lookin for info!

[MoNSTERoRBE]

ok will do!

very variable question....how much should i expect to gain?

[Phate]

where do regular potatoes stack up in there i get like 3 a day, but never sweet potatoes

http://forums.steroid.com/showthread.php?t=355037

thats a great thread that tells the difference between sweet potatos and normal potatos

read that and then if you have an questions ask, but that thread is amazing

[Phate]

ok will do!

very variable question....how much should i expect to gain?

hard question, but with a good diet, intense exercise and good pct(all of which you have right now)

i'd bet 20-25lbs, and you could keep anywhere from 15-20 of that

[MoNSTERoRBE]

wow im excited.

but i keep getting mixed opinions.

u guys agreed on 1cc of test and .5 cc of deca per shot.

yet my local source says no, 1cc of test twice a week, and 1cc of deca once a week.

whats the difference? he claims its so the oil dissolves better and u dont develop injection lumps......??

[N*E*R*D]

wow im excited.

but i keep getting mixed opinions.

u guys agreed on 1cc of test and .5 cc of deca per shot.

yet my local source says no, 1cc of test twice a week, and 1cc of deca once a week.

whats the difference? he claims its so the oil dissolves better and u dont develop injection lumps......??

Your source just wants you too buy more off him.

[one8nine]

wow im excited.

but i keep getting mixed opinions.

u guys agreed on 1cc of test and .5 cc of deca per shot.

yet my local source says no, 1cc of test twice a week, and 1cc of deca once a week.

whats the difference? he claims its so the oil dissolves better and u dont develop injection lumps......??

ha ha its cause if you listen to him you need to buy more
never take advice from a source that will cost you more money

[one8nine]

http://forums.steroid.com/showthread.php?t=355037

thats a great thread that tells the difference between sweet potatos and normal potatos

read that and then if you have an questions ask, but that thread is amazing

haha hell yes
skim cheese, reduced fat baccon bits, fat free sour cream, smart balance butter, scallions
i load mine up
but my las cycle i got down to 7% probably 15 hours cardio a week from fighting/wrestling

[MoNSTERoRBE]

either way its the same dosage, i wouldnt have to buy more.

hes saying to take the deca one cc at a time, you guys are saying to split it .5 cc with the test 2xs a week.

any reason?

[MoNSTERoRBE]

bumpp for opinions....??

[one8nine]

yes
ive shot 5ml..
the same exact reason

injection frequency
http://forums.steroid.com/showthread.php?t=355493

ester weight and active lives
http://forums.steroid.com/showthread.php?p=4131783

i already answered your question, read.

[LATS60]

yes he does
please do some research before giving out bad advice
click the injection frequency/acvive lives thread i posted

No he doesn't.
Thats not bad advice, deca can happily be shot once wk and i don't need to click your link for anecdotal evidence, i have 30 years experience of my own, maybe you should do the research and look at the pharmacology and pharmacokinetics of deca, this might help you understand the release rate of the decanoate ester and the accompanying graphs while give you an idea of the T(max) level times and serum/plasma test levels over the course of the HL.

[one8nine]

No he doesn't.
Thats not bad advice, deca can happily be shot once wk and i don't need to click your link for anecdotal evidence, i have 30 years experience of my own, maybe you should do the research and look at the pharmacology and pharmacokinetics of deca, this might help you understand the release rate of the decanoate ester and the accompanying graphs while give you an idea of the T(max) level times and serum/plasma test levels over the course of the HL.

show me
that link contains blood level stability charts and active lives
active lives are not anecdotal
congratulations, you are old and wrong

[LATS60]

Just because someone has a different opinion from you, it doesn't mean it's wrong. You are right, i'm old and you need to get your facts right.
Please take the time, you might just learn something.

Link for graphs(which prove my point) of this study are at end.
Experimental design. Twenty-three healthy volunteers were randomly allocated into four groups in two balanced blocks. The first stratum of the study involved comparing two different nandrolone esters while controlling for dose, injection site and volume. In this stratum, volunteers received either nandrolone phenylpropionate (Durabolin ; Organon) (group 1) or nandrolone decanoate (DecaDurabolin; Organon) (group 2), administered as a single deep i.m. injection of 100 mg nandrolone ester into a single injection site (gluteal) in a fixed volume (4 ml of arachis oil vehicle). In the second stratum, a single ester (nandrolone decanoate) with fixed dose (100 mg) and volume (1 ml of arachis oil vehicle) was injected into two different sites, gluteal (group 3) or deltoid (group 4) muscles. This design also allowed comparison between different injection volumes (4 ml vs. 1 ml) for a single nandrolone ester with fixed dose and injection site (i.e., group 2 vs. group 3).


