Cubbie, There is no question that I agree that the application of TRT via the Urologist method on a single injection of CYP per month has appeared to fail in effectiveness. But I am only agreeing as due to a failure in the application methods that can be corrected to increase efficiacy I speculate by at least 50% thus increasing to an overall 80% min vs potentially as low as 40% ( I speculate). I expound upon the details of this toward the bottom of this post. But the proof is really in the much greater degree of sucess I have read about and witness invovled with pellet implants. So consider the following...
You got me thinking about another and a better option to test my hypothesis about 2-3 mgs being "the perfect dose" for the LowT Male. I can not argue with some issues about the TRUE APPLICATION EFFICIACY of dosing TCyp IM. And not only based on poor injection technique, but DOES IT REALLY STICK LIKE THE PRINICPLE OF THE CYP ESTER SUGGESTS (45-60 days)?
SO would a testeosterone decanoate not be the better option? Or even just Sustanon (which is designed I think with TRT in mind as it also posesses a large component of Test decanoate). Thus guaranteeing a better "bite" of the ester in the muscle?
SADLY and due STRICKLY to ignorance. Testosterone concoctions like these with longer esters, as yet they ARE IDENTICAL in ACTIVE COMPOUND are still demonized when all along they are the same thing - Testosterone, and perhaps a more effective option for Low T males...
I would also like to elaborate on my theories about injection technique. I really dont have an opinion about Sub Q T injections yet. Obviously it would appear on the suface a poor idea to inject T directly into fat considering the estrogenic implications, HOWEVER, ONCE a depot area is saturated, how much more E's can it make? Thus leaving the remainder to trickly healthily into mainstream circulation. Who knows. Obviously again, quantification in activity via serum counts would only serve validated if measures in short term intervals (every ten mins) post injection.
ALSO, you have to wonder ON just what LEVEL is the fat related estrogen coversion REALLY OCCURRING PRIMARILY. Could it be that Estrogens are for the most part ONLY Converting once the T ester is in the blood stream and thus PERHAPS PRIMARILY ACTING ON BLOOD FAT. Or CHOLESTEROL that is.....? Specifically, is fat related ester generation confined to blood level activity and NOT from stored fatty tissue orgin? Really still, ( and we can leave this for another day) DOES FAT EVEN HAVE A DIRECT ESTROGEN METABOLIZING ABITILY, or is it just creating the conditions favorable for increased estrogen production by other means? Really? Does fat even have an estrogen receptor? Another day though.
Back on track. WOULD there be a difference in the amount of E's amomatized based on circulating blood fat?; and based on whether or not the fat is HOT & FRESH - LOL. Meaning take some different scenarios:
(1) Blood fat as a direct supply from immediate dietary injestion (animal fat, vegetable fat, TRANSFAT (synthetic)?
(2) Blood fat from natural liver production/conversion.
(3) Nutural composition of Cholesterol produced via the liver (HDL vs LDL)?
(4) Could Blood Fat inhibitors actually reduce or prevent this estrogenic activity even all together? (statins, Highly soluble oatmeal, even dietary tract means of reduction of dietary supply - via cleaner eating or Chitosan?)
Of course. Right?
Little is know to US about the true mechanism AND POTENTIAL of ESTER storage and transport within the body. JUST HOW LONG COULD AN ESTER SURVIVE IN A SUPERSATURATED BLOOD STREAM without being eliminated? And we are not talking de-esterfied TT as bound to blood protein. We are talking the ability of esterfied TT to enter, survive, and redistribute in the/via the blood. And even being redistributed throughout other fat stores in the body.? I have broached the subject with some technicals only lightly in the past and quickly received the answer - "NO", but with no merit of proof. SO I am discussing here the principle of the ester to circulate effectively throughout the body, ESPECIALLY during the SHRINKAGE/loss PERIOD that occurs AT THE TIME OF INJECTION, ... AND/OR at LARGE INUNDATION INTERVALS when GROUPS of esters (from a depot) are all effectively released by Esterase enzymes at a single time ( you have to belive this will happen based on the principles of a DEPOT and as relatet to time to interaction)....
