ChemBB
Member
I think I tried to order through their website, where it gives you a contact form to fill out post-order, and nobody ever got back to me.
In hindsight, probably should have used the Telegram.
MESO-Rx
Anabolic Steroids
Trest E/D sources?
- Thread starter ChemBB
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- ment trest trestolone
In hindsight, probably should have used the Telegram.
nutcase6174
Member
So i reached out to a few of these companies and here's what I gathered so far.
From steroid-peptide.com, I emailed them and they got back super fast. They said:
We have COA report for each of them. The purity is about 98%.
The price is as follows:
100g Trestolone Decanoate:3100USD
100g Trestolone Enanthate:3100USD
Also, I reached out to this peptide vendor that the longevity folks are using called ERP. They said that right now their production is not active but next week they can quote me for FINISHED MCT OIL Trest decanoate. The only catch is that they have an MOQ of 50 kits of 10 vials (500 total). Ill let you guys know how much they want for that.
It seems like we do have some options now. Perhaps we could convince a UGL to make a move? Even on other forums people have been looking for long ester trest every since the research chem sites went down. Huge potential market and they'd be the only domestic seller across the space to offer it.
Photon
Member
Personally i would not expect high purity on those, just fyi.
Trest is not very popular, people buy to try...that's about it lol.
nutcase6174
Member
Really? I never understood the trest hate. But to be fair, I am a super low aromatizer. Ive ran 25mg/day trest with 50mg/day dbol, 2000IU HCG/week and zero AI's with no gyno, acne, etc. Just slightly a bit puffy in the mid section but not even on the face.
In my case, trest is literally perfect (and it actually is hair safe. Ive been regrowing my temples with it, since I dont run Test and I run dutasteride for the hcg). High test gives me shedding, fever-type symptoms, and I get fatigued for a bit at the beginning of a cycle so ive moved away from it.
But yeah i guess im kind of an outlier in terms of the estrogen response. Ive heard people start getting gyno in a week.
Banana Joe
Member
Ouch, that is twice the price of Primo.
Do you have anything to read up on? This is the first time I hear about Trest being hairsafe.
Photon
Member
no hate lol
but sides rather
bp
bloat
gyno
hard to dial in e2 (doesn't show up on test reports)
cost
might need ai or more pct/pharma meds
i just finished up my last bit of Trest D from AA. As much as i like it, i never know what my actual E2 is. I don't quite like basing stuff off "feels".
bigdaddyandfriends
Member
What I’ve learned is that feels are highly dependent on DHT levels. Those with high DHT can tolerate much higher E2 levels without symptoms. Those with lower DHT levels - like me after 25 years of finasteride use and using only HRT/TRT test, are very sensitive to E2 much over 30. First thing that goes is morning wood, then libido and ED, excess emotionality like getting chocked up nearly to tears from watching videos or listening to music, even thinking about certain things. Also water retention with weight gain / bloating.
Of course DHT can be raised by taking more test, but that will increase E2 further. Unless you can get dialed in with an AI, which is not so easy with Aromasin and particularly anastrozole, where both UGL and pharma pills are almost always made at breast cancer therapeutic levels ie 25mg / 1 mg. Why UGLs catering to men using AAS don’t make smaller doses available idk.
Trest is actually hair safe at low dosages. I’ve regrown some hair on my crown and temples since using it. At high doses, it is a potent enough androgen (more so than DHT in fact) but it is not locally converted in the prostate and skin appendages so levels in those locations tend to be far lower than DHT from test.
Compared to test, mg for mg:
About 2x estrogenic
About 10-15x anabolic
About 5x androgenic
I don’t use more than 5mg/day with test, but have used up to 25mg/day without test. Those using 50-100mg/day with or without test- expect all sorts of problems.
Test isn’t needed with trestolone. However there are metabolites of DHT in the brain rhat are not unimportant - having done it both ways, I do feel better better with 70-140mg test and 17.5-35mg trest per week than either by itself at higher dosage.