Pharmacodynamics. The pharmacodynamic effects of nandrolone on plasma testosterone and inhibin were estimated by nadir concentration, time of nadir, net secretion and duration of suppression. The duration of suppression was defined as the time when plasma testosterone levels were below normal (<10 nM) or inhibin levels were reduced by 50% of base line. The effects of ester, injection site and volume were determined by parametric (testosterone) and nonparametric (inhibin) analysis of variance.

This pharmacodynamic analysis was extended by building a population pharmacodynamic model, again using the approach of Mandema et al. (1992). The pharmacodynamic model was based on one of the four basic indirect response models recently proposed by Dayneka et al. (1993). Because testosterone and inhibin secretion are both suppressed by nandrolone, model I of Dayneka et al. was physiologically the most appropriate to describe the pharmacodynamic effects of nandrolone and is shown in equation 6. (6)
R represents the measured response variable (either testosterone or inhibin concentrations), kin0 is a zero-order rate constant (the base-line testosterone or inhibin daily input rate), Cp(t) is the plasma concentration of the inhibiting drug (nandrolone) as a function of time and IC50 is the drug concentration that results in 50% of maximum inhibition of the production rate. Under steady-state base-line conditions, it is noted that kin0 = kout · R0, where R0 is R(t) at t = 0, reducing the number of parameters in the model. We have modified equation 6 to allow for incomplete inhibition of testosterone and inhibin synthesis by nandrolone and have included a parameter () to describe the steepness of this relationship (7)
where, for either testosterone or inhibin, R(t) is the measured concentration, R0 is the base-line concentration, Rmin is the minimum concentration when the input rate is maximally suppressed by nandrolone, kout is the first-order elimination rate constant, Cp(t) is the predicted plasma concentration for nandrolone (based on individual dosing and Bayesian pharmacokinetic parameter estimates) and IC50 is the concentration of nandrolone associated with 50% suppression of synthesis. The parameter was implemented as = 1 + , to enable a comparison of the full model ( > 1) and reduced model ( = 1, = 0) using the likelihood ratio test.

Alternatively, partial inhibition of the input rate can be modeled with an additional term expressing the fractional inhibition (Imax), as shown in equation 8. (8)
We used the parameterization shown in equation 7, because we were interested in estimating the base-line and maximally suppressed concentrations of testosterone and inhibin (and the interindividual variability in these parameters) directly. Based on the parameterization in equation 7, Imax is readily calculated as (9)
The interindividual errors in the model parameters (Ro, Rmin, kout, IC50 and ) were assumed to have a logarithmic-normal distribution, and the variance of the residual errors was assumed to be homoscedastic. As described for the pharmacokinetic analysis, a GAM was used to identify significant covariates, and NONMEM was used to develop the final pharmacodynamic model. All data are expressed as mean ± S.E.M.

Results
Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
Volunteers randomized into the four groups were comparable in anthropometric and hormonal variables (table 1). There were no significant differences between groups in mean dehydroepiandrosterone sulfate, LH, FSH, prolactin, insulin -like growth factor-I, hemoglobin, urea or creatinine concentrations (data not shown), which were normal for all men.





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TABLE 1
Base-line anthropometric and endocrine variables




Global statistical analysis. Considering all four groups, global statistical analysis demonstrated significant differences in the time course of plasma nandrolone concentrations (group, 2 = 84.6, 3 dF, P < .001 by Wald test; group × time interaction, 2 = 643, 66 dF, P < .001). These systematic differences were attributable to differences between different nandrolone esters (table 2). Similarly the time course of plasma testosterone concentrations varied significantly by group (group × time interaction, 2 = 266, 66 dF, P < .001) due to effects of both ester and injection site (table 2). To adjust for the dominating effect of differences between esters, a global analysis conducted for the three groups receiving nandrolone decanoate (groups 2-4) demonstrated significant effects of injection site on plasma nandrolone levels, as well as effects of injection volume and site on plasma testosterone and inhibin levels (table 3).





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TABLE 2
Global statistical analysis of plasma nandrolone and testosterone after nandrolone ester injection by time course, ester, injection site and volume







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TABLE 3
Global statistical analysis of plasma nandrolone, testosterone and inhibin after nandrolone decanoate injection by time course, injection site and volume




Pharmacokinetic analysis. Plasma nandrolone concentrations reached higher and earlier peak concentrations and had a shorter mean residence time after injection of the phenylpropionate ester (group 1; n = 7), compared with the other three decanoate ester groups (fig. 1; tables 2 and 4). Analysis of the concentration data obtained from the two subjects who received i.v. nandrolone gave the following values: area under curve/unit dose = 1.3224 × 103 days/liter, mean residence time = 25.65 ± 5.22 min, volume of distribution = 11.46 ± 0.30 liters and systemic clearance = 31.52 ± 7.26 liters/hr. From the optimal triexponential curve fit, the following parameters were estimated: A = 153.3 ± 2.7 nM, = 0.4132 ± 0.0030 min1, B = 8.8659 ± 0.4575 nM, = 0.0098 ± 0.0022 min1, C = 0.9708 ± 0.0066 nM and = 0.00043 ± 0.00045 min1. Based on the area under the curve estimates for these two subjects, the absolute bioavailability of nandrolone from i.m. injections of esters was significantly higher for nandrolone decanoate injected into gluteal muscle with a 1-ml volume (73%), compared with the other three groups (53-56%).




