haaaaaaaaaa wow, that’s amazing! Is it possible you were dehydrated on the previous blood test but well hydrated this time… Still 2 grams should be enough to stimulate an eryhropoitic response, wow it’d suck if you had falconi’s anemia (androgens tend to be a first line treatment), you’d probably be unresponsive
Be careful though, 2G is quite a biiiiiiiiiiiiiiiiittttttttttt. So what’s the full stack (just curious) is it like 1g test, 1g deca, 1g mast?
The day before a blood test is almost always the same (speaking about training and diet, hydration), so I wouldn’t suspect that my hydration status caused the result (I weigh myself everyday, I’d see a difference). The difference in the markers is in fact very small, so I’d say that they actually haven’t changed (which is surprisingly pleasant, still).
So if you want to hear more about the cycle:
The last heavy cycle I’ve done have finished about 1 year ago (I decided to educate myself intensively in the field of training and diet, I tried different ways of programming, switched to low bar squat, I worked out my heavy lifts and figured out how do clen, T3, low doses of tren work on my body; 1 year was just perfect to configure my personal TRT procedure as well).
The 1 year break was ended with about 4 months of slow, patient cutting phase (main assumptions: to be happy with the process maintaining strenght in the big 3 while still losing %BF) - finished with about 7-8% of BF (DEXA & caliper estimations), lost about ~3% with low tren (100-150 mg/wk), clen (40-80 mcg/d) and pseudoephedrine (120-240 mg/d) doses.
Current cycle is my personal best, primarily because of wise training and almost mathematically perfect E2 management. During 4 weeks I’ve linearly added about 20-25% of total load while my 5’s strenght increased by huge (at this level of advancement - intermediate++) ~12% in almost every lift. 0 injuries, 0 side effects (some positive sides only), 0 discomfort (except working out 6/7 days a week for about 2.5 h/d).
Week 1: frontloading of ND and TE (isn’t the best idea regarding to AR downregulation, but the best approach to avoid E2-related sides ASAP & to profit from ND ASAP, don’t like kicking in with orals)
Week 2: final calibration of E2 (it turned out that I needed to add roughly 20% of an AI - my TE concentration is overstated, praise my dealer) & reading signals from my body about the stack (despite actually too high dose of TE I lacked training aggression and had blurred physique way too much, libido 3/5 but no ED symptoms and so on)
Week 3: I still determine whether to add DHT derivative despite satisfying results already (drostanolone as the best solution related to profit and loss account - first shot was done on Friday), E2 is stable plus DHT comes in so I give up cabergoline (0.20 mg/e4d till this point)
Week 4: libido, sleep quality and training aggression (outside the gym agressor not) significantly improved after Masteron addition, as well as muscle hardness & strenght, physique quality; LBM increased dramatically this week what’s more interesting
Week 5 (starting in 2 days): deload time, finally; my joints and targeted muscles (directly 20 sets/wk+ per targeted muscle group, more than 30 sets/wk considering overlapping) are sore too much, I still can add weight and sets but it wouldn’t be wise or pleasant
Doses: 800-900 mg of TE, 400-500 mg of ND, 300-400 mg of DP weekly / 0.55 mg of anastrozole per day / huge amounts and variety of antioxidants for the liver, the hearth and kidneys protection; doses are way too high at this level of advancement, but no sides - no problem (0.55 of an AI daily is just stupid, TE should be lower, but this isn’t a time to change this)
Weight/BF increase: 8 kg of total body mass, about 0.5% of BF (fat folds changed slightly from 4.0 to 4.5-5.0 mm, water retention taken into account)
Weeks 6-8: if I’d hit a plateau, low doses of tren would be probably the best solution
Week 9: deload, detailed health analysis
Weeks 10-13: if everything would be acceptable, I’d maintain current approach while lowering ND / if plateau, oxymetholone at low doses as a first-line solution
Week 14: deload, detailed health analysis
Weeks 15-18: tapering off (the crucial & always the most difficult part IMO)
Weeks 19+: maintaining
EDIT: more of fresh subjective observations from drostanolone. Libido is slightly higher, but erection is much stronger and is achieved faster with the most satisfying orgasms I’ve experienced for a long time (despite being with the same woman in the same circumstances). However, cus of ND, I’m not a sex-maniac like I was on previous cycles w/o the compound. DNT “helps” in this regard - you can run more of strong androgens w/o sides related to your excessive libido or agression in life (in fact, anabolic:androgenic ratio is moved towards anabolic properties then). Nobody takes this fact into account, it’s a pity. Despite having slightly elevated E2 after adding Masteron (+12%, significant difference when on cycle, dramatic difference when on TRT) my joints are more “feelable” - I’m not sure if it’s related to anti-E2 effects of Mast or just crazy volume and weights I use & cumulative fatigue (more experience is needed in this regard, one week isn’t too much, lmao). I’m stronger as well - muscles are harder even at rest, contractions are stronger and I can feel it (DHT role in CNS-muscle neurotransmission). This is much easier to do heavy 5-10 reps of heavy compound movements to muscular failure or at 3-1 RPE w/o strong physical and mental pain (compared to just TE+ND) - that’s what I call improved training aggression. Rest periods between sets are shorter too. Muscle definition in plus, getting a pump faster. I seriously love this compound and can’t find any worthy rival for that (profit and loss account).
