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  #1241 (permalink)  
Old 06-07-2009, 01:07 AM
DatBtrue's Avatar
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Quote:
Originally Posted by DaRooster;
Could an increase of HGH release via CJC-1295 W/O dac and ghrp-6 help this?
Probably not.

Quote:
Originally Posted by DaRooster;
Could the hyper histamine production be a symptom of some hormonal deficit?
Probably not.

On the flip side does Histamine production effect GH secretion?

In animals it has an effect.

In humans it is only Histamine antagonists that have a negative effect on GH release.

For example cimetidine (Tagamet) at oral therapeutic doses for 1 mo or more to patients with peptic ulcers or normal people did not alter baseline or stimulated GH release but reduced mean nocturnal GH secretion. The drug also reduced GH response to insulin hypoglycemia when repeatedly administered and blunted the GH response to levodopa when given as an intravenous bolus injection. Higher peak plasma concentrations of cimetidine after a single intravenous bolus than after chronic oral administration explain these results." - Neuroendocrine Control of Growth Hormone Secretion, Eugenio E. Müller, Endocrine Reviews 19 (6): 717-797
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  #1242 (permalink)  
Old 06-07-2009, 03:51 AM
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Join Date: Jan 2005
Posts: 3
Hey Dat, it's CED59, and this is one of the best threads in the history of the internet. Thank you.

My rat has been using CJC-1295 (100mg) and GHRP-6 (100mg) 3x ED.

Unfortunately, [The Rat] been one of victims of the rare awful headaches that can occur. They usually hit 2-3 hours after pinning and it happens 1 out of every 5-6 shots. It seems to be a localized pain on the left temple. The headaches started 2 or 3 after beginning CJC-1295. OTC painkillers do nothing, but for some reason drinking a Coke (39g of High Fructose Corn Syrup) seems to dull it down...

Do you know why these headaches are occurring?

It is an overstimulation of the pituitary, blood pressure, or actually a blood sugar issue?

...I'm just hoping it's not a sign of a more serious issue...

I never seemed to have the problem on GHRP-6 alone. The rat has also had bouts with fatigue, so I'm using the headaches and fatigue as a sign to significantly cut down the frequency of injections.

Any thoughts?

The results are really awesome. The Rat is upset with the headaches as they very debilitating.

Last edited by Deoudes59; 06-07-2009 at 06:19 AM.
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  #1243 (permalink)  
Old 06-08-2009, 01:07 PM
Wise Guy's Avatar
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Join Date: Nov 2008
Posts: 120
Quote:
Originally Posted by Designbuilt View Post
OK, I decided to do it!! I put on a pot of coffee and I'm going to read this book start to finish today!
Go for it man!

Just know though, I spent probably 6 months reading and tearing through this thread.

My study time is limited though to an hour or two a day, as I already have my own university studies.

But go for it!
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  #1244 (permalink)  
Old 06-08-2009, 01:53 PM
DatBtrue's Avatar
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Less GH is okay; Body sculpting 101 (i.e. w/o steroids)

Quote:
Originally Posted by Deoudes59
My rat has been using CJC-1295 (100mg) and GHRP-6 (100mg) 3x ED.

Unfortunately, [The Rat] been one of victims of the rare awful headaches that can occur. They usually hit 2-3 hours after pinning and it happens 1 out of every 5-6 shots. It seems to be a localized pain on the left temple. The headaches started 2 or 3 after beginning CJC-1295. OTC painkillers do nothing, but for some reason drinking a Coke (39g of High Fructose Corn Syrup) seems to dull it down...

Do you know why these headaches are occurring?

It is an overstimulation of the pituitary, blood pressure, or actually a blood sugar issue?
Three things:
- Quality of the peptide. If the peptide is only 80% pure then it could conceivably bring on irritations. The peptides used in clinical studies are purified to the highest level (around 99%).

- GH especially when/if base level are elevated can cause sodium retention, edema, temporary carpal tunnel due to wrist swelling, elevated glucose levels/insulin resistance, etc.

This is specific to growth hormone.

CJC-1295 (if it is genuine) can cause the GH troughs/base levels to elevate. Normal pulsation continues to occur on top of this rise. I sometimes call this "growth hormone bleed".

If one doesn't know what I mean by "base levels" please envision (picture in your mind) a rise in sea (ocean ... la mer) levels due to global warming. Global warming raises the overall level by 10 centimeters. That is akin (similar ... or an analogy or comparison ...or assez même ... see I am helpful to language learners ) to what CJC-1295 does in the human body.

Note that the elevated (élevé) sea still has the same wave structure as it did before. Again so does CJC-1295.

I believe that more problems such as headache, lethargy and water come from continually elevated base levels of GH.

- acclimation may require gradually getting use to higher levels. This may mean 1 dose pre-bed for a while and a PWO dose on days you work-out. This period may need to last months before attempting to increase the dose.
Practical things:

In your case why not use the added GHRH (in the form of CJC-1295 or whatever you have) pre-bed w/ GHRP-6 and at no other times. Just stick to GHRP-6 at other dosing times.

Then at some point in time try adding just 15mcg of GHRH w/ the GHRP-6 and see how it goes. If that feels fine then increase it a little.

DO NOT suffer!!!!!!!!!!!!!!!!!!! Seriously it is absolutely not worth going through your day in a debilitated state. But you possess the ability to make small adjustments.

You do not need to flood the body with GH if it is part of a protocol. You only need the element of time (duration, ...longtemps). On these boards (hopefully not in this thread) you read about taking huge doses... and you see people ask how much GH can I get in my body?

