After reading a thread in the Steroid column, I got thinking. Just taking to opp to spew some of my bullshit. I am currently testing a hypothesis to which I will unveil down the road.
First I want to run a concept addressing hormones from a different paradigm. So hold on to your shorts here as the BBC appifany again fires off... Everyone views hormones as a PRINCIPLE FACTOR in tissue development. Well they are, but perhaps not like we are currently thinking. We already know and openly state that GENETICS will predominate any type of potential tissue development. One of the questions I will ask ahead in this post is how do we determine he lifespan of hormones and their derivatives. Perhaps the answer is simple. As long as it takes to DELIVER THE PROTIEN..... Thus the protien is not "binding the hormone as a protective measure", but the hormone is providing the key to the delivery of the protien....AND all controlled by genetic disposition - AS ONE WONT WORK WITHOUT THE OTHER.
SIDETRACK - FOR A PARAGRAPH. Of course you can eat all you want, you can work/exersise all you want. And they you follow the path all the way back up the the digestive tract, and how much is uptaked there, and how much is passed. Further now looking at caloric intake regimens as they vary in subjects. Why some may eat a ton at once, and others may need to snack all day. Just how much variation is there in different subjects as to the composition of the colon, and speed at which it passes food. Does the big eater have a fast pass rate because he eats a lot? Does the snacker absorb calories better? Does the big eater have to have more because they have a smaller section in the colon which uptakes the value?
So now you say WAIT!! Its the free T that has value, RIGHT?? Does it? Why is it in such small proportion then? Perhaps the free T is only whats left after the TT has delivered the protein.!?!? After all, WHAT is unlocking it from the protein from the hormone?? Where is the protien going? And what is the trigger? This is not to say that this "derivative of TT" does not have value, and many of the values currently thought. And what would this say about estrogens in protein?. Would they now be a SECONDARY to creation and fueling of the Muscle/value tissue as a delivery key for FAT into storage?? All the hormonal derivatives are discussed as requiring blood protein to survive. But is it the reverse, and the blood protien, or even fat, is using the hormone or derivatie to do its job. Then you have further eplaination of the life process of hormones in the body. BUT IS TT REQUIRED FOR FUNDAMENTAL TISSUE GROWTH AND AS TT ONLY? and then metabolites fueling the growth and function of ONLY SECONDARY CHARACTERISTICS and auxillary function (emotion/ensuing biological activity, etc..) Again Fat = secondary = estrogen purpose as estrogen and prior to further metabolism....?
You could consider females and hormone composition. The general genetic tissue composition in adult females further adds weight to some of my notion, but at the same time you could cite serum counts to disprove looking at it from a developmental stand point. Again, I could rebutt with "how do you know" as you never knew the testosterone trasfer rate in adolescent growing females, Or if testosterone in femaies has a "Coveted" or protected value more protected in activity. Or if testosterone has a higher growth values in them... We have testicles and they have ovaries. Pehaps they are both capable of producting the quantities of testosterone, or estrogen, either by conversion or raw production to fuel whatever actual metabolism is required for growth, development and maintenance. Why then the varying physical placement? Perhaps that is STRICTLY a factor of REPRODUCTIVE FUNCTION. One is both with a life's worth of eggs, the other makes sperm daily.. So really this begs, IS THE PHYSICAL DIFFERENCE in an ovary and a testical if laid out on a table...?!? Has anyone ever physically counted the actual total sum of testosterone an ovary can produce in a day....? I am again referring to the to prospect that TT could potentially deliver ALL muscle tissue growth factors, and that Estrogen could be a secondary as "fat type" tissue production. The actual counts metabolized again appear to reamin a mystery...
How do we even know the value of the rate at which hormones are produced at other points in the body? Male characteristics appear to come from testicular generated hormones, but they still grow larger. So what happens in a female who looses her overies at a young age?? And I am not incouraging medical science to commit an atrocity to find out! LOL...