Summarizing, the cycle gives me anabolic response I wasn’t even dreaming about. My productivity is through the roof (university successes & I can study for myself way more than when in “unnatural physiology”), I’m not emotional or having manias despite amounts used. No social or sex problems, no excessive aggression or another mental issues. I feel cool in life, I’m a beast in the gym, and I’m healthy. What more could you want?
Is this an encouragament to take AAS? Maybe, I don’t care - you decide. No drugs in the world lead to such satisfaction in a long-term manner with provided (little) sides.
DHEA
https://www.karger.com/Article/FullText/430150
“exogenous DHEA might preferentially convert to testosterone rather than estradiol due to the up-regulation of 3β-HSD and 17β-HSD protein levels and the down-regulation of aromatase protein level in primary Leydig cells” - more T, simply (so improved glucose tolerance and general health both in men and women?)
“A meta-analysis in elderly men and women has found that DHEA supplementation has no effects on blood glucose levels. However, DHEA supplementation to patients with type 2 diabetes has not been fully elucidated.”
https://www.tandfonline.com/doi/abs/10.1080/03602530600569877%20
Partial agonism towards ERalfa & ERbeta (cognitive function improvement, improved lipid profile?)
https://books.google.pl/books?id=uABKkFdPjhkC&pg=PA229&redir_esc=y#v=onepage&q&f=false
Neuroprotection (astrocytes metabolites increase), brain maturation, affects mood (TRT users claim that after adding DHEA-S to their treatment mood is elevated, probably cus of AR & ER stimulation; plus additional benefit of improved cognitive function), decreases calcium intracellular release (excitotoxicity decreases), stimulating eNOS, improves memory, an anticarcinogen, etc.
https://books.google.pl/books?id=YmQAhOeaFtUC&pg=PT349&redir_esc=y#v=onepage&q&f=false
CNS cell proliferation and neurogenesis, negative r-GABA_A modulator (excitation?), r-sigma1 agonist (modulation of cardiac miocyte contractility)
“DHEA rescued from apoptosis TrkA receptor positive sensory neurons of dorsal root ganglia in NGF null embryos and compensated NGF in rescuing from apoptosis NGF receptor positive sympathetic neurons of embryonic superior cervical ganglia. Phylogenetic findings on the evolution of neurotrophins, their receptors, and CYP17, the enzyme responsible for DHEA biosynthesis, combined with our data support the hypothesis that DHEA served as a phylogenetically ancient neurotrophic factor.”
E2 increases G6PDH activity (an important fact regarding to glucose utilization in muscle tissue towards increased hypertrophy, in a big nutshell), while T solo doesn’t!
DHEA inhibits G6PDH; “Both in vitro and in vivo experimental studies strongly indicate that DHEA and related steroids inhibit inflammation and associated epithelial hyperplasia, carcinogenesis, and atherosclerosis, at least in part, through the inhibition of G6PDH and oxygen-free radical formation.” + “Clinical trials with DHEA are encumbered by the high oral doses required as well as the conversion of DHEA into active androgens. The use of less androgenic congeners as well as non-oral formulations may facilitate testing of this class of compounds.”. Funny, if DHEA is a partial agonist of ER that makes a little nonsense.
Just few studies to confirm my statement on supplementing with DHEA-S. The supplementation is crucial for mental health while you are DHEA deficient (TRT w/o hCG, or if your testes are totally off). IMO not a significant anticarcinogen and/or antidiabetic agent. Take into account that studies “on general health” (lipid profile, glucose utilization and so on) doesn’t consider DHEA → T conversion (andropause → DHEA treatment → more T → wow), what’s crucial. DHEA isn’t the only neurosteroid, but it seems it’s the most important. However, it’s wise to keep your testes working, not just for visual aspects.