That is not where the focus should be... I myself do not stay at 100mcg of GHRH/GHRP 3 times a day chronically. I would always do that plus may add GH IF I were on a proper muscle building cycle.

But at other times lower doses not only suffice but are probably better because it allows you to ramp up when you are going into anabolic phases.

What "coast dosing" (i.e. lower) does is it keeps the body primed with a higher level of GH which does what?

Which increases the creation of IGF-1, MGF in local tissue which is used locally. So the kidneys, the brain and muscles get more cellular repair & maintenance hormone and increased protein synthesis. This reduces catabolism and still allows the body (if you are not a maxed out bodybuilder) to grow provided the factors of amino acid pool, blood flow, higher levels of physiological testosterone & or free testosterone, higher levels of physiological levels of insulin at key points are present as well as the physical workout stimulus.

At the same time provided you have "quiet periods" when insulin is not present you will have an increase of fatty acid mobilization which provided you engage in aerobic activity will eliminate fat.

Approaches to body sculpting can be subtle and need not rely on steroids. Shape change... shape change....shape change!

A 16.5" arm that is cut and has detail and is 3-dimensional is much more impressive then an 18" arm that lacks the kind of detailed etching between muscle groups that makes the smaller arm look bigger.

Need the legs to look better? Get the tear drop to pop and it will look much better then added mass.

Cords running down forearms, dense and grainy calves, the outer portion of the horseshoe on the triceps, rounded delts and chest that looks great (not massive for masses sake)...a kite shaped back...

A much smaller version of a popping pro-bodybuilder, one with less mass in the legs and back is a look most hobbiests should attempt to achieve because it looks awesome! There is no need to duplicate what a pro does such as displacing the shoulder blades to expand their back width. There are so many great body sculpting looks that can be achieved at all levels ...and can be enjoyed now as opposed to the "one day when I add more mass".

This can be accomplished with GHRH/GHRPs, Leucine+glucose, nettle root extract, eggs, the proper use of fats, staying away from protein powders, whole foods..., the use of fast periods to increase hormonal levels, etc.... plus the use of injectable sterile caprylic acid for increased androgen activity and fascia stretching... as well as understanding that GH converts some muscle fibers to the more endurance fibers so workout routines need sets with higher reps (including a set here and there of 30+ reps) ...blood flow...and understanding that hypertrophy induced by GH does not really bring strength per se... working through ROMs that put the load & peak force on the target muscle, less volume more frequency and changing exercises & patterns to avoid neurological adaptation and taking steps to avoid CNS fatigue.

C'est fini!
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  #1245 (permalink)  
Old 06-08-2009, 01:59 PM
DatBtrue's Avatar
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Join Date: Jul 2008
Location: United Kingdom
Posts: 1,701
Quote:
Originally Posted by Wise Guy;
My study time is limited though to an hour or two a day, as I already have my own university studies.
Me too! I now realize to ever gain C1 certification in the French language I need to devote 5 hours a day to active study... that is to ever get to a level where I can engage in deep conversations in French.
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  #1246 (permalink)  
Old 06-08-2009, 02:13 PM
Registered Member
 
Join Date: Mar 2009
Posts: 366
Dat, it is a pleasure reading your posts. I find myself coming to your thread more and more. I'm not ready to take the proverbial plunge into peptides just yet, but I read in here for various reasons. Much much more often as of late due to the amazing quality of your posts. I haven't learned as much, nor enjoyed the learning since I stumbled upon Dante's stuff. Actually, now that I think about it, you remind me of him alot, or he reminds me of you, who's older? lol. Wait, Dante is that you. Are you using a pseudonym? J/K.
Quote:
Originally Posted by DatBtrue View Post
Three things:
- Quality of the peptide. If the peptide is only 80% pure then it could conceivably bring on irritations. The peptides used in clinical studies are purified to the highest level (around 99%).

- GH especially when/if base level are elevated can cause sodium retention, edema, temporary carpal tunnel due to wrist swelling, elevated glucose levels/insulin resistance, etc.

This is specific to growth hormone.

CJC-1295 (if it is genuine) can cause the GH troughs/base levels to elevate. Normal pulsation continues to occur on top of this rise. I sometimes call this "growth hormone bleed".

If one doesn't know what I mean by "base levels" please envision (picture in your mind) a rise in sea (ocean ... la mer) levels due to global warming. Global warming raises the overall level by 10 centimeters. That is akin (similar ... or an analogy or comparison ...or assez même ... see I am helpful to language learners ) to what CJC-1295 does in the human body.

Note that the elevated (élevé) sea still has the same wave structure as it did before. Again so does CJC-1295.

I believe that more problems such as headache, lethargy and water come from continually elevated base levels of GH.

- acclimation may require gradually getting use to higher levels. This may mean 1 dose pre-bed for a while and a PWO dose on days you work-out. This period may need to last months before attempting to increase the dose.
Practical things:

In your case why not use the added GHRH (in the form of CJC-1295 or whatever you have) pre-bed w/ GHRP-6 and at no other times. Just stick to GHRP-6 at other dosing times.

Then at some point in time try adding just 15mcg of GHRH w/ the GHRP-6 and see how it goes. If that feels fine then increase it a little.

DO NOT suffer!!!!!!!!!!!!!!!!!!! Seriously it is absolutely not worth going through your day in a debilitated state. But you possess the ability to make small adjustments.

You do not need to flood the body with GH if it is part of a protocol. You only need the element of time (duration, ...longtemps). On these boards (hopefully not in this thread) you read about taking huge doses... and you see people ask how much GH can I get in my body?

That is not where the focus should be... I myself do not stay at 100mcg of GHRH/GHRP 3 times a day chronically. I would always do that plus may add GH IF I were on a proper muscle building cycle.