You could however consider a pre-pubescently castrated male. He will still grow, just not at the same rate and quality of the rest. This would indicative of the value of hormones produced at the testicles in relation to other body production points. At the same time it MUST indicate that TESTOSTERONE is an unlocking key, or empowering primary factor to growth - PERIOD. Hence the stunted growth.
Perhaps is am merely reiterrating what is known, but with a twist. Pehaps I am completely off base. But its food for thought at a minimum. So Bill or Doc, go ahead and correctment where I made the most obvious wrong turn. Where any of the thought is clearly proved otherwise in documentation. But I would like to see how the process works in real presentation, and perhaps I am just taking ignorant pokes at cellular biology concepts that are completely off base.
So perhaps the hormone is only the mechanism which delivers SHBG to which may be the primarily important principle, which would then identiy it as a KEY to tissue development thus unlocking the door for all protiens to activate on a cellular level - hence equalling activity and/or growth. Thus rendering hormones ONLY a trigger, or DELVIVERY MECHANISM.
So at a minimum what I am doing is again dispelling the myth - Just add T and watch it grow, This may also prelude a REAL REASON why Testosterone supplementation seems to be the FOUNDATION of all AAS cylces ANECDOTALLY and with no further explaination ever provided. Cause I will guarantee you testosterone alone is good for JACK SHIT in older males as a gym supplement for REAL GROWTH. It aint happening... So while other "Steriods" may be super for growth and development beyond genetically inclined limits, TT seems to be required as a prerequisit. Perhaps this is why.. And not saying for ALL steroids of course... But you have to wonder.
PRIMARILY the above further connotates that while excess supplies of TT may present opportunity for development (fat or muscle), it is only that. And underlying conditions and demands/stimulus will strickly govern the outsome.
So now you have an environment in the LOW-T Male where all GENETIC GROWTH is completed, and FAT STORGE potential dominates. Thus there is diminshed NEED for androgens, and only great porential for estrogens. We currently seem to associate muscle with androgens and body fat with estrogens, but only on the bluntest of UNEXPLAINED levels. So we have now turned the tables - so to speak. And placed the value again on the demands of the tissue, but with further merit, thus giving a potential explaination for the elimination lifespan of given hormones, but to only a very broad explaination of the specifics.
I am sure everyone here is aware of my notion that Serum Counts in NO WAY reflect actual testosterone metabolism rates. Meaning, the amount that is actually being made, transferred, converted, cleared, and/or wasted. Its a tool used to make a general surface observation at best, only having value bases on the conditions and sampling rates/intervals for merit of any precision. This is the primary problem with assessing hormone values in humans and thus rending ALL related medical treatments based on - A GROSSLY SERIOUS JOKE... With that said, this is the obviouis indication that I feel there is indeed a "Burn Factor", or great truth to the age old notion of "do we use testosterone when we workout", etc... Historically the answer has always been, NO - bla bla bla.... So this all leads up to my idea that the perfect dose for TRT is the one that does not increase TT serum counts. Keep in mind I am referring to the Rhelm of the "Low-T Male". This mythical beast that is somehow being screwed out of his virility for unfair biological reasons....
My concern and reason for the thought process would be that in middle aged males, the primary reason for the low T Symptoms is increased body fat and sedentary lifestyles, thus estrogen activity being the primary factor in the SYMPTOMS of LOW T. Thus, estrogen becomming the predominating control in this subject ensuing a viciousl cycle of Androgen Factor depletion - The E remaining one step ahead of the ever more starving androgen generating factors, dwendling down a bottomless pit irrecoverable and only by serious lifestyle modifycation combined with THE ABSOLUTE LOWEST SUPPLEMENTED T DOSE POSSIBLE... The obvious issue is that IF the body has reduced prodution due to estrogen factors, and estrogen factors are indeed harmfull in excess (as are androgens too I assume), then even the slightest inclrease over the current set point is accelerating the process that the body is attempting to stop. So then you have the conundrum of "feeling better' via andrgens potentially rendered from TT Supping, but is it outweighing the again refurbished estrogen production?? Now realizing the importance of lifestyle chage. So yet, TT supplementation can be a good vehicle to overcomming a controlled shortage, but changes MUST be made, and changes that may prove a real BEAR without the help - depending on the length of one's travel down the E path....
