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Hi GameChanger; You have the wrong "Ontario" person named here. I am not involved in any of this. Please review further and correct as needed. OD

@GameChanger, here is a link to what you’re talking about https://thinksteroids.com/community/threads/titan-pharma-canadian-domestic-only.134394308/ and just so you can have all your facts straight, Ontario Dude and Onterrible are not the same person. And Onterrible is also a part of your community here. ...notice how Taureau don’t give a shit about you, can’t be arsed to waste time with even the mere mention of any of you or this place, but you can’t stop talking about him,...grasping at anything you can try to twist and put his name on... He’s owns real estate in your head ...let that sink in for a minute. Happy New Year fellas!

I'm hoping the mods dont remove my post because if they do then that means they are backing some lab . I wonder if most people are aware of costs of raws in comparison to finished product. I think all us members should know some truth because understanding costs will help all of us understand motives and agendas by labs and boards. Lets take test e for example:1kg is $1000 canadian. Standard 2.5 grams per vial if dose is 250mg. That's what?$2.50 per vial,add cost of oils/ba/bb/labels/vial. Lets say $6 . Now you will see some labs bashing other labs saying ours is better and more potent because it costs $60,oh! the $40 one is bunk and fake because its so cheap. Most end users are now under the influence of a placebo effect because we have been brainwashed by the bigger people to believe that if something is cheap it has to be fake. The amount of shit talking i have seen through labs and boards amazes me. I would suggest members to go on the big boards,there are tons of raw suppliers,the cost is listed openly. Stop falling for the its more expensive its more potent BS spewed out by the board owners and the labs they control. All they are doing is ripping us off and brainwashing us because they take us as fools and most of us are. Do some homework,get street smart. If my post does not get removed,i will post a raw cost list so members have some insight. If it gets removed,then i guess this board is full of politics aswell

If you have to worry about what your girlfriend, mom or wife will think you're not in the right spot in your life to use steroids. An oral only cycle will not put on 10lb of muscle. You'll put on 10lb easily and then deflate to where you were before or less than that within 4 weeks of stopping orals.

Figure we end the new years off with a bang. We have perfected our new oil formula and now received 6 test results from janoshik. Everything can back perfect as expected. Hopefully most members can now see the politics and crap from haters. We've always been honest, transparent and offered the most compassionate pricing and people used that as a reason to slander us but test results don't lie. To everyone who supported us through all the drama, thank you. You are the reason we did this. Because now we will be going private and not accepting new clients. We are only going to support the people who stood by us through thick and thin. Bt will forever strive to improve and innovate. We will be setting the new standard for ugl labs with our pharma style oils and tabs and exact dosages. God bless and happy holidays

