I don’t. If I’m going to use something it’s going to be actual steroids. With SARMs we really don’t know what the long term effects are and of the ones we do know some about it’s pretty bad like higher rate of several different cancers (Cardarine for example). I have Anavar that I’ll take at some point but it kills my libido and that’s not something I’m willing to deal with at the moment plus if I’m going to run a cycle I need to be a bit more dialed in diet/training wise to make the most of it. I’m pretty happy where I’m at currently considering my lifestyle.
Wow that’s funny anavar was first steroid I want to try I searched it a little…it’s the safest /cleanest/most priciest oral
The thing about SARMs…yes steroids are obviously better. SARMs are exaggerated about their bad side effects…if you have reliable source start with lowest effective dose than it can be worth it but like you said it’s not going to gain as much as steroids definitely more than natural tho for sure
But why would you take something that is going to have equal at best or worse effect on you and give you less than half the results?
Well you could see it as another anabolic option so you don’t run up the dose of a real steroid where you have to change to others…Because they’re weaker than steroida side effects are a little weaker but the same. There’s one called s 23 they say should be a real steroid it’s the most potent and compared to winstrol/anavar especially cause of the drying effect. I’m going to try it next couple weeks. I don’t have a lot of experience with SARMs I did run 2 cycles before of rad 140 and cardarine with 1 cycle
@unreal24278
SARMS vs steroids
Edjumakate us please
He’s typing already!
The difference between the words “yeet” and “floop” is that “yeet” is legitimate slang whilst I made up “floop”
Sarms are generally non-steroidal in structure, but their unique chemical structure gives them affinity to the androgen receptor, with site specificity pertaining to skeletal muscle. The ideology of the perfect selective androgen receptor modulator would be one of which only binds to the AR in skeletal muscle, the reason these drugs are being worked on pertains to the notion of “we can get a drug that binds to the AR in skeletal muscle to initiate enhanced gene expression, elect a hypertrophic response without unwanted side effects”… so AR binding in the brain, prostate, cardiac muscle tissue, kidney etc could be taken out of the equation… thus amoreliating the concern for sides such as cardiac enlargement (if mediated JUST by AR binding), prostate enlargement in those predisposed, polycythemia etc…
That being said if we look at the data regarding SARM usage in LOW dosages the side effects still appear to be identical to that of anabolic steroids, profound SHBG suppression, HDL suppression, LDL increase etc… anecdotes appear to indicate hepatotoxicity to be an issue, they’re just as suppressive comparative to AAS when used in the dosages one takes for recreation. It appears certain sarms have the potential to induce ocular nerve damage by binding to (presumably) androgen receptors within the eye (S-4)
However the notion of androgen receptor site tissue specificity… (this is what constitutes as a sarm) pertains to all anabolic steroids that display site specificity, so any modified version of testosterone (say one without affinity to the 5-AR enzyme, those which have dramatically modified ratios regarding anabolic/androgenic activity etc) are considered sarms, as a matter of fact TREN has been called a “sarm” within medical literature… so I presume we are talking solely about sarms that are non-steroidal in nature
Non-steroidal sarms have
- no affinity for the 5a reductase enzyme
- potentially a higher rate of tissue specificity in terms of AR binding, meaning one MAY be able to bypass effects such as LVH and whatnot (if AR binding to cardiac myoocytes can be bypassed)
- no affinity for aromatase
- still appear to elict many of the same adverse effects on lipids, SHBG suppression etc
- may or may not be safer than AAS, we just don’t know…
- Sarms like Ostarine differ tremendously from AAS in that chemically they aren’t composed of a steroid core structure/backbone
But given they’re rather selective in action, for use in the elderly (no water retention, acne and whatnot) they may be of use… but then again… we do have oxandrolnoe
SARMs work matter of fact they’re banned in pro competition…reminds of when NBA player couple months ago got suspended 25 games for ipamorelin lol a freaken peptide.
Theyrw shouldn’t be a competition of SARMSs vs Steroids it’s more like
PEDs=steroids, SARMs, peptides
Basically just add it to your arsenal…YouTube IFBB pro Greg Doucette and the guy who’s video I embedded for the 100mg/week trt experiment. They both have SARMs(along with steroids) videos and they’re experiences with it
@Emcon456
I’m not saying they don’t work I’m just saying I’ve seen folks that use SARMS only and those that use steroids. I don’t see any reason to use something that will give less gains for the same amount of risk or more. Many of the SARMs guys use them because they are scared of needles.
I think the ones who only use SARMs and not steroids do it for price, legality, anabolic that is easier to find(some of them don’t have reliable gear source…I do…I just don’t know when I’ll start first non-testosterone steroid), and of course like you said needles which is retarted
How many times have you ran anavar and what dose? what were your results? If you want I live in Houston,TX you can e-mail me Emcon456 at gmail dot com
I ran it for two weeks and lost all libido so I stopped.
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Yep, you’re right this far…sorta…You’re not creating “delta P” between the two - you’re creating a vacuum in the syringe…you can’t conceptually treat vacuum and pressure as equivalent. The T flows from the vial to the syringe to balance the vacuum between the 2 vessels.