So via this hypothesis, you would have a male constantly starved for androgens. but just by enought to "hurt", or notice. Now you add back the missing androgen surplus and you should have a supply for androgen demands that has previously been straved by estrogen related controlling shutdown. Hence you have supplied what was lacked while circumventing the estrgoen factor causing it thus only adding what COULD NOT be made available due to THE NATURE of estrogens in males.
OBJECTIVES/PROBLEMS/POTENTIAL HIGHLIGHTS:
1. I suspect estrogens in place may interfere with androgen activity at the point of the receptor thus complicating the fundamental problem, but it could be as simple as the demand structure in place and the hormone profile only being the SYMPTOM of THUS...
2. While I propose the male body is "limited" due to estrogen controlled testical production (in most males as a current state), the limit is also primarily occurring in Low-T Males. So without a change in lifestyle (Demand factors), one will feed the body's attempted suppression of estrogen metobolism as well. Thus the required dosage should vary with time if protocol were followed.
3. Another issue that is currently unaddressed is the active lifespan of TT metabolites. Meaning, how long do androgens & estrogens go on to act effectively. Can androgens and estrogens go on to interact with other receptors once produced? Do estrogens even interact at the first receptor triggering the conversion process? Cross conversion, back and forth, and from different supply lines?
3.1 Obviously estrogens are naturally less prevalent in males. Do they have a "protection mechanism". and does the male body ahve a natural affininty tha is now backfiring, or complicating matters in these obese Roman Times...
4. Importantly and seemingly omitted by current thought is ELIMINATION. What factors are clearing what has been made? And how fast that is occurring? Obviously the blood can only hold so much hormone in cicurlation. If this is not cleared then new can not enter.
5. Hormones are protien bound in circulating supply. Does this have something to do with lifespan, and with regard to caloric demands? IS THE PRIMARY REMOVAL FACTOR WHETHER OR NOT ONE IS BURNING THESE PROTIENS AS A FUEL SOURCE, and their available supply. IS SHBG even required for testosterone to effectively operate on a cellular basis in an exogenously supplied subject? It should not be, which is further indication that hormones are a KEY and not a PRINCIPLE in growth, as it seems to be admitted there is little life outside of protiens.
6. LIver function should critical to the entire process, whether endogenous or exogenous. How does this relate in varying subjects. How does blood fat relate (cholesterol)? Again liver processing is critical to clearance. Which hormones are easier and more inclined to be Cleared?
7. I would like to know more about environmental estogens like the ones reported to come from plastics. Whats their lifespan. I think I have seen the molecular structure published but thats about it. No one seems to be talking.
Questions have been posed historically and common issues are well know. Point.. Where is all the data. Why can one not see the profiles of men diagnosed with prostate cancer, etc... How fat he was at the time. Or how sedentary they had been. MOST IMPORTANTLY what the rate of Prostate cancer is in men how have had a vasectemy, AND AT WHAT AGE? SO Is it genetics or genetic inclination to propensity of lifestyle? What about breast cancer in women? Who is counting what the relation is to application and usage of BIRTH CONTROL!?!? I really wonder if the notion is so controversial, would their docs even bring up the subject? One this is certain is that they would tell them to stop taking them if diagnosed. However, due to the age of most diagnoses, the proposition with relation to time is limited in intersecting circumstance. The fact that there is no data seemingly published is in fact the admission of the existance. Someone is taking notes.... Where is the nutshell package presentation on these matters. I am pretty sure entities are contracted to document, but most likely on in private. These are issues that government/politics does not want to recognize due to the obvious political nature of the subject and implications.