Found this amazing article while doing some research on GH for myself. Great information for all GH users! T4 is a must after reading this in my humble opinion! Enjoy! ======================================================================== Thyroid Hormone + Growth Hormone – If You Aren’t Using T4 with Your GH, You’re Not Doing It Right July 23, 2006 By Anthony Roberts Quite some time ago, I wrote a book on Anabolics, and since then, I’ve received quite a bit of feedback on it. Some of the information contained in the book is based on the 50-60 profiles I completed for Steroid.com’s main page. As a result, I get feedback on certain portions of the book from people who have read them online. When someone takes the time to send an e-mail to Steroid.com or AnabolicBooks LLC, they’re screened, and eventually some of them make their way to my e-mail account. AnabolicBooks LLC is publisher- a little known fact is that my book is actually wasn’t edited by me, nor do I own the rights to any of it. When they forward an e-mail to me, I typically consider it very carefully, and reply to the original sender. If amendments or additions are useful for anything I’ve previously written (readers frequently send me recently published studies), I typically reply and thank the person for their help. This time, something odd happened. I was forwarded an e-mail from AnabolicBooks, and the reader seemed to know what he was talking about, but (I thought) mistaken about interactions between Growth Hormone and Thyroid medication. I took a look at the e-mail, and knew that I could quickly find a study that I had saved previously, to send to the reader, to verify that the claims in my work on GH were sound. In this particular case- James Daemon, PhD- was the reader, and was correct in his assessment of the interaction between thyroid hormone and Growth Hormone. And, in direct contradiction, so was I. Thyroid medication decreases the anabolic effect of Growth Hormone. And it increases it. Huh? There’re some leaps here, because research in some of the necessary areas is sketchy (or not done yet), but if you read the entirety of this article, you’ll learn how to get a significantly more gains from Growth Hormone, for pennies a day, by the addition of a readily available (and cheap) addition to it. And yeah, it’s a drug you can get anywhere on the ‘net, very easily. And no, it’s not a steroid. In fact, I’ll go so far as to say you’re throwing away a substantial portion of your gains from growth hormone if you are not using this drug with it. Ok…I’ll explain things a bit further. First, a brief explanation of Thyroid Hormone as well as Growth Hormone may be necessary. Your thyroid gland secretes two hormones that are going to be of primary importance in understanding Thyroid/GH interaction. The first is thyroxine (T4) and the second is triiodothyronine (T3). T3 is frequently considered the physiologically active hormone, and consequently the one on which most athletes and bodybuilders focus their energies on. T4, on the other hand, is converted in peripheral tissue into T3 by the enzymes in the deiodinase group, of which there are three types- the three iodothyronine deiodinase either catalyze the initiation (D1, D2) or termination (D3) of thyroid hormone effects. The majority of the body’s T3 (about 80%) comes from this conversion via the first two types of deiodinase, while conversion to an inactive state is accomplished by the third type. It’s important to note that not all of the body’s T4 is converted to T3, however- some remains unconverted. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in your hypothalamus. So, when T3 levels go up, TSH secretion is suppressed, due to the body’s self regulatory system known as the “negative feedback loop” . This is also the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. However, it should be noted that thyroid stimulating hormone (like all other hormones) can not work in a vacuum. TSH also requires the presence of Insulin or Insulin-like Growth Factor to stimulate thyroid function (1) When thyroid hormone is present without either insulin or IGF-1, it has no physiological effect (ibid). Most people think that T3 is just a physiologically active hormone that regulates bodyfat setpoint and has some minor anabolic effects, but in actuality, in some cases of delayed growth in children, T3 is actually too low, while GH levels are normal, and this has a growth limiting effect on several tissues (2) This could be due to T3’s ability to stimulate the proliferation of IGF-1 mRNA in many tissues (which would, of course, be anabolic), or it could be due to the synergistic effect T3 has on GH, specifically on regulation of the growth hormone gene. Although it is largely overlooked in the world of performance enhancement, regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes, which are influenced by T3 levels. (3) At this point, just to give you a better understanding of what’s going on, I think it’s prudent to also give a brief explanation of Growth Hormone (GH) as well. Your body’s GH is regulated by many internal factors, such as hormones and enzymes. hormones. A change in the level of your body’s GH output begins