Nope. The flow rate goes down because the vacuum in the vial gets closer to the vacuum in the syringe. The flow rate would not change as you describe if you were pulling from an open amp rather than a vial.
No, and in fact it could be (slightly) the opposite. If you use a standard (non low dead space) syringe, you won’t get quite the 99%+ vacuum you can with an insulin pin.
I may need to re-read /correct myself later. I’m tired.
Why is that? It is an absolute difference in pressure that causes flow. I don’t see why it would matter if Delta P is formed by a vacuum vs positive pressure. Maybe I’m missing something.
No vacuum in the vial of the user injected air before pulling vacuum. A reduction in vacuum is essentially the same as a reduction of Delta P. I don’t see why we would treat them different. [quote=“louiststeinhil, post:154, topic:264487”]
No, and in fact it could be (slightly) the opposite. If you use a standard (non low dead space) syringe, you won’t get quite the 99%+ vacuum you can with an insulin pin.
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Yes but the difference pulling say 1ml into a 60 cc syringe will be faster than a 1 ml syringe. As the vacuum in the large syringe is barely impacted by 1 mL, not true with the 1 mL syringe.
I’m going on 14 months. Im still making really good gains. Adjusting my diet and training has helped to break plateaus.
OK, cutting what I said back to the simplest, barest essentials:
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Especially (but not exclusively) if you start with a “low dead space” syringe - be it 1ml or 50ml, you hit near total vacuum very quickly - like I said, you have 99% vacuum after pulling 0.1ml, regardless of the size of the syringe - assuming your dead space is 1ul.
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That means if you’re pulling against an open-air system (say, a cracked open amp), you’re getting (at sea level on a standard pressure day) somewhere around 14.5 psi of vacuum. The atmospheric pressure will then be acting trying to push your T into your syringe with 14.5psi * the cross sectional area of the inside of the needle. It will not vary with the diameter or volume of the syringe - you cannot pull more vacuum than this.
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Pulling from a sealed vial instead doesn’t change this much, it just makes the math more complex. The vial will generally be close to atmospheric initially, especially if you pre-inject air like you should. However, I’ve found the vials are not perfectly sealed, and they’ll hold vacuum better than they hold positive pressure. That is, if I put an empty syringe into a vial and pull back, when I let go the syringe returns much of the way back to empty. But not all the way. On the other hand, no matter how many times I inject a full syringe of air into a vial there’s never enough pressure to push the syringe plunger back out.
I would argue that, for TRT, an androgen agonist that has specifity mainly for muscle tissue is not ideal. Increased muscle mass is a pleasant side effect for most on TRT. But it’s not primarily the goal. Increases in well being, sexual function, assertiveness(the classic virilizing traits) are the goal. And this is would mainly be mediated via androgen receptors in the brain. Beyond that we need a better understanding of how local AR activation in specific tissues affects positive and negative outcomes with TRT. More targeted therapies could evolve fromthis research. I’m convinced that one of the big missing pieces of this TRT puzzle is the sensitivity of the androgen receptor. It can explain the wide variation of outcomes across the population. Consider these two options: Push free T to extreme levels to flood the body with androgens and overcome AR receptor insensitivity via brute force or focus on decreasing AR Insensitivity such that one can achieve a more positive outcome at a lower overall T level. To me, it is glaringly obvious which is the better long term solution.
100% agreed, though we do have men with PAIS (genetic mutation induced a lack of sensitivity within the AR) these men need very high dosages of testosterone, sometimes synthetic androgens (whilst I don’t believe in all the estrogen demonisation, if the ER remains unaffected theoretically one would have a normal response to estradiol/estrogens yet an abysmal response to testosterone/DHT)… so there’s a clear correlation in which states a lack of androgen receptor sensitivity induces an abysmal response to otherwise physiologic dosages of TRT
I’ve spoken to my endocrinologist about this issue (good god I hope she never comes across these posts)… said endocrinologists states that he/she has treated a number of patients with supraphysiologic doses of T… HCT/lipids, psa, BP and other parameters remain unaffected. If cardiac ailment stems from AR mediated gene transcription (inducing systemic alteration, I’ve been over the numerous mechanisms behind potential AAS mediated cardiac enlargement/disease), then there’s no incentive would exist to find alternative therapies as we already have acceptable means for treatment
It’s not brute force, neither is it flooding the body with anything, due to AR mutation, androgens can’t bind efficiently, so higher dosages are required for mere physiologic maintenance
Edit: shit I forgot the ER is also typically affected via PAIS, disregard the first paragraph
I get that there are unique genetic disorders that might require extreme doses. But in the general TRT population it isn’t applicable. If the line on AR stimulation in tissues that yield negative outcomes i.e. the heart are near the upper bounds of current TRT protocols. Then the goal should be to determine if changes in AR receptor sensitivity are more systemic or more local. My gut says it’s more local. Certain areas gain or lose sensitivity for various reasons. And if this is the case, what therapies(whether it be simple natural health/diet/supplement remedies or perhaps pharmacological) lead to promotion of increased AR sensitivity in the most therapeutically beneficial areas while limiting it in less beneficial areas (increase in brain, increase skeletal muscle, unchanged heart, etc)
I can guarantee the number of men taking 250+/week is not a function of PAIS