I have experiemented with unprocessed oat meal (blood level blockade as above), and noted an astounded pick up feeling that I belive was associated with a reduction of estrogen metabolism thus providing more available for androgenic activity. HOWEVER, I have not used the oatmeal while applying TRT as a FAT MAN. So I have to wonder how much more success I might have.? How much less minor GYNO activity would be supplied? But what about STATINS? If the FAT RELATED Estrogen activity is indeed due primarily to BLOOD LEVEL T-ester metobolism as a primary, could these drugs in combination hekp to solve some of the potential estrogenic issues that I am forcasting in today's LOW T MALE?? and one who is trying to do it right with exercise and diet as well.? HOW MANY OF THEM ARE REALLY GOING TO CHANGE THEIR DIET? Even if reduced, do they modify their diets FAT APPORTIONATELY to the same degrees? So then there are two potential DIET TRACKS/applications here we are analyzing.
So still if giving some of this premise any credibility at this time. What do WE even really know about cholesterol and the liver, as RESIDENT PATIENTS -LOL...... NOTHING. So what are cholesterol molecules? How are they produced. I understand that some are just going to be made by the liver as a biological function, and genetically diposed with variance in different folks. STILL, it leaves the reamining question, HOW DOES DIETARY FAT IMPACT THE PROCESS. How much is it really required to ellicit what? And how much does it determine the outcome of which types of cholesterol are PRODUCED by the liver. We have to cast doubt on dietary fat alone as the FUEL for this process of liver fat generation and speculate that the liver can turn ANY Food into cholestorol, and by gentic inclination in population type of cholesterol (ldl vs hdl). So how do the additional calories play in and to what degrees? Clearly when you eat, fat will go straight into blood thus having a dramtic impact on blood poplation as it absorbs throughout the digestive tract. So now you are left with elimination via as fuel metabolism, and liver conversion/removal. But does blood fat HAVE to get "burned or stored"? Or can it be removed directly. I am guessing not directly as a kidney path or one would see french fry grease in their urine which probably denotes a massive organ failure. BUT CLEARLY, fat is removed directly via the COLON. So another trick is how to keep it in there all the way to the CORN HOLE... LOL But as the same principle as with testosterone administration, AGAIN, the body will demand so much - and get it.!! But just what damage is the EXCESS SUPPLY doing. We allready know the anwer as a general health premise. But the point is how is this excess fat affecting SynT administration and hormone conversion with regard to estergens and androgens? I am fairly certain the answer will be similar to the answer of excess T administration. Which is to the negative, but ONLY to the degree excess can be effective either negatively or positively. It only takes so much cyanide to kill a rat, so to speak... Then there can be no further EFFECT. So again, we appear to be dealing with a CONGLOMERATION and a CUMULATIVE TOLL or continued as repeated conditions.