But at other times lower doses not only suffice but are probably better because it allows you to ramp up when you are going into anabolic phases.

What "coast dosing" (i.e. lower) does is it keeps the body primed with a higher level of GH which does what?

Which increases the creation of IGF-1, MGF in local tissue which is used locally. So the kidneys, the brain and muscles get more cellular repair & maintenance hormone and increased protein synthesis. This reduces catabolism and still allows the body (if you are not a maxed out bodybuilder) to grow provided the factors of amino acid pool, blood flow, higher levels of physiological testosterone & or free testosterone, higher levels of physiological levels of insulin at key points are present as well as the physical workout stimulus.

At the same time provided you have "quiet periods" when insulin is not present you will have an increase of fatty acid mobilization which provided you engage in aerobic activity will eliminate fat.

Approaches to body sculpting can be subtle and need not rely on steroids. Shape change... shape change....shape change!

A 16.5" arm that is cut and has detail and is 3-dimensional is much more impressive then an 18" arm that lacks the kind of detailed etching between muscle groups that makes the smaller arm look bigger.

Need the legs to look better? Get the tear drop to pop and it will look much better then added mass.

Cords running down forearms, dense and grainy calves, the outer portion of the horseshoe on the triceps, rounded delts and chest that looks great (not massive for masses sake)...a kite shaped back...

A much smaller version of a popping pro-bodybuilder, one with less mass in the legs and back is a look most hobbiests should attempt to achieve because it looks awesome! There is no need to duplicate what a pro does such as displacing the shoulder blades to expand their back width. There are so many great body sculpting looks that can be achieved at all levels ...and can be enjoyed now as opposed to the "one day when I add more mass".

This can be accomplished with GHRH/GHRPs, Leucine+glucose, nettle root extract, eggs, the proper use of fats, staying away from protein powders, whole foods..., the use of fast periods to increase hormonal levels, etc.... plus the use of injectable sterile caprylic acid for increased androgen activity and fascia stretching... as well as understanding that GH converts some muscle fibers to the more endurance fibers so workout routines need sets with higher reps (including a set here and there of 30+ reps) ...blood flow...and understanding that hypertrophy induced by GH does not really bring strength per se... working through ROMs that put the load & peak force on the target muscle, less volume more frequency and changing exercises & patterns to avoid neurological adaptation and taking steps to avoid CNS fatigue.

C'est fini!
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  #1247 (permalink)  
Old 06-08-2009, 07:54 PM
totalrecomp's Avatar
Registered Member
 
Join Date: Feb 2009
Posts: 724
Quote:
Originally Posted by DatBtrue View Post
Three things:
- Quality of the peptide. If the peptide is only 80% pure then it could conceivably bring on irritations. The peptides used in clinical studies are purified to the highest level (around 99%).

- GH especially when/if base level are elevated can cause sodium retention, edema, temporary carpal tunnel due to wrist swelling, elevated glucose levels/insulin resistance, etc.

This is specific to growth hormone.

CJC-1295 (if it is genuine) can cause the GH troughs/base levels to elevate. Normal pulsation continues to occur on top of this rise. I sometimes call this "growth hormone bleed".

If one doesn't know what I mean by "base levels" please envision (picture in your mind) a rise in sea (ocean ... la mer) levels due to global warming. Global warming raises the overall level by 10 centimeters. That is akin (similar ... or an analogy or comparison ...or assez même ... see I am helpful to language learners ) to what CJC-1295 does in the human body.

Note that the elevated (élevé) sea still has the same wave structure as it did before. Again so does CJC-1295.

I believe that more problems such as headache, lethargy and water come from continually elevated base levels of GH.

- acclimation may require gradually getting use to higher levels. This may mean 1 dose pre-bed for a while and a PWO dose on days you work-out. This period may need to last months before attempting to increase the dose.
Practical things:

In your case why not use the added GHRH (in the form of CJC-1295 or whatever you have) pre-bed w/ GHRP-6 and at no other times. Just stick to GHRP-6 at other dosing times.

Then at some point in time try adding just 15mcg of GHRH w/ the GHRP-6 and see how it goes. If that feels fine then increase it a little.

DO NOT suffer!!!!!!!!!!!!!!!!!!! Seriously it is absolutely not worth going through your day in a debilitated state. But you possess the ability to make small adjustments.

You do not need to flood the body with GH if it is part of a protocol. You only need the element of time (duration, ...longtemps). On these boards (hopefully not in this thread) you read about taking huge doses... and you see people ask how much GH can I get in my body?

That is not where the focus should be... I myself do not stay at 100mcg of GHRH/GHRP 3 times a day chronically. I would always do that plus may add GH IF I were on a proper muscle building cycle.

But at other times lower doses not only suffice but are probably better because it allows you to ramp up when you are going into anabolic phases.

What "coast dosing" (i.e. lower) does is it keeps the body primed with a higher level of GH which does what?

Which increases the creation of IGF-1, MGF in local tissue which is used locally. So the kidneys, the brain and muscles get more cellular repair & maintenance hormone and increased protein synthesis. This reduces catabolism and still allows the body (if you are not a maxed out bodybuilder) to grow provided the factors of amino acid pool, blood flow, higher levels of physiological testosterone & or free testosterone, higher levels of physiological levels of insulin at key points are present as well as the physical workout stimulus.

At the same time provided you have "quiet periods" when insulin is not present you will have an increase of fatty acid mobilization which provided you engage in aerobic activity will eliminate fat.

Approaches to body sculpting can be subtle and need not rely on steroids. Shape change... shape change....shape change!