Nah it isn’t an encouragement, I’m not an impressionable individual, if I was I’dve been knee deep in recreational drug use by now. Besides I’ve used AAS before (Anavar @25mg/day for 5 wks, stopped due to HBP) and 250mg test/wk for 9wks, not outright cycle doses or supraphysiologic, but I’m too scared of running supraphysiologic doses due to SPECIFICALLY
the results found in thesee two studies
http://circ.ahajournals.org/content/135/21/1991
(Full article is usually available for view however currently it isn’t, however some of the AAS users had LVEF’s of sub 20 percent!!!)
Another study (this one https://www.internationaljournalofcardiology.com/article/S0167-5273(12)00277-X/fulltext ), although concerning doesn’t bother me as much, while a few show no difference between subgroups of athletes, still the notion of killing myself at a young age from AAS use scares me, one because I don’t want to die yet and two because say I did acquire heart failure … It’d be a shitty life if my heart was in such bad condition I could barely even walk up a flight of stairs.
I already have a high heart rate when I exercise (intense aerobic and anaerobic exercise regularly gets it to 180BPM+, I’ve even gotten it up to 210BPM before and I can hold it for 3-4 minutes before I get tired), post exercise it goes back down to like 80-90BPM in a matter of 2 minutes or so, then it take a good 4 hours to drop down to 60BPM. When I was using all my dietary supplements something in them was causing my HR to be persistently high (90-95bpm), one time I was on all the dietary supps, took some dexmethylphenidate and a ton of caffeine to help me study and I had a REEEAAALLLY fast heart rate, shit was scary, thought I was going to die. Happened again a few days later post exercise (but nowhere near as bad) so I stopped taking all the dietary supps and everything went back to normal within two days, haven’t had an issue since. Due to anxiety about my heart (I’ve gotten an ECG, had an ECG when I was on all the dietary supps about 3-4mths ago, nothing abnormal. Also had my heart checked as an infant for defects, nothing abnormal was found. Still my sole reason for not using AAS Is because I’m scared of cardiac problems arising.
Furthermore I’m carbohydrate intolerant, glucose tolerance tests have shown I become hypoglycemic following carbohydrate consumption. I get a HUGE delayed insulin response and my blood sugar falls into the gutter, I’ll give an example, Today I ate a big packet of chips and finished it off with a nice beer (very hot today), the result was my RESTING heart rate shooting up to around 100BPM, I stood up because I was like “shit, shouldnt’ve done that, I don’t feel well” and my HR shoots up to 130BPM… from walking, coupled with that I feel dizzy and disorientated, do I have cardiomyopathy or am I just severely hypoglycemic… who knows, all I know is that I couldn’t get treatment because my glucose tolerance was 0.1 point from being out of the ref range 2 hrs post glucose tolerance test (insulin was way off though). The solution would be to try out a low carb diet/ low GI diet, however I hate the idea that I have to keep forfitting things that I like due to health issues, it’s bullshit, I’m starting to think no matter what I do I’m heading into a premature death so I might as well just enjoy the time I have left (this may factor into whether or not I ever use higher doses)
As to the DHEA, I’ve seen all those studies aside from the NGF study. However i’d like to add some counterstudies on the diabetic stuff
Hypoadrenal women given DHEA replacement notice improvements in insulin sensitivity (many variables tho, I not hypoadrenal or a woman)
Dhea lowers insulin resistance in aging men
Although in the one study, I exercise more than nearly all the people in these studies, I exercise between 12-24hrs/wk, sometimes more, that alone oughta cause some serious LVH (both concentric and eccentric given the types of exercise I do) add high doses of AAS into the mix…
Also this new study has come out (full article not yet published)
https://onlinelibrary.wiley.com/doi/abs/10.1111/joim.12850
Demonstrating mortality rates of AAS users to be 3x that of the general populace. Stuff like this gives me anxiety and makes me want to avoid ever using high doses of anything. I think I’ll be happy using 200-250mg/wk forever (depends on what bloods show). Granted I do intend to try masteron one day for its effects on libido, therefore I’ll probs one day drop the test to 125 and add 125 mast. Probs try methyltestosterone one day too. I have no use for anything else unless I have the balls to stop being anxious about every little thing in my life and decide to take the leap and try compete thus making myself happy.
As to you’re gains, 8kg is amazing, congrats. However just because you look and feel healthy doesn’t mean you inherently are, you (probably) are causing damage on a molecular level.
As to DHEA on TRT (I’m aware of DHEA’s activity as a neurosteroid and the hormones it converts to etc) I’m going to start taking 100mg/day (I’m unsure as to whether it’s a more the merrier type situation, I don’t tend to have issues with aromatase… Ever, however in a rat model absurd doses of DHEA (something like 1000mg/day or something HED equiv) resulted in cardiotoxicity. Given I can get DHEA on eBay and OTC in America in doses of up to 200mg/tablet I have no qualms about using it. A study from the 80s in men using I believe it was 1500mg of DHEA daily noticed a significant reduction in fat mass without any bodyweight decrease, suggesting an increase in muscle mass.