First I want to run a concept addressing hormones from a different paradigm. So hold on to your shorts here as the BBC appifany again fires off... Everyone views hormones as a PRINCIPLE FACTOR in tissue development. Well they are, but perhaps not like we are currently thinking. We already know and openly state that GENETICS will predominate any type of potential tissue development. One of the questions I will ask ahead in this post is how do we determine he lifespan of hormones and their derivatives. Perhaps the answer is simple. As long as it takes to DELIVER THE PROTIEN..... Thus the protien is not "binding the hormone as a protective measure", but the hormone is providing the key to the delivery of the protien....AND all controlled by genetic disposition - AS ONE WONT WORK WITHOUT THE OTHER.
SIDETRACK - FOR A PARAGRAPH. Of course you can eat all you want, you can work/exersise all you want. And they you follow the path all the way back up the the digestive tract, and how much is uptaked there, and how much is passed. Further now looking at caloric intake regimens as they vary in subjects. Why some may eat a ton at once, and others may need to snack all day. Just how much variation is there in different subjects as to the composition of the colon, and speed at which it passes food. Does the big eater have a fast pass rate because he eats a lot? Does the snacker absorb calories better? Does the big eater have to have more because they have a smaller section in the colon which uptakes the value?
So now you say WAIT!! Its the free T that has value, RIGHT?? Does it? Why is it in such small proportion then? Perhaps the free T is only whats left after the TT has delivered the protein.!?!? After all, WHAT is unlocking it from the protein from the hormone?? Where is the protien going? And what is the trigger? This is not to say that this "derivative of TT" does not have value, and many of the values currently thought. And what would this say about estrogens in protein?. Would they now be a SECONDARY to creation and fueling of the Muscle/value tissue as a delivery key for FAT into storage?? All the hormonal derivatives are discussed as requiring blood protein to survive. But is it the reverse, and the blood protien, or even fat, is using the hormone or derivatie to do its job. Then you have further eplaination of the life process of hormones in the body. BUT IS TT REQUIRED FOR FUNDAMENTAL TISSUE GROWTH AND AS TT ONLY? and then metabolites fueling the growth and function of ONLY SECONDARY CHARACTERISTICS and auxillary function (emotion/ensuing biological activity, etc..) Again Fat = secondary = estrogen purpose as estrogen and prior to further metabolism....?
You could consider females and hormone composition. The general genetic tissue composition in adult females further adds weight to some of my notion, but at the same time you could cite serum counts to disprove looking at it from a developmental stand point. Again, I could rebutt with "how do you know" as you never knew the testosterone trasfer rate in adolescent growing females, Or if testosterone in femaies has a "Coveted" or protected value more protected in activity. Or if testosterone has a higher growth values in them... We have testicles and they have ovaries. Pehaps they are both capable of producting the quantities of testosterone, or estrogen, either by conversion or raw production to fuel whatever actual metabolism is required for growth, development and maintenance. Why then the varying physical placement? Perhaps that is STRICTLY a factor of REPRODUCTIVE FUNCTION. One is both with a life's worth of eggs, the other makes sperm daily.. So really this begs, IS THE PHYSICAL DIFFERENCE in an ovary and a testical if laid out on a table...?!? Has anyone ever physically counted the actual total sum of testosterone an ovary can produce in a day....? I am again referring to the to prospect that TT could potentially deliver ALL muscle tissue growth factors, and that Estrogen could be a secondary as "fat type" tissue production. The actual counts metabolized again appear to reamin a mystery...
How do we even know the value of the rate at which hormones are produced at other points in the body? Male characteristics appear to come from testicular generated hormones, but they still grow larger. So what happens in a female who looses her overies at a young age?? And I am not incouraging medical science to commit an atrocity to find out! LOL...