A 16.5" arm that is cut and has detail and is 3-dimensional is much more impressive then an 18" arm that lacks the kind of detailed etching between muscle groups that makes the smaller arm look bigger.

Need the legs to look better? Get the tear drop to pop and it will look much better then added mass.

Cords running down forearms, dense and grainy calves, the outer portion of the horseshoe on the triceps, rounded delts and chest that looks great (not massive for masses sake)...a kite shaped back...

A much smaller version of a popping pro-bodybuilder, one with less mass in the legs and back is a look most hobbiests should attempt to achieve because it looks awesome! There is no need to duplicate what a pro does such as displacing the shoulder blades to expand their back width. There are so many great body sculpting looks that can be achieved at all levels ...and can be enjoyed now as opposed to the "one day when I add more mass".

This can be accomplished with GHRH/GHRPs, Leucine+glucose, nettle root extract, eggs, the proper use of fats, staying away from protein powders, whole foods..., the use of fast periods to increase hormonal levels, etc.... plus the use of injectable sterile caprylic acid for increased androgen activity and fascia stretching... as well as understanding that GH converts some muscle fibers to the more endurance fibers so workout routines need sets with higher reps (including a set here and there of 30+ reps) ...blood flow...and understanding that hypertrophy induced by GH does not really bring strength per se... working through ROMs that put the load & peak force on the target muscle, less volume more frequency and changing exercises & patterns to avoid neurological adaptation and taking steps to avoid CNS fatigue.

C'est fini!
Really great points in this one. I am of a similar mind set. There are days that I look at the pros and just want to say screw it and dive in head first. Then my better judgement rears its ugly/beautiful head. Slow subtle changes are what I have atempted to make over the last year and the difference is certainly noticable and was not hard n my system. As my name suggests a little muscle gain here and a little fat loss there is the route I plan to travel from now on.
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  #1248 (permalink)  
Old 06-09-2009, 02:28 AM
DatBtrue's Avatar
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Join Date: Jul 2008
Location: United Kingdom
Posts: 1,701
Post Testosterone causes lesions on the heart

Here is another reason to be natural. This latest research is not yet published but was recently released to subscribers of Cardiovascular Toxicology. The abstract was brought to my attention by likkayouth and so here are the major parts of the full study.

Scary stuff...


Cardiac Lesions Induced by Testosterone: Protective Effects of Dexrazoxane and Trimetazidine, Dalila Dalila Belhani, Cardiovascular Toxicology Published online: 12 May 2009


Abstract Further to our previous observation of post-mortem cardiac lesions after sudden death in several athletes with a history of anabolic steroid abuse, this study was intended to reproduce these lesions in rabbits administered testosterone oenanthate, a prototypic anabolic steroid abused by athletes, and to provide evidence for the protective effects of trimetazidine and dexrazoxane that are used as antianginal and cardioprotective drugs, respectively. Groups of six rabbits each were administered saline, testosterone, or a combination of testosterone and either trimetazidine or dexrazoxane for 3 months. Histologic cardiac lesions including necrosis, misshapen cell nuclei, interstitial and endocardial fibrosis, lymphocytic infiltrates, and vascular dystrophies were observed in testosterone-treated rabbits. In contrast, no significant lesions were observed in the animals treated with testosterone combined with either trimetazidine or dexrazoxane. This is the first study providing evidence for testosterone cardiotoxicity following sub-chronic exposure in laboratory animals. In addition, these results suggest the protective role of trimetazidine and dexrazoxane.


Introduction

Not infrequently athletes tend to abuse anabolic steroids derived from testosterone, and a number of sudden cardiac deaths have been reported in relation to this abuse [1–4]. Indeed, sudden deaths may be 4–6 fold more frequent in athletes with a history of anabolic steroid abuse [5, 6]. Overall, the incidence of sudden deaths has been estimated to be 2–3/100,000/year in athletes versus 0.08/100,000/year in the general population [7, 8].

In a recent study conducted with Lyon Institute of Forensic Medicine, we observed various cardiac lesions during the post-mortem examination of several athletes with a history of anabolic steroid abuse [9]. Concomitantly, we evidenced focalized as well as disseminated cardiac lesions in rabbits treated with norethandrolone, a potent anabolic steroid. These lesions were reminiscent of those observed in toxic myocarditis, e.g., myocarditis due to anthracyclines. They mostly consisted of myolysis, fibrosis, disorganized myocardial fibers, and misshapen cell nuclei, and were characterized by the presence of lymphocytic infiltrates. Moreover, arteriolar lesions suggested the possible involvement of myocardial ischemia.

The present study was undertaken to demonstrate whether the sub-chronic administration of testosterone to rabbits could induce similar cardiac lesions as testosterone cardiotoxicity has seldom been investigated in laboratory animals. In addition, the possible protective effects of trimetazidine, which exerts anti-ischemic and anti-anginal effects [10], and of dexrazoxane, which is used to prevent the cardiotoxicity of anthracycline derivatives in human cancer patients [11], were investigated in rabbits concomitantly treated with testosterone.

Materials and Methods

...

Treatment

The rabbits were randomly assigned to four groups of six animals each. All subsequent treatments were administered by the intraperitoneal route. Group I (control) animals were given saline once a day using the same volume as in treated animals. Group II animals were given 8 mg/kg of testosterone (Bayer Santé, Puteaux, France) once a month for 3 months and saline daily on the other days. Group III animals were given 8 mg/kg of testosterone once a month plus 5 mg/kg of trimetazidine (Servier laboratories, Courbevoie, France) daily for 3 months. Group IV animals were given 8 mg/kg of testosterone once a month plus 60 mg/kg of dexrazoxane (Novartis Pharma, Rueil-Malmaison, France) once a week, and saline daily on the other days for 3 months.