As to my testis, there’s a decent chance I wasn’t fertile in the first place. I noticed significant testicular atrophy prior to TRT, when on trt and other stuff (I used nandrolone very briefly, and oxandrolone) I only noticed an additional say 10-15% reduction in testicular size. With HCG the possibility of LH receptor downregulation also exists, + if my issue is primary (which it might be) then it isn’t as if it’ll do much, I’d rather take injectable FSH (which I can get) but don’t want to because why would I want to, it’s just adding more pharmaceuticals to the mix
In you’re opinion, is there any specific AAS that are of lower risk with regard to causing structural damage to the heart? If the majority of the damage and hypertrophy is mediated by binding to the AR in cardiomyocytes wouldn’t an AAS that has a large portion of its anabolic properties independent of AR binding (say stanozolol) be less damaging (I recall seeing a study in which testosterone at lesser concentrations caused cardiomyocytes to enter apoptosis when directly exposed to said hormones. That being said stanozolol is hell on the lipids… Wouldn’t touch with a ten foot pole. Prostanozolol, however could end up being one of the safer ones if my hypothesis is correct.
Sure, DHEA-S works in aspect of glucose management in elderly people and in hypoadrenal women, as it would work in every population lacking androgens and/or E2. As I’ve mentioned, these studies don’t include the fact of DHEA → T conversion (+ aromatization). In reality, improved glucose tolerance is due to physiological restoration of T&E levels (most probably). It’s common fact that T&E deficiency leads to obesity and type 2 diabetes. I wouldn’t assume that DHEA, specifically, would be able to do anything significant in this regard.
About AAS users and general population:
To tell something reliable about X factor and it’s influence on general health or mortality, a great holistics must be included (quoted studies in such isolation mislead, taken binary). YES, AAS increase risks of many diseases, DRAMATICALLY. We cycle drugs because most of sides are reversible (as cycling I mean conscious cycling, not injecting 5 g of PEDs for 3 months and then “bridging” for 3 months just on 1 g - common phenomenon). We eat good, do cardio and manage stress, avoid excess alcohol and/or smoking, and so on, to decrease possible risks. It’s not always successful, but it’s way more healthy than “general population” - if done right. We analyse our blood markers & do specific medical examinations to be sure that everything is on track. The way of prevention I described is used maybe by proverbial 5% of AAS population? Results are not surprising.
The problem of AAS induced increased mortality risk is the same if I tell you that more than 30% of guys you see in the gym have or had an experience with PEDs and still look regular and are weak. The reason is simple - they have no f*cking idea what they’re doing (when they think exactly the opposite) in regards to both training, diet and health.
Ventricular hypertrophy is mainly caused by AR stimulation as you say, plus cus of anaerobic conditions of strenght training (the second is reversible in 100%), plus increased RBC level, plus cus of water retention when E2 management is incorrect (and all another causes of elevated BP). Cardiac myocyte is a tissue, biochemically and structurally very similar to skeletal muscles. So every anabolic steroid with A:A ratio directed towards androgenic properties (and lower anabolism) should provide decreased AR stimulation in the heart - from simple deduction, you won’t find any studies on that (the problem of disturbed lipidogram remains, obviously).
LISS cardio should be included in each AAS user to compensate the fact by increasing ventricular volume (not to mention another benefits). As well as proper diet, low sodium intake, cholesterol management, low stress environment, etc.
Define too much, I probs drink 2 beers/month, don’t use recreational drugs or smoke (because why would I, i see absolutely no possible benefit that could be gained from smoking cigarettes or using recreational drugs other than a wonderful escape from reality that would simply draw me back to using drugs again and hence I’d probably develop a problem therefore I just stay away.)
5 grams? What the fuck? Are you sure about that… 1 gram cruising? That’s got to be a joke, I thought the 10-100x physiologic doses was a wild exxageration. I do get bloods but I don’t have a doc to moniter my health, I simply moniter my blood pressure (always PERFECT), blood sugar and whatnot. Today on the bench press machine (I don’t have a partner to workout with therefore I don’t barbell bench in case of dropping the bar on myself which I’ve done before and it hurts) I did 120kg for 12 reps. I’m very happy with that in general. Thats probs equiv to bench pressing like 80-90kg for 12 reps, not great but for someone with chronic pain I think it’s pretty good.