in the hypothalamus with somatostatin (SS) and growth hormone-releasing hormone (GHRH). Somatostatin exerts its effect at the pituitary to decrease GH output, while GHRH acts at the pituitary to increase GH output. Together these hormones regulate the level of GH you have in your body. In many cases, GH deficiency presents with a low level of T3, and normal T4(4). This is of course because conversion of T4-T3 is partially dependant on GH (and to some degree GH stimulated IGF-1), and it’s ability to stimulate that conversion process of T4 into T3. Interestingly, the hypothalamus isn’t the only place where SS is contained; the thyroid gland also contains Somatostatin-producing cells. This is of interest to us, because in the case of the thyroid, it’s been noted that certain hormones which were previously thought only to govern GH secretion can also influence thyroid hormone output as well. SS can directly act to inhibit TSH secretion or it may act on the hypothalamus to inhibit TRHsecretion. So when you add GH into your body from an outside source, you are triggering the body into releasing SS, because your body no longer needs to produce its own supply of GH…and unfortunately, the release of SS can also inhibit TSH, and therefore limit the amount of T4 your body produces. But that’s not the only interaction we see between the thyroid and Growth Hormone. As we learned in high-school Biology class, the body likes to maintain homeostasis, or “normal” operating conditions. This is the body’s version of the status quo, and it fights like hell to maintain the comfort of the status quo (much like moderators on most steroid discussion boards). What we see with thyroid/GH interplay is that physiological levels of circulating thyroid hormones are necessary to maintain normal pituitary GH secretion, due to their directly stimulatory actions. However, when serum concentrations of thyroid hormone increase above the normal range we see an increase in hypothalamic somatostatin action, which suppresses pituitary GH secretion and overrides any stimulatory effects that the thyroid hormone may have had on GH. The suppression of GH secretion by thyroid hormones is probably mediated at the hypothalamic level by a decrease in GHRH release(5). In addition, as IGF-I production isincreased in the hypothalamus after T3 administration and T3 may participate in IGF-1 mediated negative feedback of GH by triggeringeither increased somatostatin tone and/or decreased GHRH production (6). IGF, interestingly, has the ability to mediate some of T3’s effects independent of GH, but not to the same degree GH can (7.) In fact, IGF-I production isincreased in the hypothalamus after T3, administration it may plausibly participate in negative feedback by triggeringeither increased somatostatin tone and/or decreased GHRH production.So we know that GH lowers T4 (more about this in a sec), but an increase in T3 upregulates GH receptors (8) as well as IGF-1 receptors (9,10). As can be previously stated, and due to the ability of GH to convert inactive T4 into active T3, GH administration in healthy athletes shows us an entirely predicatble increase in mean free T3 (fT3), and a decrease in mean free T4 (fT4)levels.(11) Interaction between GH, IGF-I, T3, and GC. GH stimulates hepatic IGF-I secretion and local production of growth plate IGF-I, and exerts direct actions in the growth plate. Circulating T3 is derived from the thyroid gland and by enzymatic deiodination of T4 in liver and kidne.. The regulatory 5′-DI and 11ßHSD type 2 enzymes may also be expressed in chondrocytes to control local supplies of intracellular T3 and GC. Receptors for each hormone (GHR, IGF-IR, TR, GR) are expressed in growth plate chondrocytes. So, with the use of GH, what we see is an increased conversion of T4-T3, and possible inhibition of Thyroid Releasing Hormone by Somatostatin, and therefore even though T3 levels may rise, there is no increase in T4 (logically, we see a decrease). Now, as we’ve seen, GH is HIGHLY synergistic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body. As noted before, T3 enhances many effects of GH by several mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below: Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3) As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study which provided the graph above concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphysiological if we’re going to be using supraphysiological levels of GH, right? Otherwise, the GH we’re using is going to be limited by the amount of T3 our body produces. However, since we’re taking GH, and it is converting more T4 into T3, T4 levels are lowered substantially, and this is the problem with GH. and may actually be THE limiting factor on GH…if we assume that at least some of GH’s effects are enhanced by thyroid hormone, and specifically T3, then what we are looking at is the GH that has been injected is being limited by a lack of T3. But that doesn’t make sense, because if we use T3 + GH, we get a decrease in the anabolic effect of GH. This is where Mr. Daemon, who had contacted me via an e-mail to my publisher, about Thyroid + GH interaction, was able to shed some light on