special receptor in the hippocampus vs prefontal cortex, etc., I have difficulty relating these to corresponding real-life phenomena.

As for the SSRI, yes, it is doc prescribed. Actually, it’s the same doc that approved of my idea to have my T levels checked when the SSRI proved to yield inconsistent results. It’s since then that I’ve been on TRT (and T4).
The SSRI is escilatopram, btw, and the official reason is PTSD.

So, I don’t think I’d want to mess with ND, but allegedly NPP is safer when used wisely. I’m trying a T-only light blast now, and am thinking about later blast(s). The combo in the title is one candidate, but triggering psychological issues that I seem to mostly have under control now is simply not worth it.

So, in conclusion, do you think NPP is a clear risk in my case if combined with double the amount T (say, 200 NPP & 400 T /w) and minimal AI?


#18

Impressive! When you said you were a student I figured you were young like me (but about four years older, so 21-22), now I’d assume you’re in you’re mid to late twenties though. Wait I got confused, I thought MS was a master’s degree, is it? I’m confused

Have you competed before?


#19

A recent meta-analysis on PTSD pharmacotherapy (please consider changing the medicine):
https://onlinelibrary.wiley.com/doi/abs/10.1002/da.22511

I’m currently studying CNS pharmacology (started about 2 months ago, will take an exam in 1 month). To be honest, CNS diseases are so complicated that a chance to hit a proper drug is like playing a roulette. CNS drugs pharmacology is known only partialy, not to mention getting to know overall pathophysiology of a disease. That sucks, I know. Good psychiatrist is a man who will perfectly combine symptoms with a given drug, luck plays a big role, not certainty, unfortunately. That’s why I hate neuro-science.

I’m not a theorist - I personally got out of a depression, w/o any drugs. Self psychotherapy and patiency were the key on my example. I don’t say that SSRI are a bad thing, but in the end you’ll leave them, what then?

Nor-19 are known for weird mental sides. I’ve used trenbolone and nandrolone separately for few times. Contrary to most people experiences, trenbolone gives me a quite good sleep, while nandrolone makes me to wake up at 4 AM each day (5-6 h of total sleep, sometimes it’s hard, sometimes it’s highly practical), and other mental disturbances. Anyway, let’s assume all we know about nor-19 AAS is that they increase problems with CNS more than another compounds. You don’t want to worsen your problem, so just choose another compound.


#20

Thanks a lot, mate!

There’s another question that’s been keeping my brain busy. That’s the real, overall role of SHBG in men. (I guess the “it’s a baddie” idea is an oversimplification, but I struggle to grasp its true evolutionary/physiological role) It’s fully off-topic here, so I’m happy to take it offline, or to another thread, whatever rocks your boat. Cheers!