I due believe stress induced by my chronic pain and my anxiety will significantly shorten my lifespan alone. As to LISS, what’s a good example of this? I bike to and from gym (so probs average nearly 100 kilometres a week), however I bike hard and fast for long periods of time, fast enough to sustain my HR in the 160-180 range.
So by deduction then, AAS like drostanolone, methenolone, methandriol (pro-hormone) and testosterone (100/100) should provide the least risk for LVH and cardiomyopathy. I think I’ll just stick to test for the timebeing though, don’t see any point stacking on TRT (aside from libido boost, however mast will/ should have a fairly negative impact on my lipid profile, therefore if not cycling it’s probably not worth it)
This is kind of a catch 22 is it not? (barring primary hypogonadism) as obesity is associated with hypogonadism and type 2 diabetes, type 2 diabetes is associated with obesity and hypogonadism and whatnot, all three are interlinked. That being said there is a distinct, strong correlation between testosterone and insulin sensitivity in men (hence men undergoing androgen deprivation therapy tend to develop insulin resistance)
What I don’t understand is… why on earth would a normal individual who isn’t competing or anything inject 5 grams/ week, that sounds absurd to me. I can’t imagine how big I’d get off a mere 400mgs per week let alone 5000mg per week haha (although there’s def a point in which AR saturation occurs then it’d be diminishing returns and more sides.
But yeet you’re likely right about DHEA, berberine shows serious promise for improving glucose tolerance and insulin sensitivity.
What’s the highest dose you’ve personally ever heard of anyone using? One of the studies I should mention took away the variables of illicit drug use (didn’t factor in dieting) and found LV dysfunction was still present, albeit not as significant (still P value over .05 tho), I believe the average doses in these studies are typically around 800-1500mg/wk. The higher the average dose, the more concerning the results, most case reports don’t specify doses or compounds used. Two of the most concerning case reports I’ve seen was a bodybuilder who supposedly took one cycle of test, primo and deca and died suddenly, heart was found to be nearly 600 grams… My first thought about the study was “they didn’t know the extent of his abuse, one 3 month cycle won’t cause such hypertrophy of the heart in the absence of cardiovascular disease such as inherited HCM/ dialated cardiomyopathy” the other was a male in his mid 60s who did one 3 month cycle and developed CHF, my thought was “he’s lying, the report said he’d been training for 4 decades, he’s probably had an extensive past use of PED’s” both of these reports made clear that there was no familial history though. Finally there was a case report in which a man had CHF with a TT of only 2800ng/dl, once again given the man was a competitive weightlifter I thought to myself “he had used tons of shit in the past”
I believe for reasons like this case reports tend to be very flawed, it is impossible to know the full extent of the subjects abuse, many times compounds and doses aren’t mentioned nor is familial history (sometimes), presence of illicit drug abuse etc. Still the amount of case reports piling up concerns me greatly. I’ll very, very likely try 300mg of test one day (say 12-16 months from now). Thats a cycle dose (albeit very low end) is it not?
I’m not sure how long I want to live, I just want to live as long as I can function properly and exercise (in old age my joints will probably be absolutely shot, I don’t want to be alive at the point where I can barely walk/ get out of bed therefore im fine with shaving a decade or two off, however I don’t want to drop in my 20s or 30s (I think 70-75 is a good age to target, although I might be bedridden before then, depends on the progression of my issues)
Yes you are right, I exaggerated those 5 grams. Considering many guys who inject more than 0.5 g of trenbolone (multiply it by 5 by reason of it’s power related to T), almost 1.5 grams of T plus 1.0 g of nandrolone, plus more compounds at lower doses we actually exceed those symbolic “5 grams”. 1.0 g of T cruising dose is very common, seriously, when 0.5 g is a total standard in my circle and on many forums.
Dimishing returns and “close to total” receptor saturation is an awesome (cus mysterious, no serious data) topic considering AAS. Some studies suggest that T and derivatives stimulate AR synthesis (in physiology, more T → more AR → more AR-T and so on); on the other hand, there’re studies where supraphysiological amounts where given and AR downregulation was observed. You will see the same looking at LBMgrowth-time curve at the same dosage (6-8 weeks of linear growth, then plateau - confirms some mechanism of adaptation). The same about LBMgrowth-concentration curve - the curve flattens after some critical range (too bad any reliable studies stop dosing at ~600 mg of TE). There’s nothing to dream about - negative feedback exists for sure. That’s why every individual should find his sweetspot for each compound (ofc taking most benefits with the lowest sides). On my example, I shouldn’t exceed 0.5 g of TE because of dramatic aromatization (4 mg of an AI/wk is just economically stupid and illogical, well, I had give it a try). On the other side, I tolerate trenbolone and nandrolone very good, so I will program my future cycles on them.