FINALLY, one has to ask the question, HOW TO METABOLIZED FATS REACT WITH THE BODY? That is, the fats we are releasing when on a calorie restrictive diet, or that are metabolized for fuel based on exercise.. What is the returned fat product in circulation effectively? Is ONLY enough fat released as required to immediately burn? Or can additional fats be released when during this process that actually just move around with the same properties as fats JUST INGESTED IN EXCESS? We are animals and we are what we eat, so you would think cracking into the stores can have the same temporaray potential as pigging out on food (but which type of food fat, animal only?) Or do these metabolised fats, or fats summonsed for fuel even ever possess their same original properties at any point between release and burning? I would think YES, but only as animal fat. We are in short EATING OURSELVES, right? This also begs the question of the varance of PLANT and SYNTHETIC (trans) fats. How do they store in us? Or do they at all? Are they just creating HAVOK as the body is FORCED TO CONVERT or IMMEDITELY DEAL WITH THEM. Hence the proof in the primary problem with transfats (margerine, etc..) These were created solely as a PRESERVATIVE and via the means LONGER or more complex BONDING that makes it DIFFICULT for the body to process them. So then what toll are they taking on our ability to healthily metabolize the natural or healthy fats. Is there a SYNERGY created by ingesting transfats that is thus allowing healthy natural fats (inclusive of YES - Butter) that is causing these fats to now how toxic potential whereas they otherwise would not AT ALL. Has the workload created to metabolize trans fats now created a monster out of otherwise normally healthy fats? Perhaps even the "healthy", natural fats DO indeed have a stronger propensite to harm the body, or "stick" to arteries, BUT ONLY when allowed to fourish as when HINDERED by trans fat processing? Now they have become deadly whereas othewise normal and healthy. SO what is the composition of a fat blockage in an artery. I dont think all of them are even fat?? SO would this have stuck in the absence of the transfats? This would mean that healthy fats are not the evil, and that at the same time, trans fats are not the supply of arterial blockages, but it is ONLY the combination of the both - the trans fats being the primary catalyist. And to what degree varying on the individuals genetic propensity to metabolise fat/cholesterol. For that matter and speaking of cholestorol SERUM COUNTS. Could a high level simply mean that while more may be present, the individual even has a HIGH propensity to keep it harmlessly in circulation, and not biting the walls of arteries.
I have sidetracked now. But this all still has application to blood fats as the related to testosterone and estrogen metabolism certainly. Finally what are the differences in how vegetable, animal, and sythetic fats HOLD and TRANSFER esters. Obviously vegetable oil allows for ester saturation, hence the cottonseed or peanut oil as a primary solvent in Testosterone cypionate and the like. Obviously vegetable oil readily releases it as well. So here is an interesting point. JUST HOW MUCH MORE EFFICIENT IS ANIMAL FAT AT STORING Cypionate and its ester? Obviously it is much greater as it is cited as holding it in the body for 45-60 days. So then the ester transferred from the veggie oil in a matter of hours to days into body(animal fat) to be stored up to two months!?!?! There is some proof of variance in holding affinity of fats. Now thats a strong affinity. So now consider blood composition of fat, cholesterol, etc.. Does someone eating a shitload of vegetable oil (olive oil persay) have less of an ability to carry non-protien bound "depot shrinkage" for an extended time, but at the same time have a faster affinity to pick it up and transport it? Does a healthy component of vegetable oil perhaps provide a vehicle for the mobilization of fat stored esters from the animal fat (your fat) in which it is stored? Does a person with lower vegetable fat in their diet HOLD AND ESTER LONGER? Does a person with a high level of TRANSFATS (synthetic) have a further diminished ability to pick up or excecute the ester from stroage, and yet whatever IS picked up by transfats is held a longer time whereever? Are transfats actually held within human adipose tissue stores - AS TRANS FATS withing animal fat? Is this part of the initial dieting and FAT RELEASE process that seems so slow at first, and actually a primary obstacle to health fat metabolism/removal when incepting a dietary and excercise change in regimen? SO now how much of the ester was stored in TRANS FAT? AND will it ever released converting to effective TT, or is it forever bound as far as the lifespan in our bodies until the liver has to destroy the whole transfat ester "package" in the end to never realize the effect of that Syn T? Could transfats contribute to the failure of TRT, or Steroid use even.
This all begs the question. HOW much is a condition of fatty stasis, or NO CHANGE critical to having a good blood profile for effective T ester metabolism, or a healthy testosterone metabolism to minimal Estrogen conversion? Does the condition of WEIGHT LOSS as a general, whether, dietary restrictive, exercise, or whatever, PROVIDE A POOR BLOOD PROFILE REGARDLESS? Is stasis in fat metabolim required for a health Syn T conversion? Can INHIBITORS like statins, Blood soluble fibers (Oatmeal) benfit the SynT metabolism process? Could ELIMINATION EXPEDITORS even benefit this process by expediting the removal of blood fats ( amphetamines, ephederine, Clenbuteral, caffine) thus not allowing RELEASE RATE esters OR Circulating TT as a general to interact with blood fat and readily convert to estrogens?