Treat is also progesterogenic - maybe more so than tren - so higher doses starting causing those issue too, ie hyperprolactinemia symptoms (typically without hyperprolactinemia in blood work, so via sensitization/upregulation of PLR) and anorgasmia. Libido can go either way - excessive to absent, depending on the individual.
nutcase6174
Member
So with hair safety, I have to say a few things.
AGA: This is what causes male pattern baldness. It is when the follicles get miniaturized and permanently (at least for the most part with current technology) get thinner and thinner.
When people say something made them start shedding in a few weeks, that is not AGA. That rapid of a response is far too fast and acute for it to be genuine follicle miniturization and death.
Shedding/TE: This is what happens due to rapid changes in your environment/stress levels. This can happen as a result of tragic emotional distress, weight loss, medication changes, etc. The key difference here is that it starts all at once and is a TON of hair being shed. Not a gradual process of thinning. It also is not localized to any particular region usually, so your hair all across your head or in random patches will get thinner.
You could almost go bald within a few months and it would grow back to normal once the body adjusted to the stress or the environment changed. This is not what AGA is at all.
Issues with adding Testosterone to a cycle
The persistent addition of testosterone to all steroid cycles in the modern era is what i believe causes all the permanent hair loss (AGA) from steroids.
Testosterone converts to DHT. Even with dutasteride/finasteride, small amount of it still get converted. Additionally, people often site the serum decreases in DHT but that's largely irrelevant for AGA. IIRC Dut only decreases scalp DHT by 70% at the high end.
Adding high enough doses of test will eventually cause enough to convert to DHT to cause AGA.
DHT is the only thing confirmed to cause AGA
We know from studies on men without 5AR due to genetic disorders that they have 0 incidence of AGA. Also, they tend to have higher levels of testosterone since none of it converts to DHT.
This is why we know that testosterone itself actually does not cause AGA, despite people like moreplatesmoredates pushing this rumor that test can actually cause AGA too.
If you look at the transcription activity of DHT and Testosterone when they bind to the androgen receptor, they have a ton of differences.
People assume that because a compound is 'androgenic' and strongly binds to the androgen receptor, that this will result in the same transcription. But this idea is completely false. There will be overlap, but just because it is the same receptor does not mean it does the same thing.
If the other compounds don't actually cause AGA, why do they cause me to shed?
Simple. First, any shift in anything you take, medications, diet, etc has the chance to cause shedding. Obviously going from natty/trt levels and quadrupling the amount of hormones in your body will cause shedding in some people, just like how it causes acne in others.
19-nors:
tend to drive up prolactin which itself causes hair loss, but not AGA.
Using an AI OR AI-effect compounds like primo and EQ:
Crashes E2 and causes shedding, and E2 is critical for extending the growth phase of hair follicles as well as counteracting DHT effects on the follicle.
Extremely prolonged use of liver-toxic compounds:
If you're cooking your liver and basically feel like dying, I think this one is common sense.
High doses of anything:
High enough doses of any compound will cause a (temporary probably, but better not to find out the hard way) shed due to the shock of having such a rapid shift in hormones.
But xyz did make my hair permanently thinner:
SHBG crashing compounds:
Less SHBG = More free test. More free test converts to DHT at a higher rate in the scalp. Hence, AGA.
Stacking with compounds with high androgen receptor affinity:
These would theoretically occupy more of the androgen receptors in the body that testosterone would be able to bind to, kicking it back into circulation where it would be more suceptible to 5AR conversion into DHT
Real world evidence:
When you look at the cycles guys ran back in the day of just Deca, Primo, Dbol, very few of them had slick heads. I believe the primary cause is that they literally had essentially zero DHT in their body.
If we think about it, they were not running HCG or TRT doses. They had essentially no testosterone in their body, and hence essentially zero DHT. And this would be even more safe than taking dut/fin since as I mentioned before, those aren't as effective at reducing scalp DHT as they are at serum DHT.