things. You see, I knew that it couldn’t just be the actual presence of enough T3 along with the GH that was limiting GH’s anabolic effect, because, simply adding T3 to a GH cycle will reduce the anabolic effect of the GH (12.). Originally, he had said to me that T3 was synergistic with GH, wheras I said that T3 actually reduced the anabolic effects of GH- now I realize we were both correct. Logically this presents a bit of a problem, which I believe can be solved. This came from reading several studies provided to me by Dr.Daemon. the trend I was seeing was that even when Growth Hormone therapy was used, T3 levels needed to be elevated in order to treat several conditions caused by a lack of natural growth hormone. And even if the patient was on GH, T3 levels still needed to be elevated. And what I noticed was that those levels were elevated successfully by using supplemental T4 but not T3. Here’s why I think this is: Additional T3 is not all that’s needed here. What’s needed is the actual conversion process of T4-T3, and the deiodinase presence and activity that it involves. This is because Local 5′-deiodination of l-thyroxine (T4) to active the thyroid hormone 3,3′,5-tri-iodothyronine (T3) is catalyzed by the two 5′-deiodinase enzymes (D1 and D2). These enzymes not only “create” T3 out of T4, but actually regulates various T(3)-dependent functions in many tissues including the anterior pituitary and liver. So when there is an excess of T3 in the body, but normal levels of T4, the body’s thyroid axis sends a negative feedback signal., and produces less (D1 and D2) deiodinase, but more of the D3 type, which signals the cessation of the T4-T3 conversion process, and is inhibitory of many of the synergistic effects that T3 has! Remember, Type 3 iodothyronine deiodinase (D3) is the physiologic INACTIVATOR of thyroid hormones and their effects (13)and is well known to have independent interaction with growth factors (which is what GH and IGF-1 are).(14) This is because with adequate T4 and excess T3, (D1 and D2) deiodinase is no longer needed for conversion of T4 into T3, but levels of D3 deiodinase will be elevated. When there is less of the first two types of deidinase, it would seem that the T3 which has been converted to T4 can not exert it’s protein sparing (anabolic effects), as those first two types are responsible for mediation of many of the effects T3 has on the body. This seems to be one of the ways deiodinase contributes to anabolism in the presence of other hormones. All of this would explain why anecdotally we see bodybuilders who use T3 lose a lot of muscle if they aren’t using anabolics along with it- they’re not utilizing the enzyme that would regulate some of T3’s ability to stimulate protein synthesis, while they are simultaneously signaling the body to produce an inhibitory enzyme (D3). And remember, for decades bodybuilders who were dieting for a contest have been convinced that you lose less muscle with T4 use, but that it’s less effective for losing fat when compared with T3? Well, as we’ve seen, without something (GH in this case) to aid in the conversion process, it would clearly be less effective! Since the deiodinase enzyme is also located in the liver, and we see decreased hepatic nitrogen clearance with GH + T3, it would seem that the D3 enzyme is exerting it’s inhibitory effects, but in the absence of the effects of the first two deiodinase enzymes, it remains unchecked and therefore not only limits the GH’s nitrogen retention capability. In other words, if we have enough to GH in our body aid in supraphysiological conversion of T4 into T3, but we already have the too much (exogenous) T3, the GH is not going to be converting any excess T4 into T3 after a certain point- which would be a limiting factor in GH’s anabolic effects, when coupled with the act that we’ve allowed the D3 enzyme to inhibit the T3/GH synergy that is necessary. As further evidence, when we look at certain types of cellular growth (the cartilage cell in this case) we see that GH induced rises in IGF-I stimulates proliferation, whereas T3 is responsible for hypertrophic differentiation. So it would seem that in some tissues, IGF-1 stimulates the synthesis of new cells, while T3 makes them larger. In this particular case, The fact that T4 and (D1) deiodinase is am active component in this system is noted by the authors. They clearly state (paraphrasing) that: “T4 is is converted to T3 by deiodinase (5′-DI type 1) in peripheral tissues…[furthermore]GH stimulates conversion of T4 to T3 , suggesting that some effects of GH may involve this pathway.” The thing I want you to notice is that the authors of this paper state that the that the conversion PATHWAY is probably involved, and not the simple presence of T3. (15 ) Also, that same study notes that T3 has the ability to stimulates IGF-I and expression in tissues that whereas GH has no such effect (ibid). So what are we doing when we add T3 to GH? We’re effectively shutting down the conversion pathway that is responsible for some of GH’s effects! And what would we be doing if we added in T4 instead of T3? You got it- we’d be enhancing the pathway by allowing the GH we’re using to have more