The long and short and one of the things that began this rant, was the concept of the the true efficiacy of the cypionate ester as a form of TRT. Can it really be applied to ellicit a 45-60 DEPOT in the body? I was leading into POOR INJECTION TECHNIQUES and how to resolve best possible. Do you really think some nurse just closing her eyes and pinning your ass in 5 seconds is effective? Was that one little rub with a cotton ball an effective clamping of the leakage into fat/circulation? Think again. Have you ever pinned a dose only to see it leak back out of the skin.? Well, if it came ALL THE WAY back out of the muscle and INUNDATED the void or fatty area between the muscle and skin to the point that it seeped back through a hole in the skin this should tell you something. BB's say a max pin in the buttock is 2mls. This would have to be a GORILLLA. The average Low T male I speculate could take about .5 ML AT BEST without severe detrimental shrinkage/loss. I do propose that WE, as TRT males, can get a ful ML to stay in the muscle on a single injection (or 90% of it).
So here is how to do it:
(1) You will obviously have to hit the muscle centrally, IF NOT CLOSER TO THE INSIDE LOWER PERIMETER. Think about it like this. Any leakage is going to follow the path it came in on. The injection IS UNLIKELY to just migrate out the back side of the muscle as there has been no hole created ( and proof in that the juice does not just go right into muscle, else it would not be quirting back up and out!). So go ahead and get to the deeper side of the muscle group, with care not to go through.
(2) Spend a good 2-3 mins injecting, even moving back out as much as a path of a cm or two while proceeding thus increasiing potential absorbtion area. But there has to be a diminishing effective application as time moves forward. This is proven in the problem we are discussing. The best you can hope to effect to get the mucle to relax, expand a little, and START ABSORPION.
(3) I belive the critical point is indeed the capping off of the puncture with PRESSURE. So what is the effective STOPPER to keep this PRESSURIZED depot in place utlimately? Its going to be in the DEPOT COMPONENTS / specifically the Benzyl benzoate. This component of a TCYP injection is not only a carrier, solvent, and preservative - IT IS THE ESSENCE OF THE "DEPOT". It is greatly responsible for any inflammation resulting, and solely if there is not longer any allergy the the ester resulting. The premise of the BB in T cyp is to help retain the injection at the LOCAL site so that it will be properly uptaked by the muscle/fat at that SPECIFIC SITE. So go ahead and cap it with a finger, or PALM EVEN. Apply pressue and rub the bastard a bit. You goal is to force the depot to stay in the muscle for a short time by blocking the pucture alone. The assistance will come in the bodies ability to close a wound in combination with the BB hepling as a solvent to in keeping the cyp "powder" from precipitating into not READILY dispersible powder form too quicly so that it can inundate into the 2-3 inch surrounding tissue. And finally the mildly inflammatory reaction of the BB will help to seal the pucture to some degree. So its a give and take OF BORDERLINE histaminic reaction. BB providing solubility for migration into muscle tissue (primary pupose of BB) vs an propensity for tissue aggrivation thus slowing the process or leakage at the same time. I DO Believe that inflamation and pain is primarily based on the ester itsself and not so much the BB. But I am certain the BB does cause aggrivation and pain to some degree and varying again based on individuals and their experience .immunity to the reactino by time.
The point is. I agree that there is great potential for a once per month injection to fail. I believe this is caused primarily due to the failure of the injection its self. How much failure could be overted by proper injection techique/application remains unclear. THiS IS the greatest OVERSIGHT in TRT application today as it is obviously EVERYTHING in the once per month Urologist recommended dosage. It is clearly a conundrum as a GROSS OVERSIGHT and an example of a CATASTROPHIC FAILURE due to THE MOST BASIC PRINCIPLE of the application. So again, we have a situation where THE GRAVITY and implications of the BIG PICTURE have caused SOCIETY to TOTALLY fly by the obvious failure that has reduced the EFFECTIVE RESULT BY PROBABLY AT LEAST 60-70% considering... To examine the far side of the syn tcyp application process. How much more efficient could body builders be in application? Just how much would they really need.?