Discussion

In this study, the administration of testosterone was found to induce various histologic cardiac lesions in rabbits including misshapen cell nuclei, necrosis, interstitial, and endocardial fibrosis. Similar lesions of the myocardium have been previously reported in athletes with a history of anabolic steroid abuse [3, 6, 12]. We also observed dysplasia of the precapillary arterioles, which can cause ischemia leading to morphologic changes including contraction bands, acidophilia, and undulation of myocardial fibers. At a later stage, liquefaction necrosis is a common finding. Finally, we found that testosterone can induce acute inflammatory lesions of cardiomyocytes as previously reported [13–15]. Testosterone has been reported to exert pro-inflammatory effects with the release of TNF-a and IL-1ß, and this in turn resulted in apoptosis of cardiac cells [16]. Interestingly, as compared to non-castrated males, castrated rats had lesser cytokine release and reduced apoptotic response measured from caspase-1, caspase-3, and caspase-11 activation, and Bcl-2 expression. That no evidence of apoptosis was found in the present study may be explained by the sensitivity of the method used, or more probably by the conditions of exposure, i.e., sub-chronic versus acute.

No cardiac hypertrophy was observed in animals treated with testosterone alone in this study. This may be due to the rather short duration of treatment (3 months) as the development of cardiac hypertrophy in athletes has been suggested to require chronic testosterone exposure [17]. Following prolonged exposure, testosterone can induce hypertrophic cardiac lesions [2, 6] leading to sudden death via a reduction of ventricular compliance [2] and/or the induction of disorders of diastolic relaxation [18]. The sudden death of a 32-year-old transsexual woman treated with intramuscular testosterone 125 mg/kg once or twice monthly for 2 years has been reported [19]. Her post-mortem examination revealed hypertrophic cardiopathy and atheromatous plaques on the left and right coronary arteries that resulted in over 90% coronary stenosis in the proximal end of the anterior interventricular artery.

In contrast to testosterone alone, the combination of testosterone with trimetazidine was not associated with the development of any consistent cardiac lesions in rabbits after 3 months of treatment. Although the mechanism of the cardioprotection achieved by trimetazidine in this study is not clearly elucidated, several mechanisms can be proposed. Trimetazidine can decrease intracellular acidosis and alterations in transmembrane ion movements caused by ischemia, and thus reduce the migration and infiltration of neutrophils and lymphocytes to the cardiac tissue during ischemia/reperfusion [20]. Thus, trimetazidine could reduce the release of pro-inflammatory cytokines induced by testosterone. Second, trimetazidine exerts protective effects during ischemia in inhibiting the opening of mitochondrial permeability transition pores during ischemia/reperfusion [21]. Kajstura et al. [22] showed that the extent of cardiac lesions, such as myocardial necrosis and apoptosis during myocardial ischemia is significantly reduced by trimetazidine. Thirdly, Ruixing et al. [23] found that capase-3 activation and mitochondrial cytochrome C release were decreased in rabbits treated with trimetazidine as compared to untreated animals. In addition, the apoptotic index was negatively correlated to serum superoxide dismutase activity, and positively correlated to malondialdehyde levels, which suggests that trimetazidine could prevent myocardial lesions during ischemia-reperfusion. Based on these data, it is suggested that the anti-apoptotic effects of trimetazidine could inhibit apoptosis induction by testosterone, and thus prevent the development of cardiac lesions in rabbits treated with testosterone alone.

Similarly to rabbits treated with trimetazidine, rabbits treated with dexrazoxane did not develop any consistent cardiac lesions despite concomitant testosterone exposure. Dexrazoxane plays an important role in the cardioprotection of patients treated with anthracycline derivatives [11, 24]. It is indeed well recognized that these derivatives can induce various histological lesions of the heart, such as myocardial necrosis, cellular infiltrates, myofibrillar loss, and cytoplasmic vacuolization. The mechanism of this protective effect of dexrazoxane is not fully understood. It is at least in part related to the prevention of apoptotic and necrotic lesions involving the reduced formation of Fe3+-anthracycline complexes that generate the production of free radicals that induce alterations of mitochondria [25]. Therefore, the cardioprotection evidenced during the present study following treatment with either trimetazidine or dexrazoxane in testosterone-treated rabbits could result from similar mechanisms involving decreased mitochondrial alterations.

In conclusion, this study provides confirmative evidence that anabolic steroids, and in particular testosterone, induce cardiotoxic effects resulting in heart lesions similar to those seen in toxic myocarditis. The lack of cardiac lesions in testosterone-treated rabbits when given trimetazidine or dexrazoxane concomitantly suggests that either drug can have a cardioprotective effect, which warrants further investigation.
References:

1. Deligiannis, A., Björnstad, H., Carre, F., Heidbüchel, H., Kouidi, E., Panhuyzen-Goedkoop, N. M., et al. (2006). ESC study group of sports cardiology position paper on adverse cardiovascular effects of doping in athletes. European Journal of Cardiovascular Prevention and Rehabilitation, 13, 687–694. doi:10.1097/01.hjr.0000224482.95597.7a.


2. Kindermann, W. (2006). Cardiovascular side effects of anabolic-androgenic steroids. Herz, 31, 566–573. doi:10.1007/s00059-006-2856-0.


3. Di Paolo, M., Agozzino, M., Toni, C., Luciani, A. B., Molendini, L., Scaglione, M., et al. (2007). Sudden anabolic steroid abuse-related death in athletes. International Journal of Cardiology, 114, 114–117. doi:10.1016/j.ijcard.2005.11.033.