T4 to convert to T3, thus giving us more of an effect from the GH we’re taking. Adding T4 into our GH cycles will actually allow more of the GH to be used effectively! Remember, the thing that catalyzes the conversion process is the deiodinase enzyme. This is also why using low amounts of T3 would seem (again, anecdotally in bodybuilders) to be able to slightly increase protein synthesis and have an anabolic effect – they aren’t using enough to tell the body to stop or slow down production of the deiodinase enzyme, and hence .Although this analogy isn’t perfect, think of GH as a supercharger you have attached to your car…if you don’t provide enough fuel for it to burn at it’s increased output level, you aren’t going to derive the full effects. Thyroid status also may influence IGF-I expressionin tissues other than the liver.So what we have here is a problem. When we take GH, it lowers T3 levels…but we need T3 to keep our GH receptor levels optimally upregulated. In addition, it’s suspected that many of GH’s anabolic effects are engendered as a result of production of IGF-1, so keeping our IGF receptors upregulated by maintaining adequate levels of T3 seems prudent. But as we’ve just seen, supplementing T3 with our GH will abolish Growth Hormone’s functional hepatic nitrogen clearance, possibly through the effect of reducing the bioavailability of insulin-like growth factor-I (12.) So we want elevated T3 levels when we take GH, or we won’t be getting ANYWHERE NEAR the full anabolic effect of our injectable GH without enough T3. And now we know that not only do we need the additional T3, but we actually want the CONVERSION process of T4 into T3 to take place, because it’s the presence of those mediator enzymes that will allow the T3 to be synergistic with GH, instead of being inhibitory as is seen when T3 is simply added to a GH cycle. And remember, we don’t only want T3 levels high, but we want types 1 and 2 deiodinase to get us there- and when we take supplemental T3, that just doesn’t happen…all that happens is the type 3 deiodinase enzyme shows up and negates the beneficial effects of the T3 when we combine it with GH. And that’s where myself and Dr. Daemon ended up, after a week of e-mails, researching studies, and gathering clues. If you’ve been using GH without T4, you’ve been wasting half your money – and if you’ve been using it with T3, you’ve been wasting your time. Start using T4 with your GH, and you’ll finally be getting the full results from your investment. T4 – thyroxine – thyroid hormones References: GrowthFactors. 1990;2(2-3):99-109.Interaction of TSH, insulin and insulin-like growth factors in regulating thyroid growth and function. Eggo MC, Bachrach LK, Burrow GN. F, Rumpler M, Klaushofer K 1994 Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3- E1. FEBS Lett 345: 67–70 Relationship of the rate of transcription to the level of nuclear thyroid hormone-receptor complexes.J Biol Chem. 1984 May 25;259(10):6284-91. Yaffe BM, Samuels HH. Thyroid morphology and function in adults with untreated isolated growth hormone deficiency. J Clin Endocrinol Metab. 2006 Mar;91(3):860-4. Epub 2006 Jan 4. Eur J Endocrinol.1995 Dec;133(6):646-53.Influence of thyroid hormones on the regulation of growth hormone secretion. Giustina A, Wehrenberg WB. Binoux M, Faivre-Bauman A, Lassarre C, Tixier-Vidal A 1985 Triiodothyronine stimulates the production of insulin-like growth factor I (IGF-I) by fetal hypothalamus cells cultured in serum free medium. Dev Brain Res 21:319–323 Eur J Endocrinol. 1996 May;134(5):563-7.Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans: comparison with growth hormone.Hussain MA, Schmitz O, Jorgensen JO, Christiansen JS, Weeke J, Schmid C, Froesch ER Harakawa S, Yamashita S, Tobinaga T, Matsuo K, Hirayu H, Izumi M, Nagataki S, Melmed S. In vivo regulation of hepatic insulin-like growth factor-1 messenger ribonucleic acids with thyroid hormone.Endocrinol Jpn 37(2):205-11, 1990 Hochberg Z, Bick T, Harel Z Alterations of human growth hormone binding by rat liver membranes during hypo- and hyperthyroidism. Endocrinology 126(1):325-9, 1990 Matsuo K, Yamashita S, Niwa M, Kurihara M, Harakawa S, Izumi M, Nagataki S, Melmed S Thyroid hormone regulates rat pituitary insulin-like growth factor-I receptors. Endocrinology 126(1):550-4, 1990 The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 11 5221-5226, 2003. High Dose Growth Hormone Exerts an Anabolic Effect at Rest and during Exercise in Endurance-Trained Athletes M. L. Healy, J. Gibney, D. L. Russell-Jones, C. Pentecost, P. Croos, P. H. Sönksen and A. M. Umpleby J Hepatol. 1996 Mar;24(3):313-9. Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man.Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO Huang, SA. Physiology and pathophysiology of type 3 deiodinase in humans. Thyroid. 2005 Aug;15(8):875-81. Review. Hernandez. A. Structure and function of the type 3 deiodinase gene.Thyroid. 2005 Aug;15(8):865-74. Review. F, Rumpler M, Klaushofer K 1994 Thyroid hormones increase insulin-like growth factor mRNA levels in the clonal osteoblastic cell line MC3T3- E1. FEBS Lett 345: 67–70 https://thinksteroids.com/articles/thyroid-hormone-growth-hormone/