I again resign for now....
You got me thinking about another and a better option to test my hypothesis about 2-3 mgs being "the perfect dose" for the LowT Male. I can not argue with some issues about the TRUE APPLICATION EFFICIACY of dosing TCyp IM. And not only based on poor injection technique, but DOES IT REALLY STICK LIKE THE PRINICPLE OF THE CYP ESTER SUGGESTS (45-60 days)?
SO would a testeosterone decanoate not be the better option? Or even just Sustanon (which is designed I think with TRT in mind as it also posesses a large component of Test decanoate). Thus guaranteeing a better "bite" of the ester in the muscle?
SADLY and due STRICKLY to ignorance. Testosterone concoctions like these with longer esters, as yet they ARE IDENTICAL in ACTIVE COMPOUND are still demonized when all along they are the same thing - Testosterone, and perhaps a more effective option for Low T males...
I would also like to elaborate on my theories about injection technique. I really dont have an opinion about Sub Q T injections yet. Obviously it would appear on the suface a poor idea to inject T directly into fat considering the estrogenic implications, HOWEVER, ONCE a depot area is saturated, how much more E's can it make? Thus leaving the remainder to trickly healthily into mainstream circulation. Who knows. Obviously again, quantification in activity via serum counts would only serve validated if measures in short term intervals (every ten mins) post injection.
ALSO, you have to wonder ON just what LEVEL is the fat related estrogen coversion REALLY OCCURRING PRIMARILY. Could it be that Estrogens are for the most part ONLY Converting once the T ester is in the blood stream and thus PERHAPS PRIMARILY ACTING ON BLOOD FAT. Or CHOLESTEROL that is.....? Specifically, is fat related ester generation confined to blood level activity and NOT from stored fatty tissue orgin? Really still, ( and we can leave this for another day) DOES FAT EVEN HAVE A DIRECT ESTROGEN METABOLIZING ABITILY, or is it just creating the conditions favorable for increased estrogen production by other means? Really? Does fat even have an estrogen receptor? Another day though.
Back on track. WOULD there be a difference in the amount of E's amomatized based on circulating blood fat?; and based on whether or not the fat is HOT & FRESH - LOL. Meaning take some different scenarios:
(1) Blood fat as a direct supply from immediate dietary injestion (animal fat, vegetable fat, TRANSFAT (synthetic)?
(2) Blood fat from natural liver production/conversion.
(3) Nutural composition of Cholesterol produced via the liver (HDL vs LDL)?
(4) Could Blood Fat inhibitors actually reduce or prevent this estrogenic activity even all together? (statins, Highly soluble oatmeal, even dietary tract means of reduction of dietary supply - via cleaner eating or Chitosan?)
Of course. Right?
Little is know to US about the true mechanism AND POTENTIAL of ESTER storage and transport within the body. JUST HOW LONG COULD AN ESTER SURVIVE IN A SUPERSATURATED BLOOD STREAM without being eliminated? And we are not talking de-esterfied TT as bound to blood protein. We are talking the ability of esterfied TT to enter, survive, and redistribute in the/via the blood. And even being redistributed throughout other fat stores in the body.? I have broached the subject with some technicals only lightly in the past and quickly received the answer - "NO", but with no merit of proof. SO I am discussing here the principle of the ester to circulate effectively throughout the body, ESPECIALLY during the SHRINKAGE/loss PERIOD that occurs AT THE TIME OF INJECTION, ... AND/OR at LARGE INUNDATION INTERVALS when GROUPS of esters (from a depot) are all effectively released by Esterase enzymes at a single time ( you have to belive this will happen based on the principles of a DEPOT and as relatet to time to interaction)....