What would be the most hair safe then?
In theory, anything without testosterone OR HCG. Even HCG will provide testosterone that could be converted to DHT at a higher rate due to the other compounds in the mix.
Aromatizing compounds as a base for estrogen like Trestolone, Deca/NPP, Dbol would work, or even any anabolic with exogenous estrogen administration.
I'd be curious if someone would run a Tren/Estrogen cycle to test out this hypothesis.
This is just a collection of my thoughts but I've been meaning to write this all down at some point.
AlexDavis43
Member
Not trest hate imo, but the only reason I ordered a kit was to see how I responded personally (specifically regarding muscle gainz)... which was *meh* so I never got it again... no hate, just not a keeper for me
bigdaddyandfriends
Member
Very well said
It’s the high local concentrations of potentiated androgens (eg DHT) that cause male pattern baldness. High systemic levels of similarly potent androgens like tren/trest/DHB could eventually cause it, too; there is nothing specific to DHT other than the extremely high concentrations in tissues highly expressing 5α-reductive (type I mostly, in skin appendages including hair follicles).
Best bet is to keep DHT levels in check by limiting test/HCG, not having excessive free test at lower doses by displacing it all off SHBG, and using an effective topical anti-androgen like RU-58841 - that blocks everything at the follicle, not just DHT. It’s similar to Casodex/bicalutamide, used for androgen deprivation therapy in prostate CA patients, but topical so effects largely limited to scalp. Spillover always occurs but it’s not significant in enhanced individuals.
This is why I use low dose test + trestolone, rather than more typical levels of test. And use RU-58841. The spray I made also has finasteride and minoxidil but they have a more limited effect, finasteride is a type II 5αR which has limited effect in the scalp, duta is a dual type I/II so more effective, but is less suited to topical administration. I did get results from 25 years of 0.5-1mg/day fina, so it does still have an effect.
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nutcase6174
Member
A key point that I don't think is talked about is one that I mentioned:
Just because something binds strongly to androgen receptors / offers typical 'androgenic' effects like aggression, libido, dryness, etc. doesn't mean it will have the same transcriptional activity as DHT.
Testosterone and DHT are literally two molecules different than each other, yet those two molecules cause DHT to have basically neglible activity for anabolism while testosterone is among the best we have available for tissue gain.
But those two molecules also COMPLETELY disarm testosterone as a threat to hair follicles.
Now if just that small change causes such a vast difference in transcriptional activity, you can imagine how much of a difference that compounds with 4, 5, or 6+ modifications would have.
Just from a probability perspective, its highly unlikely that things like 19-nors which are far more different from DHT than testosterone is would somehow also cause the same activity that DHT does in the scalp, especially given how unique DHT is in terms of that specific effect.
The fact of the matter is we have zero evidence in either direction, and every single person who has gone permanently bald (not just shedding) from AGA as a consequence blasting also were using testosterone.
nutcase6174
Member
Fair, Primo and Test Prop is like that for me. Ive tried multiple different suppliers but for some reason I get horrible PIP and sick feeling. But they seem to be the hottest stuff nowadays.
bigdaddyandfriends
Member
Only reason DHT is not anabolic is there is an enzyme in skeletal muscle that quickly breaks it down - 3α-HSD. That’s why DHT (and DHB) derivatives with high anabolic:androgenic ratios exist, they are mostly attenuated androgens but resist that degradation in skeletal muscle, so typically have less androgenicity than DHT and much more anabolism.
Primo is a DHB derivative, the c1 methylation is basically useless other than increasing oral bioavailability for acetate tabs, but the Δ1 AAS are all resistant to 3α-HSD to some degree - much more so with C2 modification ie methyl group (stenbolone from DHB, masteron from DHT), C>O substitution (anavar), or pyrazole ring addition (winstrol).
A 3α-HSD inhibitor would be quite interesting. But I would think it would have other unwanted effects.
