AndroidHealthClinic

Ik zie door de bro science het bos niet meer

Test e om de dag geeft nog stabielere waarde dan test p om de dag.
Test-e elke dag geeft nog een stabielere waarde, maar het word niet significant beter. Ik vind zelf dat je minimaal binnen 50% van de halveringstijd van het ester moet injecteren. Voor een prop ester is de halveringstijd 4 dagen en werkt om de dag dus ideaal. Een enanthaat ester heeft een halveringstijd van 10 dagen en is mijn mening dat je maximaal 5 dagen tussen elke injectie moet laten.
 
Test-e elke dag geeft nog een stabielere waarde, maar het word niet significant beter. Ik vind zelf dat je minimaal binnen 50% van de halveringstijd van het ester moet injecteren. Voor een prop ester is de halveringstijd 4 dagen en werkt om de dag dus ideaal. Een enanthaat ester heeft een halveringstijd van 10 dagen en is mijn mening dat je maximaal 5 dagen tussen elke injectie moet laten.

Hoezo wordt het niet significant beter?
 
  • Topic Starter Topic Starter
  • #25
Belangrijker zijn de doses (mg/ml) waar je prikt (bil - arm - subq ), de bolus en hoe de substantie is klaargemaakt (carrier (olie) en oplosmiddelen etc).

The effect of steroid esters | JuicedMuscle.com

Influences on the halflife and potency of steroids | JuicedMuscle.com

Conclusies betreft inject spots zijn wel bizar.. Tot wel 30% meer effectiviteit van AAS wanneer je in de glute injecteert t.o.v. delts. Vind ik heel opmerkelijk.

Er zijn ook studies die beweren dat de absorptie veel beter is bij een delt injectie.

@Galen
Hoe sta jij hierin? Zijn bepaalde injectiespots superieur?
 
Laatst bewerkt:
Conclusies betreft inject spots zijn wel bizar.. Tot wel 30% meer effectiviteit van AAS wanneer je in de glute injecteert t.o.v. delts. Vind ik heel opmerkelijk.
I have never heard anyone provide an explanation for how this would work. The same quantity of the esterfied drug is inside the body with either injection spot. The only way for the drug to leave the body is to first enter the blood circulation, then having the ester removed by enzymes, and then to be metabolized and secreted by liver and kidneys. It's not like any of the drug could just magically disappear in the delts. The only difference between injection spots is how fast the esterfied drug enters the blood stream. So absent of any valid theoretical explanation, I would argue that there is some measurement error in the studies. But hey I'm biased since I'm too immobile to pin my glutes :treuren:
 
  • Topic Starter Topic Starter
  • #27
I have never heard anyone provide an explanation for how this would work. The same quantity of the esterfied drug is inside the body with either injection spot. The only way for the drug to leave the body is to first enter the blood circulation, then having the ester removed by enzymes, and then to be metabolized and secreted by liver and kidneys. It's not like any of the drug could just magically disappear in the delts. The only difference between injection spots is how fast the esterfied drug enters the blood stream. So absent of any valid theoretical explanation, I would argue that there is some measurement error in the studies. But hey I'm biased since I'm too immobile to pin my glutes :treuren:

Sounds logical and I really want to believe it too. Since I hate sticking long needles in my ass and love pinning with insuline needles in lats/delts/pecs.
 
Test-e elke dag geeft nog een stabielere waarde, maar het word niet significant beter. Ik vind zelf dat je minimaal binnen 50% van de halveringstijd van het ester moet injecteren. Voor een prop ester is de halveringstijd 4 dagen en werkt om de dag dus ideaal. Een enanthaat ester heeft een halveringstijd van 10 dagen en is mijn mening dat je maximaal 5 dagen tussen elke injectie moet laten.

Een enanthaat ester heeft een halveringstijd van 5 dagen

About SteroidGraph
 
I have never heard anyone provide an explanation for how this would work. The same quantity of the esterfied drug is inside the body with either injection spot. The only way for the drug to leave the body is to first enter the blood circulation, then having the ester removed by enzymes, and then to be metabolized and secreted by liver and kidneys. It's not like any of the drug could just magically disappear in the delts. The only difference between injection spots is how fast the esterfied drug enters the blood stream. So absent of any valid theoretical explanation, I would argue that there is some measurement error in the studies. But hey I'm biased since I'm too immobile to pin my glutes :treuren:
Injection site affects the steroids pharmacokinetics and therefore also it's effectivity. There isn't much substance on this, but there's a good paper detailing the pharmacokinetics (and to some extent the pharmacodynamics) of nandrolone depending on ester, injection site and oil volume: Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. - PubMed - NCBI
 