I have experiemented with unprocessed oat meal (blood level blockade as above), and noted an astounded pick up feeling that I belive was associated with a reduction of estrogen metabolism thus providing more available for androgenic activity. HOWEVER, I have not used the oatmeal while applying TRT as a FAT MAN. So I have to wonder how much more success I might have.? How much less minor GYNO activity would be supplied? But what about STATINS? If the FAT RELATED Estrogen activity is indeed due primarily to BLOOD LEVEL T-ester metobolism as a primary, could these drugs in combination hekp to solve some of the potential estrogenic issues that I am forcasting in today's LOW T MALE?? and one who is trying to do it right with exercise and diet as well.? HOW MANY OF THEM ARE REALLY GOING TO CHANGE THEIR DIET? Even if reduced, do they modify their diets FAT APPORTIONATELY to the same degrees? So then there are two potential DIET TRACKS/applications here we are analyzing.
So still if giving some of this premise any credibility at this time. What do WE even really know about cholesterol and the liver, as RESIDENT PATIENTS -LOL...... NOTHING. So what are cholesterol molecules? How are they produced. I understand that some are just going to be made by the liver as a biological function, and genetically diposed with variance in different folks. STILL, it leaves the reamining question, HOW DOES DIETARY FAT IMPACT THE PROCESS. How much is it really required to ellicit what? And how much does it determine the outcome of which types of cholesterol are PRODUCED by the liver. We have to cast doubt on dietary fat alone as the FUEL for this process of liver fat generation and speculate that the liver can turn ANY Food into cholestorol, and by gentic inclination in population type of cholesterol (ldl vs hdl). So how do the additional calories play in and to what degrees? Clearly when you eat, fat will go straight into blood thus having a dramtic impact on blood poplation as it absorbs throughout the digestive tract. So now you are left with elimination via as fuel metabolism, and liver conversion/removal. But does blood fat HAVE to get "burned or stored"? Or can it be removed directly. I am guessing not directly as a kidney path or one would see french fry grease in their urine which probably denotes a massive organ failure. BUT CLEARLY, fat is removed directly via the COLON. So another trick is how to keep it in there all the way to the CORN HOLE... LOL But as the same principle as with testosterone administration, AGAIN, the body will demand so much - and get it.!! But just what damage is the EXCESS SUPPLY doing. We allready know the anwer as a general health premise. But the point is how is this excess fat affecting SynT administration and hormone conversion with regard to estergens and androgens? I am fairly certain the answer will be similar to the answer of excess T administration. Which is to the negative, but ONLY to the degree excess can be effective either negatively or positively. It only takes so much cyanide to kill a rat, so to speak... Then there can be no further EFFECT. So again, we appear to be dealing with a CONGLOMERATION and a CUMULATIVE TOLL or continued as repeated conditions.
FINALLY, one has to ask the question, HOW TO METABOLIZED FATS REACT WITH THE BODY? That is, the fats we are releasing when on a calorie restrictive diet, or that are metabolized for fuel based on exercise.. What is the returned fat product in circulation effectively? Is ONLY enough fat released as required to immediately burn? Or can additional fats be released when during this process that actually just move around with the same properties as fats JUST INGESTED IN EXCESS? We are animals and we are what we eat, so you would think cracking into the stores can have the same temporaray potential as pigging out on food (but which type of food fat, animal only?) Or do these metabolised fats, or fats summonsed for fuel even ever possess their same original properties at any point between release and burning? I would think YES, but only as animal fat. We are in short EATING OURSELVES, right? This also begs the question of the varance of PLANT and SYNTHETIC (trans) fats. How do they store in us? Or do they at all? Are they just creating HAVOK as the body is FORCED TO CONVERT or IMMEDITELY DEAL WITH THEM. Hence the proof in the primary problem with transfats (margerine, etc..) These were created solely as a PRESERVATIVE and via the means LONGER or more complex BONDING that makes it DIFFICULT for the body to process them. So then what toll are they taking on our ability to healthily metabolize the natural or healthy fats. Is there a SYNERGY created by ingesting transfats that is thus allowing healthy natural fats (inclusive of YES - Butter) that is causing these fats to now how toxic potential whereas they otherwise would not AT ALL. Has the workload created to metabolize trans fats now created a monster out of otherwise normally healthy fats? Perhaps even the "healthy", natural fats DO indeed have a stronger propensite to harm the body, or "stick" to arteries, BUT ONLY when allowed to fourish as when HINDERED by trans fat processing? Now they have become deadly whereas othewise normal and healthy. SO what is the composition of a fat blockage in an artery. I dont think all of them are even fat?? SO would this have stuck in the absence of the transfats? This would mean that healthy fats are not the evil, and that at the same time, trans fats are not the supply of arterial blockages, but it is ONLY the combination of the both - the trans fats being the primary catalyist. And to what degree varying on the individuals genetic propensity to metabolise fat/cholesterol. For that matter and speaking of cholestorol SERUM COUNTS. Could a high level simply mean that while more may be present, the individual even has a HIGH propensity to keep it harmlessly in circulation, and not biting the walls of arteries.