4. Fineschi, V., Riezzo, I., Centini, F., Silingardi, E., Licata, M., Beduschi, G., et al. (2007). Sudden cardiac death during anabolic steroid abuse: Morphologic and toxicologic findings in two fatal cases of bodybuilders. International Journal of Legal Medicine, 121, 48–53. doi:10.1007/s00414-005-0055-9.


5. Pärssinen, M., Kujala, U., Vartiainen, E., Sarna, S., & Seppälä, T. (2000). Increased premature mortality of competitive power lifters suspected to have used anabolic agents. International Journal of Sports Medicine, 21, 225–227. doi:10.1055/s-2000-304.


6. Luke, J. L., Farb, A., Virmani, R., & Sample, R. H. (1990). Sudden cardiac death during exercise in a weight lifter using anabolic androgenic steroids: Pathological and toxicological findings. Journal of Forensic Sciences, 35, 1441–1447.


7. Maron, B. J., Epstein, S. E., & Roberts, W. C. (1986). Causes of sudden death in competitive athletes. Journal of the American College of Cardiology, 1, 204–214.

8. Corrado, D., Basso, C., Pavei, A., Michieli, P., Schiavon, M., & Thiene, G. (2006). Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. Journal of the American Medical Association, 296, 1593–1601. doi:10.1001/jama.296.13.1593.


9. Fanton, L., Belhani, D., Vaillant, F., Tabib, A., Gomez, L., Descotes, J., et al. (2008). Heart lesions associated with anabolic steroid abuse: Comparison of post-mortem findings in athletes and norethandrolone-induced lesions in rabbits. Experimental and Toxicologic Pathology, (Nov), 20. Epub ahead of print.

10. Bertomeu-Gonzalez, V., Bouzas-Mosquera, A., & Kaski, J. C. (2006). Role of trimetazidine in management of ischemic cardiomyopathy. The American Journal of Cardiology, 98(5A), 19J–24J. doi:10.1016/j.amjcard.2006.07.005.


11. Wiseman, L. R., & Spencer, C. M. (1998). Dexrazoxane. A review of its use as a cardioprotective agent in patients receiving anthracycline-based chemotherapy. Drugs, 56, 385–403. doi:10.2165/00003495-199856030-00009.


12. Hartgens, F., & Kuipers, H. (2004). Effects of androgenic-anabolic steroids in athletes. Sports Medicine (Auckland, N.Z.), 34, 513–554. doi:10.2165/00007256-200434080-00003.


13. Rossi, M. A. (1991). Patterns of myocardial fibrosis in idiopathic cardiomyopathies and chronic Chagasic cardiopathy. The Canadian Journal of Cardiology, 7, 287–294.


14. Cavasin, M. A., Tao, Z. Y., Yu, A. L., & Yang, X. P. (2006). Testosterone enhances early cardiac remodeling after myocardial infarction, causing rupture and degrading cardiac function. American Journal of Physiology. Heart and Circulatory Physiology, 290, 2043–2050. doi:10.1152/ajpheart.01121.2005.


15. Wang, M., Tsai, B. M., Kher, A., Baker, L. B., Wairiuko, G. M., & Meldrum, D. R. (2005). Role of endogenous testosterone in myocardial proinflammatory and proapoptotic signaling after acute ischemia-reperfusion. American Journal of Physiology. Heart and Circulatory Physiology, 288, H221–H226. doi:10.1152/ajpheart.00784.2004.


16. Inoue, H., Nishida, N., Ikeda, N., Tsuji, A., Kudo, K., Hanagama, M., et al. (2007). The sudden and unexpected death of a female-to-male transsexual patient. Journal of Forensic and Legal Medicine, 21, 1–7.

17. Hartgens, F., Cheriex, E. C., & Kuipers, H. (2003). Prospective echocardiographic assessment of androgenic-anabolic steroids effects on cardiac structure and function in strength athletes. International Journal of Sports Medicine, 24, 344–351. doi:10.1055/s-2003-40705.


18. Gauthier, J. (2001). Cardiovascular effects of doping. Annales de Cardiologie et d’Angeiologie, 50, 293–298. doi:10.1016/S0003-3928(01)00032-4.


19. Ren, G., Dewald, O., & Frangogiannis, N. G. (2003). Inflammatory mechanisms in myocardial infarction. Current Drug Targets. Inflammation and Allergy, 2, 242–256. doi:10.2174/1568010033484098.


20. Meldrum, D. R., Wang, M., Tsai, B. M., Kher, A., Pitcher, J. M., Brown, J. W., et al. (2005). Intracellular signaling mechanisms of sex hormones in acute myocardial inflammation and injury. Frontiers in Bioscience, 10, 1835–1867. doi:10.2741/1665.


21. Argaud, L., Gomez, L., Gateau-Roesch, O., Couture-Lepetit, E., Loufouat, J., Robert, D., et al. (2005). Trimetazidine inhibits mitochondrial permeability transition pore opening and prevents lethal ischemia-reperfusion injury. Journal of Molecular and Cellular Cardiology, 39, 893–899. doi:10.1016/j.yjmcc.2005.09.012.


22. Kajstura, J., Liu, Y., Baldini, A., Li, B., Olivetti, G., Leri, A., et al. (1998). Coronary artery constriction in rats: necrotic and apoptotic myocyte death. The American Journal of Cardiology, 82, 30K–41K. doi:10.1016/S0002-9149(98)00535-9.


23. Ruixing, Y., Wenwu, L., & Al-Ghazali, R. (2007). Trimetazidine inhibits cardiomyocyte apoptosis in a rabbit model of ischemia-reperfusion. Translational Research; the Journal of Laboratory and Clinical Medicine, 149, 152–160. doi:10.1016/j.trsl.2006.11.004.