You could however consider a pre-pubescently castrated male. He will still grow, just not at the same rate and quality of the rest. This would indicative of the value of hormones produced at the testicles in relation to other body production points. At the same time it MUST indicate that TESTOSTERONE is an unlocking key, or empowering primary factor to growth - PERIOD. Hence the stunted growth.
Perhaps is am merely reiterrating what is known, but with a twist. Pehaps I am completely off base. But its food for thought at a minimum. So Bill or Doc, go ahead and correctment where I made the most obvious wrong turn. Where any of the thought is clearly proved otherwise in documentation. But I would like to see how the process works in real presentation, and perhaps I am just taking ignorant pokes at cellular biology concepts that are completely off base.
So perhaps the hormone is only the mechanism which delivers SHBG to which may be the primarily important principle, which would then identiy it as a KEY to tissue development thus unlocking the door for all protiens to activate on a cellular level - hence equalling activity and/or growth. Thus rendering hormones ONLY a trigger, or DELVIVERY MECHANISM.
So at a minimum what I am doing is again dispelling the myth - Just add T and watch it grow, This may also prelude a REAL REASON why Testosterone supplementation seems to be the FOUNDATION of all AAS cylces ANECDOTALLY and with no further explaination ever provided. Cause I will guarantee you testosterone alone is good for JACK SHIT in older males as a gym supplement for REAL GROWTH. It aint happening... So while other "Steriods" may be super for growth and development beyond genetically inclined limits, TT seems to be required as a prerequisit. Perhaps this is why.. And not saying for ALL steroids of course... But you have to wonder.
PRIMARILY the above further connotates that while excess supplies of TT may present opportunity for development (fat or muscle), it is only that. And underlying conditions and demands/stimulus will strickly govern the outsome.
So now you have an environment in the LOW-T Male where all GENETIC GROWTH is completed, and FAT STORGE potential dominates. Thus there is diminshed NEED for androgens, and only great porential for estrogens. We currently seem to associate muscle with androgens and body fat with estrogens, but only on the bluntest of UNEXPLAINED levels. So we have now turned the tables - so to speak. And placed the value again on the demands of the tissue, but with further merit, thus giving a potential explaination for the elimination lifespan of given hormones, but to only a very broad explaination of the specifics.
I am sure everyone here is aware of my notion that Serum Counts in NO WAY reflect actual testosterone metabolism rates. Meaning, the amount that is actually being made, transferred, converted, cleared, and/or wasted. Its a tool used to make a general surface observation at best, only having value bases on the conditions and sampling rates/intervals for merit of any precision. This is the primary problem with assessing hormone values in humans and thus rending ALL related medical treatments based on - A GROSSLY SERIOUS JOKE... With that said, this is the obviouis indication that I feel there is indeed a "Burn Factor", or great truth to the age old notion of "do we use testosterone when we workout", etc... Historically the answer has always been, NO - bla bla bla.... So this all leads up to my idea that the perfect dose for TRT is the one that does not increase TT serum counts. Keep in mind I am referring to the Rhelm of the "Low-T Male". This mythical beast that is somehow being screwed out of his virility for unfair biological reasons....
My concern and reason for the thought process would be that in middle aged males, the primary reason for the low T Symptoms is increased body fat and sedentary lifestyles, thus estrogen activity being the primary factor in the SYMPTOMS of LOW T. Thus, estrogen becomming the predominating control in this subject ensuing a viciousl cycle of Androgen Factor depletion - The E remaining one step ahead of the ever more starving androgen generating factors, dwendling down a bottomless pit irrecoverable and only by serious lifestyle modifycation combined with THE ABSOLUTE LOWEST SUPPLEMENTED T DOSE POSSIBLE... The obvious issue is that IF the body has reduced prodution due to estrogen factors, and estrogen factors are indeed harmfull in excess (as are androgens too I assume), then even the slightest inclrease over the current set point is accelerating the process that the body is attempting to stop. So then you have the conundrum of "feeling better' via andrgens potentially rendered from TT Supping, but is it outweighing the again refurbished estrogen production?? Now realizing the importance of lifestyle chage. So yet, TT supplementation can be a good vehicle to overcomming a controlled shortage, but changes MUST be made, and changes that may prove a real BEAR without the help - depending on the length of one's travel down the E path....