Nice to talk with you, BTW - it’s always a pleasure to answer. Could you invite more users to the conservation? I’m rarely active on forums, maybe I’m doing something wrong?
Well, it does appear that supraphysiologic doses of AAS promote the creation of new androgen receptors, however saturation (even with new androgen receptors being synthesized) probably DOES exist if we look at the data given. Here is a chart from a study in which multiple doses of test was given to healthy men (you’ve def seen this study, it’s “testosterone dose response relationships in healthy young men” very commonly cited study on BB forums.
Anyhow the difference between 300-600mg isn’t exactly 2x the amount of muscle mass and strength gained, therefore one could hypothesize the difference might be even smaller between 600-1200mg and so on, therefore while diminsihing returns has been demonstrated to exist (higher doses more harsh on lipids, haematological parameters for some and generally more risky on the cardiovascular system), androgen receptor saturation may exist in regard to that a certain dose (say 4000mg vs 5000mg) may not make much of, if any difference at all.
Feelings mutual (talking to you), you’re a very interesting individual with lots of solid info and advice to share. As to inviting more users to the conversation, sure (you’re not doing anything wrong, it’s hit or miss whether others reply to you’re threads, what you do to make people reply is tag them), I’ll see if I can get anyone to join in
@studhammer @iron_yuppie @physioLojik @flipcollar @WolfDiana @flappinit @newbvet
Anyone want to join the convo?
Thank you. I know this study very well, each book on AAS cite that (too bad that dosing ends at 0.6 g). Most studies on the topic find that androgens upregulate AR synthesis. Acutely, what’s the key fact here!
This is a study with higher doses (albeit the full text requires one to be part of the medical community or one has to purchae it to access said full text, I can access the full text later on behalf of someone else)
Sadly it only measures renal function and parameters, not cardiac function or strength and muscle mass gained (shame). There are two studies in which participants use exorbitant (self reported) doses of AAS and have cardiac function and parameters measured.
“prospective Echocardiographic Assessment of Androgenic-Anabolic Steroids and Effects on Cardiac Structure and Function in Strength Athletes”, I have access to the full paper on PDF, I’ll upload the entire paper via screenshots (probs not supposed to though, as the paper isn’t generally accessable to the general populace, however people can purchase it, therefore meh I think it’ll be fine)
Page oooooooooooooooneeeeeeeeeeeeee
Page two (half of)
other part of page two
PAAAAAAAAAAAAGE THREEEEEEEEEEEEEEEEEEEEEEEEEEEEEEE
PAGE FOURRRRRRRRRR
Page six
Page seven
Here’s another good and accessable one
I’m unsure if I’ll get into trouble for posting this or not, potentially.
I’m unsure as to why more people aren’t joining the conversation, it’s a good one with a ton of valuable information, when physiolojik comes back to posting he might join in.
As to the books on AAS, are you talking about like… anabolics from William Llewellyn’s Anabolics and such? I find that while helpful, to garner a deep understanding of these chemicals one must read through biochemistry and hormone physiology textbooks (specifically the parts related to hormone synthesis), I’m sure you know that though lol because you almost have a masters degree in pharmacy!
Yes, I’m talking about books like Llewellyn’s one. Such books provide reasonably good foundation of knowledge, but what’s more important, they’re a perfect source of references (it helped me hard at the beginning). As you can assume, AAS chemistry and pharmacology isn’t researched well (maybe with an exception of 3 compounds) - so subjective experiences from another users, often unbelievable, are for a weight of gold (the main reason I read forums).
With some knowledge of medical chemistry (structure-activity relationship), physiology & patophysiology, pharmacokinetics, pharmacology, biochemistry, drug development technology, and so on, you are actually able to (with a lot of probability) predict the effects of the drug. With the addition of some studies and users experiences - it comes out well.
It would be awesome to specifically inhibit 3HSD activity in the muscle tissue and/or myostatin. Stamulumab was a hope.
What are your plans after finishing school?
Are you meaning to tell me 500mg cruising is a standard? My left ventricle hurts looking at these doses!!! If these doses are common among normal people I can’t even IMAGINE how much the pro’s must be using, I know Dallas Mccarver had a TT of 55,000ng/dl, thus was probably on 5 grams + of test/wk ALONE!
Would be awesome, however concept of satalite cell depletion form myostatin deficiency is a scary thought, supposedly follistatin (available from various peptide clinics) is an antagonist to myostatin, (binding to TGF and whatnot) GDF-8 (myostatin) is a member of TGF is it not?