Injection site affects the steroids pharmacokinetics and therefore also it's effectivity. There isn't much substance on this, but there's a good paper detailing the pharmacokinetics (and to some extent the pharmacodynamics) of nandrolone depending on ester, injection site and oil volume: Pharmacokinetics and pharmacodynamics of nandrolone esters in oil vehicle: effects of ester, injection site and injection volume. - PubMed - NCBI
I took a quick look at the study. The finding that injection site influences plasma nandrolone levels is not statistically significant in a multivariate regression model (Neither were the coefficient estimates statistically significant for other dependent variables such as testosterone and inhibin levels). And the difference in AUC between deltoid and gluteus injection is only statistically significant at the 10% level in the empirical model. In their fitted model, the difference in AUC is significant, but given how many free parameters are in their model, that's basically a foregone conclusion.

So the empirical evidence for differences in pharmacokinetics based on injection site is very weak. Furthermore, the paper provides no explanation of, or data for, how specifically the pharmacokinetics would differ. They did find that gluteal injections are associated with slower release kinetics than for deltoid injections, which they argue may be due to differences in blood flow and intramuscular fat deposits. In my mind, this is the only mechanism through which drug metabolism between the two groups may differ. But how exactly? No clue. And would that lead to a 30% difference in AUC plasma concentrations? Very unlikely.
 
It's not like any of the drug could just magically disappear in the delts. ...
W Schänzer 1996:
Anabolic androgenic steroids (AAS) are misused to a high extent in sports by athletes to improve their physical performance. Sports federations consider the use of these drugs in sports as doping. The misuse of AAS is controlled by detection of the parent AAS (when excreted into urine) and (or) their metabolites in urine of athletes. I present a review of the metabolism of AAS. Testosterone

There are many excretion profiles available on the net. Studies from the fifties already found that excretion increased when people took T3, newer research also investigated other metabolism enhancers such as caffeine.. verrek ben ik alweer in het engels bezig en dat op een nederlands site ...lol..
I posted about here How to use oral anabolic steroids | JuicedMuscle.com
 
It's not like any of the drug could just magically disappear in the delts. ...
W Schänzer 1996:
Anabolic androgenic steroids (AAS) are misused to a high extent in sports by athletes to improve their physical performance. Sports federations consider the use of these drugs in sports as doping. The misuse of AAS is controlled by detection of the parent AAS (when excreted into urine) and (or) their metabolites in urine of athletes. I present a review of the metabolism of AAS. Testosterone

There are many excretion profiles available on the net. Studies from the fifties already found that excretion increased when people took T3, newer research also investigated other metabolism enhancers such as caffeine.. verrek ben ik alweer in het engels bezig en dat op een nederlands site ...lol..
I posted about here How to use oral anabolic steroids | JuicedMuscle.com
My point is that the drug still has to go through the blood stream before being further metabolized and then secreted in urine. So it cannot disappear in the muscle tissue before entering the blood, and thus I don't see how AUC of the drug's plasma levels can vary much for different IM injection sites. Your article is mostly about the absorption of oral drugs into the blood stream, so I don't really see the connection to be honest.
 
I took a quick look at the study. The finding that injection site influences plasma nandrolone levels is not statistically significant in a multivariate regression model (Neither were the coefficient estimates statistically significant for other dependent variables such as testosterone and inhibin levels). And the difference in AUC between deltoid and gluteus injection is only statistically significant at the 10% level in the empirical model. In their fitted model, the difference in AUC is significant, but given how many free parameters are in their model, that's basically a foregone conclusion.
Why only look at the AUC? You'd mainly expect differences in other pharmacokinetic variables when looking whether or not injection site or carrier has any effect.

So the empirical evidence for differences in pharmacokinetics based on injection site is very weak.
With the exception of AUC, all pharmacokinetic parameters were significantly different between groups.

Furthermore, the paper provides no explanation of, or data for, how specifically the pharmacokinetics would differ. They did find that gluteal injections are associated with slower release kinetics than for deltoid injections, which they argue may be due to differences in blood flow and intramuscular fat deposits. In my mind, this is the only mechanism through which drug metabolism between the two groups may differ. But how exactly? No clue. And would that lead to a 30% difference in AUC plasma concentrations? Very unlikely.
Well, the release of an esterified steroid from the oily depot is determined by its partition coefficient, which is influenced by what directly borders the oily depot and thus also depends on the surface area the oil depot borders the surrounding tissue with. Imagine a perfect sphere, it's surface area bordering surrounding tissue will be much smaller than when the same volume of oil would form a layer exactly 1 molecule thick (which would yield the largest possible surface area).
Depending on the muscle you've injected, it might be that the oil depot has more or less surface area to be in contact with the surrounding tissue.

