My layman's presentation would be based on this information which I have interpreted over the years. The LONGER the reported "half-life" an injectible esterfied steroid is stated as having, the LARGER/more complex the molecular structure. These larger molecular structures tend to INTERACT/BIND with "FAT" or muscle - BUT FURTHEST FROM LIKELIHOOD OF BINDING WITH
WATER. Thus they are not very "dynamically or Fluidly active" in the body the way my mind see's it. But it would STAND TO REASON that for a for a FUNDAMENTAL STATIC BODY PRINCIPLE to involve with a foreign molecule, there would have to be at least (1) fundamental chemically attractive properties, (2) certain encouraging conditions and co-factors to some degree, (3)
and ROOM in the PHYSICAL COMPLEXITY of the intended cellular/molecular target VIA COMPLEXITY IN STRUCTURAL DESIGN OF SAID.... Else your principle target is WATER, which is very dynamic in action in the body and not a "Static Principle" as incorporated.
Whether or not these longer ester molecular structures bind with "fat" as
"FORCED" (as "large molecular structures like "FAT" are the ONLY ONEs that CAN accept them) - OR -
"INCLINED" (due to structural design ideology/similarity) - I DON'T RECALL... You can consider that WATER does not involve its self with "fat" in the body any more than its SERVICING INTENDED NATURE. So I would speculate water(H20) is used Concomitantly in the body as this example - beyond any PRIMARY INCORPORATION into a particular cells structure. Personally, I do think that ester binding to 'FAT" as an injectable steroid application is more of a FORCED EVENT. "Else you'd 'just have to look at it and it would stick - right??"
You may also consider that one of the primary purposes of the SECONDARY SOLVENT - BB - Is to help the esterfied steroid to interact with the LOCAL TISSUE at the point of the injection/application.
Keep in mind a lot of the stuff I WRITE is CONJECTURE FOR THOUGHT and based ONLY on basic understanding of biology and chemistry on the most primitive level. So I am ASKING as well, and not attempting to PREACH a bible - although it may seem. SO SOMEONE CORRECT ME IF YOU CAN...!
BACK ON TRACK - to my intended reply -
IN EXPERIENCE with application to animals, Some of the factors will be as follows:
1. You MUST first understand that a steroid "half-life" in reference to esterfied injectables IS NOT EVEN CLOSE to the description of the "active metabolism half-life" ("active drug half-life") of a steroid or drug in blood circulation or as involved with the body for its full intended EFFECTIVE metabolic action. AS EXAMPLE, if you consider the amphetamine Ritalin has a 3 hour half life. You eat it, it goes into blood and cells, and starts working - and getting "worked on" by the body. NOW CONSIDER that testosterone has a drug half life of seconds to minutes once in blood circulation, and only depending on factors like whether or not its picked up by blood protein, and other things life general blood population, metabolism action, and Clearance/elimination. So if you compare to Ritalin HITTING THE BLOOD STREAM and then having a 3 hour HL, the Testosterone hitting the blood is 3 minute HL.
2. So the REPORTED steroid half lives are really SOLELY BASED on how long they will sit in the body BOUND TO "FAT" prior to their release de-esterfication VIA Esterase ENZYMES - which must FIRST REACH and AFFECT the esterfied testosterone WHILE its bound to fat,muscle, whatever that had a COMPATIBLE MOLECULAR STRUCTURE enough for it to stick in the first place.
3.
IMPORTANTLY - IN A VACUUM - Esterfied steroids MUST HAVE A DEFINITE Time to be de-esterfied by Esterase enzymes...! There can be no other way. Therefore there MUST be FUNCTIONAL Biological factors in play which are CAUSING this DELAY of up to 6-8-10 weeks even depending. So the MAGIN QUESTION IS - "how long does it take to get to the center of the tootsiepop". There is no easy answer as the factors are many, and can be subdivided even:
- THE FIRST TWO CLASSIFICATIONS have to be DEMAND vs SUPPLY. AKA - Does the body NEED to GO TO THE TROUBLE to "de-esterfy" Fat bound EXOGENOUS HORMONES?? After all, if there is plenty already in blood circulation, this will prohibit the NEED, Limit the "blood space", & result in a natural gravitation to process what is READILY Available.
I do not discount that there is also a general SUPPLY BASED Proximity effect also occurring. If not even FORCING ester involvement with the body due to the nature of the principle HOSTING/INVOLVED "fat" cell to naturally want to return to stasis. But in WHAT Conditions and end effect must vary based on overall current body handling protocols pertaining to FAT/muscle metabolism.
- The Second Most influential I SUSPECT would be PHYSICAL INVOLVEMENT of the ester with the body. AKA - pertaining to how applied. If we go back to the original POINT of this reply, which is TIME TO DE-ESTERFY a steroid in the body in a vacuum. Now take an esterfied steroid, PHYSICALLY/MANUALLY Place it in proximity with a compatibly involving tissue (fat/muscle primarily)- and whacher stick.....! but the magic question we are discussing is for how long? So it stands to reason that if you stuck an ester to a muscle in a body with plenty of endogenous supply already available, the demand or resources may not be in place to quickly go after it. But if you stuck that same ester in the same place in a body starved of hormones and will all the effective co-factors (esterase enzyme, etc..) in place, it may very well get picked up immediately.