24. Paiva, M. G., Petrilli, A. S., Moises, V. A., Macedo, C. R., Tanaka, C., & Campos, O. (2005). Cardioprotective effect of dexrazoxane during treatment with doxorubicin: A study using low-dose dobutamine stress echocardiography. Pediatric Blood & Cancer, 45, 902–908. doi:10.1002/pbc.20488.


25. Chen, B., Peng, X., Pentassuglia, L., Lim, C. C., & Sawyer, D. B. (2007). Molecular and cellular mechanisms of anthracycline cardiotoxicity. Cardiovascular Toxicology, 7, 114–121. doi:10.1007/s12012-007-0005-5.
NOTE:

Trimetazidine is a drug for angina pectoris, sometimes referred to by the brand name Vastarel MR. Each tablet contains 35 mg of trimetazidine. Trimetazidine is an anti-ischemic (anti-anginal) metabolic agent, which improves myocardial glucose utilization through stopping of fatty acid metabolism. Trimetazidine is usually prescribed as a long-term treatment of angina pectoris, and in some countries (including France) for tinnitus and dizziness. It is taken twice a day.

Trimetazidine has high safety and tolerability profile. It has no known drug interactions

Dexrazoxane hydrochloride (Zinecard [Pfizer for USA & Canada]; Cardioxane [Novartis for EU & ROW]) is a cardioprotective agent.

It is used to protect the heart against the cardiotoxic side effects of anthracyclines, such as doxorubicin.

FDA has also approved a dexrazoxane hydrochloride drug, brand name Totect or Savene (developed by TopoTarget), for use as a treatment of extravasation resulting from IV anthracycline chemotherapy. Extravasation is an adverse event in which chemotherapies containing anthracylines leak out of the blood vessel and necrotize the surrounding tissue.

As a derivative of EDTA, dexrazoxane chelates iron, but the precise mechanism by which it protects the heart is not known.
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Old 06-09-2009, 05:20 AM
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Me too! I now realize to ever gain C1 certification in the French language I need to devote 5 hours a day to active study... that is to ever get to a level where I can engage in deep conversations in French.
Good luck Dat.

I have found Vinpocetine and a Choline source to be a great combo for memory enhancement and retention.
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Old 06-09-2009, 03:26 PM
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Good luck Dat.

I have found Vinpocetine and a Choline source to be a great combo for memory enhancement and retention.
I would highly suggest PEA and Hup A as a potent learning stack. Got me through some tough courses this year.


Dat,
Read that test study above and noticed that the dosage was not all that high. How dose a rabbit-> human dose vary? Also I am in the process of reading some of Vince Girondas writings and I believe he wrote about a study that showed cholesterol/heart disease correlation that used rabbits. Vince went on to sat that this was no surprise as rabbits did not have the ability to process cholesterol, or at least something to that effect. Wondering if this would carry over into test? Can we assume that sides of test in rabbits carries over into human subjects? I might be grasping here but I hate to see negatives(health wise) associated with something that is used extensively by the BB community.
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Old 06-09-2009, 03:30 PM
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givin the dose they gave the rabbits, i extrapolated that dose to someone my size and it was almost a gram of test, which I consider to be a hefty dose. Im a firm believe in Phil's 1cc a week theories and I adhere to that and have liked the long term results.
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Old 06-09-2009, 03:30 PM
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Dat-
Out of the following: SAM-e, Centrophenoxine, mucuna puriens, 5-htp, picamilon, what would you say is a keeper, and what can be eliminated from a regimen...all are taken with the goal of reducing stress/tension, and improving mood/calming a bad temper.
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Old 06-10-2009, 12:49 AM
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Dat-
Out of the following: SAM-e, Centrophenoxine, mucuna puriens, 5-htp, picamilon, what would you say is a keeper, and what can be eliminated from a regimen...all are taken with the goal of reducing stress/tension, and improving mood/calming a bad temper.
Mucuna pruriens, I would always keep. I dose EOD and I think it is important for balancing (not jacking up) dopamine levels. It also is IMO one of the best non-peptide ways to increase GH pre-bed. It is also important for maintaining healthy sexual desire, satisfaction and performance. ...again not dosed to achieve anything beyond normalcy. (Too much will make you too happy and too much everything... this is not sustainable or desirable long-term).

5-HTP is something that is subjective. Do you need to increase serotonin?

For me the answer is no and 5-HTP does more harm then good.

One thing though is that people who crave carbs and I mean crave carbs on a diet to the point where it is always a fight... many of them have lower levels of serotonin and this doesn't change as you lose bodyfat. Supplementing so as to increase serotonin reduces intense cravings for carbohydrates on a diet.

Serotonin (in my body) is not something I play with. First I am not deficient and when I use something like 5-HTP it screws me up and it takes weeks to get back to feeling normal again. It is subjective but it gives me an edgy irritated mood.

The other three I don't really have a personal basis from which to speak.
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Old 06-10-2009, 01:00 AM
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givin the dose they gave the rabbits, i extrapolated that dose to someone my size and it was almost a gram of test, which I consider to be a hefty dose. Im a firm believe in Phil's 1cc a week theories and I adhere to that and have liked the long term results.
The wider messages:
Trimetazidine is interesting because it is safe and well tolerated and will protect the heart on a test cycle.

Chronic exposure was not needed , just 3 months to show lesions.

This study is just part of an overall concern about use of steroid cycles causing cardio-problems in humans. Autoposies show this type of damage when done on athlete users/abusers.