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nutcase6174
Member
DHT is not anabolic purely because of 3a-HSD. It has fundamentally varied transcriptional activity from testosterone as shown in this in vitro study:
Modulation of androgen receptor activation function 2 by testosterone and dihydrotestosterone - PubMed
The androgen receptor (AR) is transcriptionally activated by high affinity binding of testosterone (T) or its 5alpha-reduced metabolite, dihydrotestosterone (DHT), a more potent androgen required for male reproductive tract development. The molecular basis for the weaker activity of T was...
pubmed.ncbi.nlm.nih.gov
Now I am not saying the 3a-HSD doesn't play a role. But 3α-HSD also acts as a backdoor pathway to synthesize DHT as well, in fact IIRC the preferred direction in the reaction is from from one of the androgen neurosteroids into DHT.
Also, clearly even the c1 methylation in Primo is not 'useless'. Otherwise, DHB and Primo wouldn't have such different effects. Primo literally has metabolites that act as AI's that are absent from DHB.
Even small modifications of these compounds, while they might seem small and for other reasons, can and usually will cause drastic differences in the actual effects they have.
bigdaddyandfriends
Member
Thanks for posting that article. It is interesting and it’s interactions with cofactors likely explains some of the antiestrogenic effects of DHT and its derivatives.
What hasn’t been studied much if at all is the transactivation of other highly potent synthetic androgens ie ment, tren, and DHB. They probably do similar things but local vs systemic concentrations will be very disparate.
3α-ΗSD has at least four subtypes found in different tissues. One in skeletal muscle removes the 3-hydroxyl group and can then pass it on to the back door pathway for DHT and neurosteroids like 3α-done in the brain.
Primo remains a bit of a mystery to me. I am immune to or do not produce the Ai metabolite. I’ve run it 2x my test and no effect. One metabolite it doesn’t produce, except in fungi, is atamestane. Majority of metabolites are 3α-degradation products so it’s partially susceptible to that enzyme. But different people likely produce different metabolites in different amounts. I suppose it takes is for one of them to be ligand for aromatase with a long dissociation time for it to have an AI effect. The non-competitive steroidal AIs all share the same Δ1 & Δ4 A-ring feature, which boldenone has, primo does not. I’m currently testing boldenone to see if it affects my estradiol.
The c1 methylation does significantly weaken the androgen - if you’ve ever used DHB it is very apparent. Maybe that is why it considered relatively side effect free. But I saw far more results running DHB @ 105mg/wk then Primo at 3x that for several months. Other than that feature, they are interestingly molecularly identical, as is stenbolone with c2 rather than c1 methylation. I did not have any issues running low dose DHB (from DutchParmaUS, a source on another board), taking a break because of its purported toxicity but will definitely use it again. Only thing I noticed from it was a lot of extra strength and a fuller/harder look without gaining weight.
What hasn’t been studied much if at all is the transactivation of other highly potent synthetic androgens ie ment, tren, and DHB. They probably do similar things but local vs systemic concentrations will be very disparate.
3α-ΗSD has at least four subtypes found in different tissues. One in skeletal muscle removes the 3-hydroxyl group and can then pass it on to the back door pathway for DHT and neurosteroids like 3α-done in the brain.
Primo remains a bit of a mystery to me. I am immune to or do not produce the Ai metabolite. I’ve run it 2x my test and no effect. One metabolite it doesn’t produce, except in fungi, is atamestane. Majority of metabolites are 3α-degradation products so it’s partially susceptible to that enzyme. But different people likely produce different metabolites in different amounts. I suppose it takes is for one of them to be ligand for aromatase with a long dissociation time for it to have an AI effect. The non-competitive steroidal AIs all share the same Δ1 & Δ4 A-ring feature, which boldenone has, primo does not. I’m currently testing boldenone to see if it affects my estradiol.