THiS PERTAINS TO PHYSICAL REAL CONDITIONS/supply/demand/general body BUT.... With further specific reference to HOW or WHERE APPLIED (Stuck).. I wonder if IN A VACUUM, when would a an ester detach from a compatible molecule.?? Would it be related to this fat just wanting to find stasis and shed the extra load? Would it be related to the chemical nature of the ester, and it just "wearing out", or breaking down in the presence of ZERO destructive stimulus - but as an inherent failure by design?? NO ONE KNOWS...~!
4. SO WHAT FACTORS SLOW ESTER METABOLISM?
a) Does that saturation of the body with the esterfied steroid as a SYSTEM actually in fact compound upon its self by population related to supply/demand?
b) Does the physical PROXIMITY as APPLIED have an influence? Do adipose tissue cells effectively hold esters longer than muscle. COULD FAT even hold an ester PERMANENTLY if that adipose tissue cell was never again actively metabolzed as a fuel source (like a heavy metal in fat)?? Do esters sitting ATOP muscle tissue get ACCESSED faster or slower? Do Esters closer to the physical central area of a given muscle group get accessed by esterase enzymes at a slower or faster rate? Do esters provide "protective shields" as effective "DEPOTS" via MORE of them applied at the same location, thus INHIBITING Normal blood access (consider you are "pickeling" the tissue cells in many ways)...? Does the physical location within the body with reference to blood flow slow or expedite ester release (consider the extremities of the body simply process less total blood volume at the end of a given day, and the same goes for microcillary involved tissue)..? How does general blood population of EVERYTHING - ranging from other hormones, hormonal derivatives, blood fat, liver enzymes, general co-factors, and
even hydrolic stasis with regard to ELECTROLytes is HUGE in reality.. How do vitamins and Minerals (METALS which DRIVE the body's ELECTRICAL FIRING) come into play? THE LIST GOES ON...
IN SHORT
, the time for which de-esterfication occurs in completely variable based on a MYRIAD of COnditions specific to each individual and ANY TIME varying greatly. You can attempt to split, cut, and shit hairs, but THE REALITY of the situation is that this TIMELINE Changes greatly STATISTICALLY CURVING with Application as AMOUNTS and DURATION of TIME. The curve will be NON-linear in REAL ACTION based on other APPLICATION FACTORS not discussed here as well. Therefore its simplified as a "Half-Life".
What the above paragraph SAYS. Is that IF,,, you pin test cypionate for the first time in a year, and center Bullsye of a large muscle group, in conditions which could 'use a little hormone"; it will most likely have effective action DATES running from starting in as little as 2 days, peaking in 4-6 days, and fully metabolized to nothing in 2 weeks tops. The first 48 hours would be the IPS. (It should also be noted that BB in the solution is touted as having up to a 72hr active effective time to "assist the ester into fat", and I suspect this diminished with biological exposure/experience) NOW IF YOU CONTINUE TO PIN MORE Cypionate, and with consideration of that SAME LOCATION, there appears to be a "Compounding effect" to which extends the "half-life" of the steroid as - THE MORE YOU PUT IN, and THE LONGER YOU DO IT - The MORE STAYING POWER THIS DEPOT WILL HAVE EFFECTIVELY IN THE BODY.. (at the same time it may also reduce the effective half life WHILE increasing INSTANT EFFECT pertaining to IPS.. This is where variables like how often you pin, how much each time, site rotation, body loca, etc come into play as well and importantly!). The Proof of this effect is the fact that a first time pin by a previously experienced user will be " completely gone" in as little as two weeks, if no more is applied.!!!. And ONCE he continues to pin testosterone, if considering the same location, the effective 7 day half life starts to apply moreso now, and the total effective time (not "half life" )that the ester appears to have action in real life now moves to 14,21, or even 30 days (exaggerated but point being INCREASING). If you MATHED out a 7 day half life calculating effective supply available from exogenous steroid as pinned, you get the following as a FULL LIFE CALCULATION. (initial set up time) +7 days, + 3.5 Days + 1.75 Days + .87 days to not negligible as EXCESS SUPPLY for the body. That total is about 14-18 days total lifespan - for one single pin with no more.. Still, not you can go and consider “half-lives” as measured in available blood serum and tout longer times, which is ILLOGICALLY the basis for much of the “half-life concept if scientifically attempted from a “Visible Angle”. The problem with this is that it DOES NOT take into account how much is processing and at what rate, and further does not examine current esterfied steroid present in the body. These two failures are big and devaluing minimally. Again the truth being that the real fair calculation lies somewhere between the manual time count, and the “visible blood count”. BUT this variance in ACCOUNTING is also PROOF of the massive failure of the use of the TERM "Half-Life" as pertaining to injectable esterfied steroids.!!! There can be no other way as this presentation is packaged. But there are so many variables not discussed here.!! So its an example as "thought-fuel". So feel free to blast me now.
But the PROOF which I attempt to hang a hat, is the FACT that steroid TOTAL Active life DOES APPEAR to VARY ranging as much as 7-14 days OR Single-to-double (which are not really the same).
Make no mistake. Bill Roberts is an EXPERT. I am a construct of free thought designed only to encourage further thought.