Using the lowest doses is better for many reasons. This just adds to that list.

Finally the young idiots (who are hobbiests not competitors) that love to create stacks of high dose this steroid and high dose that steroid really are idiots I'm afraid. No need to single out todays group as idiots... I am guilty of youthful stupidity at times in this area as well.... in the distant past.
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Old 06-10-2009, 04:10 AM
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SAM-e taken at 400-800mg a day is quite valuable, from joint support to liver support to mood enhancement.
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Old 06-10-2009, 09:10 AM
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One thing though is that people who crave carbs and I mean crave carbs on a diet to the point where it is always a fight... many of them have lower levels of serotonin and this doesn't change as you lose bodyfat. Supplementing so as to increase serotonin reduces intense cravings for carbohydrates on a diet.

Serotonin (in my body) is not something I play with. First I am not deficient and when I use something like 5-HTP it screws me up and it takes weeks to get back to feeling normal again. It is subjective but it gives me an edgy irritated mood.
I go through cycles where I can not fill satisfied no matter what I eat, then it goes a way for a few days then returns. (Carbs especially)
Its not a hypoglycemic type of hunger, just a "never fill satisfied" feeling.
Is there a trick or OTC sup that would help take the edge off?
I'm sure I'm one of a few billion or so who also experience this...LOL
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Old 06-10-2009, 11:58 AM
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The wider messages:
Using the lowest doses is better for many reasons. This just adds to that list.

Dat,
As you know, anti-aging protocols prescribe low doses of testosterone (e.g. cyp) perpetually starting in the 40s into old age. If a dose was, say, 90 mg per week to replace any deficiency one might have would you speculate the these lesions would develop over time? Or is there a safe reference range that one could occupy, even if it were in the upper quartile, on into old age?
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Old 06-10-2009, 01:57 PM
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I go through cycles where I can not fill satisfied no matter what I eat, then it goes a way for a few days then returns. (Carbs especially)
Its not a hypoglycemic type of hunger, just a "never fill satisfied" feeling.
Is there a trick or OTC sup that would help take the edge off?
I'm sure I'm one of a few billion or so who also experience this...LOL
Most places that sell complete amino acids lie. They leave out L-Tryptophan.

This important amino acid is required to produce serotonin in the brain which helps control feelings of satiety. Supplementing w/ it by taking it with your carbs could help reduce the amount you eat. See study below:

Tryptophan administration may enhance weight loss by some moderately obese patients on a protein-sparing modified fast (PSMF) diet, Eric Heraief, M.D, International Journal of Eating Disorders Volume 4 Issue 3, Pages 281 - 292 2006

Abstract

Drugs thought to enhance serotonin-mediated neurotransmission have been shown to diminish appetite for carbohydrates. Therefore, we examined the ability of tryptophan (TRP), serotonin's amino acid precursor, or a placebo to influence weight loss among 62 obese Swiss outpatients who were on a reducing diet [the protein-Sparing Modified Fast (PSMF) Diet] which can be associated with severe carbohydrate craving. This diet provides relatively large amounts of protein (1.2-1.4 g/kg ideal body weight/day) but little carbohydrate (40 g/day or less), thus stimulating ketone body production. Its consumption also reduces the ratio of plasma TRP to the summed concentrations of the other large neutral amino acids, thereby probably diminishing brain TRP and serotonin levels. During the initial month of the PSMF diet all patients received the placebo; thereafter 30 received TRP (750 mg, twice daily, orally, for 3 months) and 32 the placebo, according to a double-blind protocol.

Among moderately obese patients (140-159% of ideal weight; n = 25), the TRP significantly enhanced weight loss (p lt;.05), especially during the first treatment month (3.4 ± 2.8 vs 7.7 ± 1.7 kg lost; means ± standard deviation) but also during the total 3-month test period (2.6 ± 2.3 vs 1.5 ± 1.6 kg lost/month). The JRP didn't modify the reported adherence to the PSMF diet. The partial efficacy of TRP among our moderately obese subjects does not presently justify its routine use as an adjunct to a PSMF diet. However, greater efficacy may be obtained with better patient selection and under metabolic conditions designed to amplify the uptake of TRP into the brain (i.e., administration along with a carbohydrate).


I posted a while back what my favorite appetite suppressant was: http://www.professionalmuscle.com/fo...d.php?p=489695

The fineness of the powder and apple pectin in it make the gel that forms in your belly better and it s l o w s down digestion of carbohydrates and also instantly cuts hunger (maybe 10x better then straight Psyllium Fiber which forms the base of this powder). You take this before you eat high GI foods and your blood glucose profile will be a lower GI profile.
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Old 06-10-2009, 02:01 PM
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What about 5-htp in place of tryptophan?
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Old 06-10-2009, 02:07 PM
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Dat,
As you know, anti-aging protocols prescribe low doses of testosterone (e.g. cyp) perpetually starting in the 40s into old age. If a dose was, say, 90 mg per week to replace any deficiency one might have would you speculate the these lesions would develop over time? Or is there a safe reference range that one could occupy, even if it were in the upper quartile, on into old age?
No I don't think that true HRT dosing that keeps you in the upper ranges of normal present a problem.

I always wondered though about the possibility of mimicking natural release of testosterone instead of steady administration. That might mean an earlier in the day IM administration of a tiny bit of test suspension and then let it clear and spend the rest of the day with your own natural levels (plus mild natural AIs ...things like DIM, Resv, Nettle Root).

Anyway my general sense of it is that very low levels & very high levels present health problems in the long run and that being in the upper normal range is great for reducing diabetes, etc.

This is for true HRT though, not what some people use as a way to get into pharmacological levels.
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