The c1 methylation does significantly weaken the androgen - if you’ve ever used DHB it is very apparent. Maybe that is why it considered relatively side effect free. But I saw far more results running DHB @ 105mg/wk then Primo at 3x that for several months. Other than that feature, they are interestingly molecularly identical, as is stenbolone with c2 rather than c1 methylation. I did not have any issues running low dose DHB (from DutchParmaUS, a source on another board), taking a break because of its purported toxicity but will definitely use it again. Only thing I noticed from it was a lot of extra strength and a fuller/harder look without gaining weight.
LGOP528
Member
We need more of this! Order it, pin it, give unbiased individual response.
I enjoy nerding out on this stuff as much as the next guy but people’s response carry more weight to me.
LGOP528
Member
Interestingly, I have the opposite response to primo but the same response to DHB that you do. Primo turns me into an asshole within 2-3 days. It isn’t even enough time to crash my E2 so there has to be something else going on with a metabolite.
Were you eating in a surplus with DHB? Interesting that you didn’t gain weight. My cycle was cut short due to surgery. I wanted to save what I have for a bulk but maybe that isn’t the best use for it, if you were not gaining weight.
bigdaddyandfriends
Member
I generally stay in a slight deficit as I prefer to be lean and not trying to add much muscle @ 57 yo. Typically every 4-5 days I eat a little over maintenance. My diet is not typical bodybuilder, I limit carbs to about 100-150gm/day pre-, during- and post-workout most days; so it's inherently a higher fat diet (probably why my HDL stays decent on gear).
I've tried about everything and nothing put on strength as much or as fast as DHB - trestolone included. My weight didn't change significantly, but I added reps and or pounds to all my exercises and my abs looked noticeably better - my wife told me "you got a 8-10 pack". So it was definitely a recomp effect. So far it has not noticeably elevated liver enzymes, hs-CRP, or Hct during short cycles. And other than what it did to my strength and body, I noticed absolutely nothing from it re: mood, libido, sleep, etc. In my body it acts as a pure anabolic steroid.
I think DHB could be useful for a cut, recomp, or bulk - just depends on food intake really. More strength is a combination of nervous system stimulation and muscle growth, so more food probably would mean more muscle.
Primo at least up to 30mg/day (added to 30mg/day masteron) didn't seem to add anything or reduce my aromasin requirement, it just add mg to my perma-cycle; that may not seem like a lot, but it was double my test dose. I never tested it myself but my stash is all from Axle, Opti, Hunter (old stock when he was excellent), and APharma/P-Labs - all solid sources. And same thing every time. I have a bunch and will try it again at some point, but it just doesn't seem to have much effect in me at least at 210mg/wk, other than raising my Hct some. I know that's a low dose, but at my age I'm not wanting to do high mg cycles; I like to stay around 5mg/kg/wk total - part of the reason I like potent compounds. My mood has not been the greatest when running primo either, same thing with nandrolone, it doesn't agree with me. Everything else including MENT/tren and I am fine. I also would see more hair in the sink with primo than when not running it.
Masteron, I get all the typical effects - including some extra anabolism and my skin staying dry/thin and some gyno protection. And peeing every 2-3 hours starting at 4 a.m. and dropping 4-6 lbs of water overnight by 9-10 a.m. when I sleep in. Happens every time I run it, and still doing it at only about 140mg/wk right now. And it's not a prostate issue because my bladder is full every time. Gotten to the point where I basically sleepwalk to the bathroom and get back in bed and continue whatever dream I was in... but I like mast and will keep running it, otherwise only good effects from it. No hair loss; those claiming to lose hair running it I suspect are using higher test and the mast (like proviron) is increasing free test which can they be converted to DHT. I don't run very high doses, but when taken in sufficient quantity any androgen will probably cause some hair loss.
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LGOP528
Member
This is how I saw it too, just wanted to make sure!
I got a really good mental drive and thermogenic effect. My dose was 105 mg per week. I am excited to run a longer cycle but right now I am running a longer cycle of test/EQ/trest E.
Photon
Member
I ended up purchasing DHB because of all your DHB posts lol
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