First - gap year, travel for a month or two, get back, get a job dedicate myself to bodybuilding for the entire year (like live the entire bodybuilding lifestyle and everything)
Second- Biomed, pharmacy or a science degree
Third- post-grad medicine (under graduate is too hard to get into)
Fourth- specialise (endocrinology or pain specialist)
Fifth- help people, likely move to a different country to work.
Sixth- be content with my accomplishment and die a happy man at any age…
I’ve just taken 25 mg of oxymetholone that waits for me. Quick observations (~2 h after it was taken):
Damn, this shit really works. I’ve decided to include low oxymetholone’s doses for following weeks (for 4, maybe 5 weeks (depends on training schedule) @ 25-75 mg, linear elevating - I should take an advantage of a fact that I’m still lean and have great health status), then probably will switch to trenbolone as a finisher.
can’t relate there haha, not usually happy, not sad either, just neutral. I’m probably going to see a cardiologist about my heart, it became very elevated following a meal (without carbohydrates). It jumped to resting 80 and standing 130, can visibly feel palpitations (though regular beat), uncomfortable, I feel dizzy when it happens. I’ll mention this, however I don’t think it’s important, my BP is always very low, recent test had it at 106/47 (yea, the diastolic BP is very low). It pisses me off to think that I might have something seriously wrong with my heart at this age (despite having never used outright supraphysiologic doses of gear). Only one doctor knows of my steroid use (however that doctor doesn’t know much about them, doses or whatnot). I’m sure if I tell him what’s going on i’ll be told it’s the steroids that I took (last 250mg shot was five weeks ago). I’m gonna get my heart checked out for piece of mind, I’ve noticed it happens even when I’m not anxious, my HR variability is ridiculous, I’ve had it as low as 49BPM and as high as 120BPM resting, I’ve come to the conclusion I’m almost certain something isn’t right, I’d rather know if my death is imminent that not know and drop.
Going to try get a referral to cardiologist (need referrals to go anywhere here, and the docs don’t exactly make it easy to get one either)
hah, I’d be in the bathroom for a few hours if I took that much.
Hmmmmmmmmmmm what genre of music?
Keep an eye on lipids, oxymetholone can destroy them fast, granted 25mgs is a low dose (prescribing guidelines for aplastic anaemia were like 1-5mg/kg/day and for wasting before anadrol-50 was available but 5-10m tabs were I believe it was 10-15mg/day but up to 30mg wasn’t uncommon.
Abdominal discomfort? Where in the abdomen, upper right side?
I’ve forgotten to add:
Abdominal discomfort after oral AAS intake is very unspecific (deep, diffused, painless) in my experience. It absolutely doesn’t feel like dyspepsia and/or hyperacidity and/or another common GI tract acute disorder. Maybe just a strong blood supply to the liver and intestines due to high toxicity gives the symptom?
Dancing to “E. Clapton - I Shot the Sheriff (Live)” this time! During weekends I listen to blues, jazz and classical music (studying). When on the gym, heavy metal, rap and energetic electronic music fit me best.
Aren’t your heart issues caused mainly by GAD?
probably plays a huge factor, however I’d rather have piece of mind and be sure. There’s potentially something else too it, (undiagnosed endocrine disorder or something, worst case scenario is something like wolff parkinsons white syndrome), my heart has been very variable recently in the absence of extreme anxiety (hr variability is ridiculous), I do believe something might be wrong (tachycardia induced cardiomyopathy is a thing however I doubt I had that), I just need to make sure everything is alright, if everything checks out and it is anxiety then I need to be properly managed with regards to my anxiety. Due to my nature of planning everything out I see these scenarios (it’s like a tree diagram) I get checked out, if nothings wrong I try get my anxiety managed properly (without benzodiazepines). If something is wrong and it’s mild I try get it sorted out (say WPW syndrome= cardiac ablation), if something is severely wrong (heart failure, dialated cardiomyopathy from an unknown cause (genetics, HCM or DCM from AAS induced toxicity is extreeeeeemely unlikely given the doses I’ve used unless I had some kind of issue to begin with and AAS made it worse (in which case I’d’ve been a ticking timebomb anyway). Anyhow if I have like… full on heart failure (I’ve had some concerning symptoms recently that I’m not going to get into), I hypothesize I’d give up at that point and live a hedonistic, irresponsible lifestyle (the exact opposite of how I currently live) until my heart gave out, which would probably be fairly quickly. If I have something moderate like mild-moderate LVH or subclinical dysfunction I’ll just take the meds required. I only worry about this stuff as I’ve had fairly shitty luck in the past, and I believe (sometimes) that in certain aspects of my life I hit the lottery and in others I’ve been cursed, my health is not exactly something I’ve hit the jackpot on, I’ve yet to acquire anything serious however I believe it’s only a matter of time. (not to say I believe in fate, however I do believe life is a lottery and some hit the jackpot and some are forever losers, it sucks but that’s just how it is).