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Alrighty. Now to start, I’m recovering from a torn tricep. Tore it at the Canadian open powerlifting meet WITH MY FUCKIN OPENER!!! Anyway, I ordered my first cycle since the meet. Cycle will look like this 1 gram test c 600 mg deca 75-100 mg dbol this is low dose for me, I’m not afraid to Boston Loyd this shit. But I’ll be telling you how it goes. I’m not training at 100 % yet, but I am training well enough to push for results. Never ran a cycle using only one lab. No holds barred review

Do not order from a person that goes by hawk33 it’s a scammer scam lab keeps changing Labs name but always uses hawk33 that doesn’t change. Stay far far away guys .

For the record.. and to end the bullshit... ONTerrible and Taureau are NOT affiliated in any manner whatsoever. My source is 100% accurate. I don't get my info from the internet or another forum, or repeating some post from somewhere. People may want to talk about people and that's fine. But it has to be the truth. From here on out... I will delete any information in this thread to the contrary. Rig pig was bang on. There is no talk about BT or their owners by him. So to quote, "If you're talking about him, he must be doing something right." I'm not picking sides... just stating the obvious.

How is your cycle coming around bro?

I posted that thread on another board and got the BS from ONTerrible himself. trying to pass himself off like the shit of shits. I got my hands slapped my the mods there, but I'm all for REAL transparency and fairness. If it's one thing, if you're not legit, your going to get your a$$ raped on the meso board. I've been onto this guy for close to 2 months now. Yes he his here but hasn't posted recently. I haven't checked recently where else he is playing his games.

Great work ! Thanks for sharing pics and your experience with sibutramine

Thank you guys. We did this to shut up people like taureau who try slandering us to promote their business. And thank you all for standing by us and being patient while we played our cards right to expose the politics that are involved in the game. One thing I learnt in life, you are not successful till people are shit talking you. The shit talkers are also our number one fans because they are constantly thinking about us. So a special thanks to the haters because you gave us further exposure for free. Now it's time to take over in 2019

Amazing brother Thank you !

Too many hearts on the second picture ?. Kidding aside (or was I) the physique is looking good

Just a quick discussion about the test base. Ok, so yeah, I really like this stuff at 2ml per day. Like really like it. Pumps are ridiculous and my intensity is really high on this.

One of the very few posts in this thread that is rational. Thank you for posting.

I’ve ran 3 grams it didn’t last long as I couldn’t stand the lethargy. if I didn’t have to work I’d do it again but I couldn’t function but imo 2 grams is better than 1 and 3 grams is better than 2 Thing is don’t jump into it all at once. I believe diminishing returns aren’t as prevalent as people think. If you start at 750 and add 250 a week I can personally guarantee the gains will keep coming IF you are training and eating right. Throw some GH and slin in there and look out

high doses of anything feels like shit eventually. Its the price we pay

Have run 2g week. But that was building up having run test for two years straight. Started at 500mg/week

2000 mg/week Test C w/ 1500 mg Tren E ... lots of sides and less results that I feel that I get with lower doses.

Hi folks, hope this is the right section to post this. I've been away for a bit (damn, life gets in the way sometimes, lol) and thought I would post some pics of my (messy) garage setup. Nothing fancy, a cage with pull down attachment, some power blocks and a few accessories. But most important is the beer fridge and the 90's JBL big ass speakers, lol. Hope everyone is doing fine! ?

this is what I meant, we are being spoon fed all the bs about expensive gear being more potent. It only benefits the boards and the labs they endorse,we end users only gain a lighter wallet. I'm thankful you guys did not delete my post,it shows this is a neutral board compared to others. I will only pay for quality but will never pay for the hype that goes behind the $50 test vial labs,that is straight up robbery

Exactly. That's why I have never bought into the "you get what you pay for" argument a lot of people throw around. Almost every lab is using the same or similar supplier for their raws. The quality is virtually the same. The process of making the oils is the same? Glass vials are the same for the most part. Yes there is risk to be considered. A man's time etc... as well. But is a vial of test really worth $50+? My first ever cycle was on Teragon test-e. I bought it at $35 a vial. it worked as it should. No complaints. I continued to use them solely until I had access to other labs. Yea I get seduced by reviews and the rhetoric. But at the end of the day the more expensive lab wasn't any more or less effective than the cheaper one. The under-dosing argument is all they have. It's the common line used to legitimize their rationale for getting you to pay more for their gear. People can do whatever the fuck they want. Buy from whomever they want. I don't care. We all have our favorites. But common sense needs to be prevail sometimes. Unless a lab is doing some uniqure brewing, exotic blends, and new carriers... there is no reason to buy into the "sales pitch." There are lots of good labs all the way through the price spectrum. Do your research, and buy what you feel comfortable buying. But the only way to know if a lab is good or not is to use them. I personally never buy a compound I've never used before from a new "to me" lab. I always buy some test-e and something else I've already ran. So I know what the results should be.