So via this hypothesis, you would have a male constantly starved for androgens. but just by enought to "hurt", or notice. Now you add back the missing androgen surplus and you should have a supply for androgen demands that has previously been straved by estrogen related controlling shutdown. Hence you have supplied what was lacked while circumventing the estrgoen factor causing it thus only adding what COULD NOT be made available due to THE NATURE of estrogens in males.
OBJECTIVES/PROBLEMS/POTENTIAL HIGHLIGHTS:
1. I suspect estrogens in place may interfere with androgen activity at the point of the receptor thus complicating the fundamental problem, but it could be as simple as the demand structure in place and the hormone profile only being the SYMPTOM of THUS...
2. While I propose the male body is "limited" due to estrogen controlled testical production (in most males as a current state), the limit is also primarily occurring in Low-T Males. So without a change in lifestyle (Demand factors), one will feed the body's attempted suppression of estrogen metobolism as well. Thus the required dosage should vary with time if protocol were followed.
3. Another issue that is currently unaddressed is the active lifespan of TT metabolites. Meaning, how long do androgens & estrogens go on to act effectively. Can androgens and estrogens go on to interact with other receptors once produced? Do estrogens even interact at the first receptor triggering the conversion process? Cross conversion, back and forth, and from different supply lines?
3.1 Obviously estrogens are naturally less prevalent in males. Do they have a "protection mechanism". and does the male body ahve a natural affininty tha is now backfiring, or complicating matters in these obese Roman Times...
4. Importantly and seemingly omitted by current thought is ELIMINATION. What factors are clearing what has been made? And how fast that is occurring? Obviously the blood can only hold so much hormone in cicurlation. If this is not cleared then new can not enter.
5. Hormones are protien bound in circulating supply. Does this have something to do with lifespan, and with regard to caloric demands? IS THE PRIMARY REMOVAL FACTOR WHETHER OR NOT ONE IS BURNING THESE PROTIENS AS A FUEL SOURCE, and their available supply. IS SHBG even required for testosterone to effectively operate on a cellular basis in an exogenously supplied subject? It should not be, which is further indication that hormones are a KEY and not a PRINCIPLE in growth, as it seems to be admitted there is little life outside of protiens.
6. LIver function should critical to the entire process, whether endogenous or exogenous. How does this relate in varying subjects. How does blood fat relate (cholesterol)? Again liver processing is critical to clearance. Which hormones are easier and more inclined to be Cleared?
7. I would like to know more about environmental estogens like the ones reported to come from plastics. Whats their lifespan. I think I have seen the molecular structure published but thats about it. No one seems to be talking.
Questions have been posed historically and common issues are well know. Point.. Where is all the data. Why can one not see the profiles of men diagnosed with prostate cancer, etc... How fat he was at the time. Or how sedentary they had been. MOST IMPORTANTLY what the rate of Prostate cancer is in men how have had a vasectemy, AND AT WHAT AGE? SO Is it genetics or genetic inclination to propensity of lifestyle? What about breast cancer in women? Who is counting what the relation is to application and usage of BIRTH CONTROL!?!? I really wonder if the notion is so controversial, would their docs even bring up the subject? One this is certain is that they would tell them to stop taking them if diagnosed. However, due to the age of most diagnoses, the proposition with relation to time is limited in intersecting circumstance. The fact that there is no data seemingly published is in fact the admission of the existance. Someone is taking notes.... Where is the nutshell package presentation on these matters. I am pretty sure entities are contracted to document, but most likely on in private. These are issues that government/politics does not want to recognize due to the obvious political nature of the subject and implications.