Some other stuff which influences the partition coefficient is indeed what the surrounding tissue is made up of, the rate of bloodflow (which will influence the concentration gradient as it will remove the steroid from the area), osmotic pressure from tissue fluids, activity of local esterases, lymphatic drainage, etc. etc.

Do note that I'm not suggesting these differences are huge. It's just without a doubt that any measured differences are not just due to measurement errors.
 
Laatst bewerkt:
Why only look at the AUC? You'd mainly expect differences in other pharmacokinetic variables when looking whether or not injection site or carrier has any effect.

With the exception of AUC, all pharmacokinetic parameters were significantly different between groups.
You are referring to table 4?. 'Time of peak', 'Peak concentration', 'Mean residence time', 'Half-time', 'Duration' and 'Clearance' were all significantly different between groups in table 4. But I'm not sure what the null hypothesis there actually is. I reckon the null is that all 4 estimates are identical. So for example if there were only a difference between column 1 and 4, that would cause the low p value even when columns 3 and 4 are not significantly different statistically.


If you consider Table 3 on the other hand, you see that there were no statistically significant differences in Nandrolone, Testosterone and Inhibin plasma levels between the 2 injection sites. But I might be wrong here, my stats is very rusty plus I'm not familiar with some of the statistical techniques they use. If I'm correct, however, this would mean that even if the researchers did make no errors in the measurement process (Which for stuff like the AUC is tricky I have been told), then there is still no credible evidence that injection site matters for total plasma levels. The finding that there are no differences in plasma levels after controlling for covariates is also consistent with there being no difference in AUC.

Even with my reservations about the interpretation of Table 4 though, you are right that there ate differences in the pharmacokinetics, as evidenced by the interaction term of time and volume/site. So the timing of the drug release from the injection site does differ.

The reason I am focusing on total plasma levels and AUC is because this is arguably the most important determinant of physiological action. If, as cited in the reporting on this paper, the AUC/bioavailibility of gluteus injections were really 30% higher, then that would make a huge difference in terms of the drug's overall efficacy. But as I argue above, this finding is not robust at all. On the other hand, there is evidence that the timing of release differs significantly between injection sites, something for which there is a multitude of well founded potential explanations as you point out above.

So I agree that the pharmacokinetics differ between injection sites, but I would argue that this is inconsequential in terms of the drug's efficacy if a regular injection frequency such as e5d is used. The only pharmacokinetic variable that would make a difference, AUC\total plasma levels, is no different between injection sites, as opposed to what has been reported in all those bodybuilding articles about the paper.

559d3758ea297b9f32737c867d8ad2f0.png
 
Oh no, I agree with that; if you have quite stable levels because you inject frequently enough it doesn't matter in the slightest.
 
Halve waardetijd is een niet bestaand fenomeen, gewoon theoretisch. Zoals gezegd zijn er ontzettend veel omstandigheden die bepalen hoe lang een in olie opgeloste steroïde werkt.
Kijk alleen deze studie naar Nebido.
Intramuscular injection of testosterone undecanoate for the treatment of male hypogonadism: phase I studies. Behre et al

OBJECTIVE:

In the search for long-acting testosterone preparations suited for substitution therapy of hypogonadal men, testosterone undecanoate (TU) dissolved in either tea seed oil or castor oil was investigated.

DESIGN:

In study I, 1000 mg TU in tea seed oil (125 mg/ml) were injected in equal parts into the gluteal muscles of seven hypogonadal men. In study II, 1000 mg TU in castor oil (250 mg/ml) were injected into one gluteal muscle of 14 patients.

RESULTS:

In comparison with published data on testosterone enanthate, most widely used for i.m. injections, the kinetic profiles of both TU preparations showed extended half-lives and serum levels not exceeding the upper limit of normal. The castor oil preparation had a longer half-life than TU in tea seed oil (33.9+/-4.9 vs 20.9+/-6.0 days (mean pm S.E.M.)). Dus een verschil van 34 dagen vs 21 dagen in halve waardetijd !!! Wat is het verschil? ...de bolus en de gebruikte carrier olie.

CONCLUSION:

The longer half-life and the smaller injection volume make TU in castor oil a strong candidate for further applications in substitution therapy and in trials for male contraception.

Dat werkt voor diverse variabelen
Dimethyl nandrolon

En vooral tegenwoordig, nu kleinere bolussen nodig zijn voor HRT/TRT
Subcutaan Injecteren
 
Terug
Naar boven