I have sidetracked now. But this all still has application to blood fats as the related to testosterone and estrogen metabolism certainly. Finally what are the differences in how vegetable, animal, and sythetic fats HOLD and TRANSFER esters. Obviously vegetable oil allows for ester saturation, hence the cottonseed or peanut oil as a primary solvent in Testosterone cypionate and the like. Obviously vegetable oil readily releases it as well. So here is an interesting point. JUST HOW MUCH MORE EFFICIENT IS ANIMAL FAT AT STORING Cypionate and its ester? Obviously it is much greater as it is cited as holding it in the body for 45-60 days. So then the ester transferred from the veggie oil in a matter of hours to days into body(animal fat) to be stored up to two months!?!?! There is some proof of variance in holding affinity of fats. Now thats a strong affinity. So now consider blood composition of fat, cholesterol, etc.. Does someone eating a shitload of vegetable oil (olive oil persay) have less of an ability to carry non-protien bound "depot shrinkage" for an extended time, but at the same time have a faster affinity to pick it up and transport it? Does a healthy component of vegetable oil perhaps provide a vehicle for the mobilization of fat stored esters from the animal fat (your fat) in which it is stored? Does a person with lower vegetable fat in their diet HOLD AND ESTER LONGER? Does a person with a high level of TRANSFATS (synthetic) have a further diminished ability to pick up or excecute the ester from stroage, and yet whatever IS picked up by transfats is held a longer time whereever? Are transfats actually held within human adipose tissue stores - AS TRANS FATS withing animal fat? Is this part of the initial dieting and FAT RELEASE process that seems so slow at first, and actually a primary obstacle to health fat metabolism/removal when incepting a dietary and excercise change in regimen? SO now how much of the ester was stored in TRANS FAT? AND will it ever released converting to effective TT, or is it forever bound as far as the lifespan in our bodies until the liver has to destroy the whole transfat ester "package" in the end to never realize the effect of that Syn T? Could transfats contribute to the failure of TRT, or Steroid use even.
This all begs the question. HOW much is a condition of fatty stasis, or NO CHANGE critical to having a good blood profile for effective T ester metabolism, or a healthy testosterone metabolism to minimal Estrogen conversion? Does the condition of WEIGHT LOSS as a general, whether, dietary restrictive, exercise, or whatever, PROVIDE A POOR BLOOD PROFILE REGARDLESS? Is stasis in fat metabolim required for a health Syn T conversion? Can INHIBITORS like statins, Blood soluble fibers (Oatmeal) benfit the SynT metabolism process? Could ELIMINATION EXPEDITORS even benefit this process by expediting the removal of blood fats ( amphetamines, ephederine, Clenbuteral, caffine) thus not allowing RELEASE RATE esters OR Circulating TT as a general to interact with blood fat and readily convert to estrogens?