YEEEEEEEEEET, i’ve posted thoughouly on heavy metal in a few threads, it’s my bread and butter, I’ve been listening to it since I was about 6 y/o. I also like blues and jazz, rap… not so much, it depends on what they sing about, the girls, money and drugs songs never really appealed to me. Certain raps which take serious subject matter into hand and deal with it in a mature or satirical way I don’t mind.
Potentially, however the hepatotoxicity of oxymetholone (in my opinion) is wildly overstated, I can find studies in which people are administered 100-150mg/day for many many months without any serious liver complications besides elevated ALT/AST (other side effects abound though, lipids go in the trash). Upper right side of the abdomen is typically where one would feel pain if it was liver related. Not to say you aren’t extremely sensitive to the toxicty of oxymetholone and/or C17AA’s, if you are then you’ll find out when you’re eyes turn yellow lol (in which case stopping the oxymetholone should reverse jaundice, the liver is remarkably regenerative). Are you taking any liver detox supps (tudca, nac, curumin etc.) The reason oxymetholone has been PARTICULARLY implicated in the development of hepatocellular carcinoma and pelosis hepatis (in my opinion) is due to the prescribed doses given to people with AA. 1-5mg/kg is nothing to scoff at, while it is more hepatotoxic than say, anavar mg for mg, if one was given 5mg/kg of oxandrolone for a prolonged period of time (say for me that’d be about 365mg/day for the highest dose) toxicity would likely become an issue, 365mg/day of any C17AA compound is going to cause issues… Other orals haven’t been used in a clinical setting at similar doses to what oxymetholone has been used at. (aside from methyltestosteorne, however still 150-200mg/day isn’t exactly 5mg/kg/day)
Yeet, also I forgot to mention I take a selective alpha 2 adrenergic receptor agonist off label for anxiety, it’s why my blood pressure is always frighteningly low (a diastolic of 47 is veeeeeeeeeeeeeeerrrrrrrrrrrrrrrrryyyyyyyyyyyyy low), I do have post orthostatic hypotension (I get dizzy when I stand up and walk around), I’m thinking I might have POTS (post orthostatic tachycardia syndrome).
Oxymetholone’s mysterious estrogenic activity doesn’t let me sleep. Anadrol’s main 5 metabolites (all lacking C2 hydroxymethylene fragment) from Bi H et al; J Steroid Biochem Mol Biol 42 (2): 229-42 (1992):
In the face of the above, the fact that oxymetholone is a DHT derivative (as well as mestanolone), it’s estrogenic activity must results from (and because of C2 fragment):
The thing is, ER is very specific for it’s substrates (compared to other representatives of SHSF; the least amount of crossover - LBD similarity to another family members is very low). From medical chemistry, I don’t accept the theory of any oxymetholone’s or it’s known metabolites potential to affect ER in anyway.
As a potential PR antagonist with relatively long time of activity basing on it’s t1/2 in the blood I support the theory of ER upregulation. Mifepristone as well-known anti-PR agent leads to gynecomastia (among others, because of the upregulation):
Solution for E-sides from oxymetholone - more AI and/or SERM administration (the other one won’t deal with water retention and elevated BP), more drostanolone or another DHT derivative, cabergoline if needed.
My water retention and BP are perfect after 4 weeks of juicing on TE, ND & DP - E2 @ 190-200 pmol/L. Great strenght and LBM increase while %BF is still constant, ABS and veins are visible everywhere (4000-4500 kcal/d, 20% fats). The physique is blurred a little bit (E2 is slightly elevated for anabolic & safety purposes) and it’s totally fine. No health sides so far. Started to love to sleep from 9 PM to 4 AM (nandrolone)!
However, I’ll add oxymetholone to the stack next Monday. Will start with 25 mg/ed most probably (basing on it’s A:A index it gives me another 25 x 7 x 3 ~ 500 mg of T equivalent, plus water so strenght and safety). I’ve tried it @ 50 mg for 2 (not following) days last week, I’ve described the experience. Water retention haven’t been observed, obviously, because of acute manner of the administration. Hunger and energy increase were most felt, as well as abdominal discomfort and slight headache. BP & HR increase were noted (so headache, slight weakness after some time). Water retention could only worsen the problem. Finding a compromise is tough.
If water retention would be as powerful as literature & guys describe, I’d add even more AI and I’d increase diuresis and Na+ output possibly non-invasively.