The long and short and one of the things that began this rant, was the concept of the the true efficiacy of the cypionate ester as a form of TRT. Can it really be applied to ellicit a 45-60 DEPOT in the body? I was leading into POOR INJECTION TECHNIQUES and how to resolve best possible. Do you really think some nurse just closing her eyes and pinning your ass in 5 seconds is effective? Was that one little rub with a cotton ball an effective clamping of the leakage into fat/circulation? Think again. Have you ever pinned a dose only to see it leak back out of the skin.? Well, if it came ALL THE WAY back out of the muscle and INUNDATED the void or fatty area between the muscle and skin to the point that it seeped back through a hole in the skin this should tell you something. BB's say a max pin in the buttock is 2mls. This would have to be a GORILLLA. The average Low T male I speculate could take about .5 ML AT BEST without severe detrimental shrinkage/loss. I do propose that WE, as TRT males, can get a ful ML to stay in the muscle on a single injection (or 90% of it).
So here is how to do it:
(1) You will obviously have to hit the muscle centrally, IF NOT CLOSER TO THE INSIDE LOWER PERIMETER. Think about it like this. Any leakage is going to follow the path it came in on. The injection IS UNLIKELY to just migrate out the back side of the muscle as there has been no hole created ( and proof in that the juice does not just go right into muscle, else it would not be quirting back up and out!). So go ahead and get to the deeper side of the muscle group, with care not to go through.
(2) Spend a good 2-3 mins injecting, even moving back out as much as a path of a cm or two while proceeding thus increasiing potential absorbtion area. But there has to be a diminishing effective application as time moves forward. This is proven in the problem we are discussing. The best you can hope to effect to get the mucle to relax, expand a little, and START ABSORPION.
(3) I belive the critical point is indeed the capping off of the puncture with PRESSURE. So what is the effective STOPPER to keep this PRESSURIZED depot in place utlimately? Its going to be in the DEPOT COMPONENTS / specifically the Benzyl benzoate. This component of a TCYP injection is not only a carrier, solvent, and preservative - IT IS THE ESSENCE OF THE "DEPOT". It is greatly responsible for any inflammation resulting, and solely if there is not longer any allergy the the ester resulting. The premise of the BB in T cyp is to help retain the injection at the LOCAL site so that it will be properly uptaked by the muscle/fat at that SPECIFIC SITE. So go ahead and cap it with a finger, or PALM EVEN. Apply pressue and rub the bastard a bit. You goal is to force the depot to stay in the muscle for a short time by blocking the pucture alone. The assistance will come in the bodies ability to close a wound in combination with the BB hepling as a solvent to in keeping the cyp "powder" from precipitating into not READILY dispersible powder form too quicly so that it can inundate into the 2-3 inch surrounding tissue. And finally the mildly inflammatory reaction of the BB will help to seal the pucture to some degree. So its a give and take OF BORDERLINE histaminic reaction. BB providing solubility for migration into muscle tissue (primary pupose of BB) vs an propensity for tissue aggrivation thus slowing the process or leakage at the same time. I DO Believe that inflamation and pain is primarily based on the ester itsself and not so much the BB. But I am certain the BB does cause aggrivation and pain to some degree and varying again based on individuals and their experience .immunity to the reactino by time.
The point is. I agree that there is great potential for a once per month injection to fail. I believe this is caused primarily due to the failure of the injection its self. How much failure could be overted by proper injection techique/application remains unclear. THiS IS the greatest OVERSIGHT in TRT application today as it is obviously EVERYTHING in the once per month Urologist recommended dosage. It is clearly a conundrum as a GROSS OVERSIGHT and an example of a CATASTROPHIC FAILURE due to THE MOST BASIC PRINCIPLE of the application. So again, we have a situation where THE GRAVITY and implications of the BIG PICTURE have caused SOCIETY to TOTALLY fly by the obvious failure that has reduced the EFFECTIVE RESULT BY PROBABLY AT LEAST 60-70% considering... To examine the far side of the syn tcyp application process. How much more efficient could body builders be in application? Just how much would they really need.?
I again resign for now....
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