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Fig. 1. Time course of plasma nandrolone concentrations in 23 healthy men over 32 days after i.m. injection of 100 mg of nandrolone phenylpropionate in 4 ml of arachis oil vehicle into the gluteal muscle (group 1) () or injection of 100 mg of nandrolone decanoate into the gluteal muscle in 4 ml of arachis oil vehicle (group 2) (), into the gluteal muscle in 1 ml of arachis oil vehicle (group 3) () or into the deltoid muscle in 1 ml of arachis oil vehicle (group 4) (). Results are expressed as mean and S.E.M., unless the S.E. is smaller than symbol.







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TABLE 4
Pharmacokinetic variables




The final population pharmacokinetic model incorporated ester, site and volume of injection and height as significant covariates. Height was significantly superior to weight, body surface area or lean body mass as a covariate. The type of ester influenced the absorption profile of nandrolone, such that the phenylpropionate ester was best described by a one-compartment absorption model and the decanoate ester was best described by a two-compartment absorption model. This was implemented in the model with parameter P (table 5). The interpretation of this parameter was that, effectively, the total dose of the phenylpropionate ester is administered into the "fast" compartment characterized by the rapid absorption rate constant (k1), whereas only ~14% of the total dose of the decanoate ester is administered into this compartment, with the remaining ~86% of the total dose being administered into the "slow" compartment characterized by a slower absorption rate constant (k2). This basic difference in the profiles of the nandrolone concentration data is shown in figure 2. In figure 2, the individual in each of the four groups with the median mean absolute prediction error was selected to represent the Bayesian predictions based on the individual pharmacokinetic parameters. In addition, the rate of absorption from the fast compartment (k1) was greater for the deltoid muscle than the gluteal muscle.




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TABLE 5
Nandrolone population pharmacokinetic model







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Fig. 2. Observed and model-predicted time course of plasma nandrolone concentrations in four healthy men over 32 days after i.m. injection of 100 mg of nandrolone ester. The four men were selected from each of the treatment groups according to the median predicted error in nandrolone concentrations, so that they were most representative of that group. Note the logarithmic vertical scale. , observed data; , individual Bayesian predictions.




A two-compartment disposition function performed significantly better than a one-compartment disposition function. Site and volume of injection were important covariates for the two parameters, with bioavailability as a component (F·A1 and F·A2). F·A1 was greater in the gluteal muscle, compared with the deltoid muscle, and F·A2 was greater with a smaller injection volume (1 ml vs. 4 ml). Although the slow hybrid rate constant 2 was difficult to estimate accurately, it describes the very slow terminal elimination phase (fig. 2) and significantly improved the logarithmic-likelihood objective function of the model, as exemplified by the improved fit of the two-compartment, compared with one-compartment, disposition function.

Pharmacodynamic analysis. Plasma testosterone concentrations were most rapidly and completely suppressed within the first week after injections of the phenylpropionate ester (fig. 3; tables 2 and 6), but this suppression was sustained for the shortest time. The duration of suppression was significantly longest after the gluteal 1-ml injection. Plasma testosterone concentrations returned to base line by day 13 after the phenylpropionate ester but required >20 days to return to base-line levels after the decanoate ester. Among the decanoate ester injections, both injection volume and site significantly influenced plasma testosterone concentrations (tables 3 and 6). Plasma inhibin levels after decanoate ester injections were suppressed to significantly lower nadir levels after 1-ml gluteal injection (fig. 3; table 6). Plasma inhibin was not assayed after nandrolone phenylpropionate (group 1) injection.




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Fig. 3. Time course of plasma testosterone concentrations in 23 healthy men over 32 days after i.m. injection of 100 mg of nandrolone phenylpropionate in 4 ml of arachis oil vehicle into the gluteal muscle (group 1) () or injection of 100 mg of nandrolone decanoate into the gluteal muscle in 4 ml of arachis oil vehicle (group 2) (), into the gluteal muscle in 1 ml of arachis oil vehicle (group 3) () or into the deltoid muscle in 1 ml of arachis oil vehicle (group 4) (). Results expressed as mean and S.E.M., unless the S.E. is smaller than the symbol.







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TABLE 6
Pharmacodynamic variables




The GAM analysis detected no statistically significant covariates for the testosterone pharmacodynamic model (table 7). The inclusion of a parameter to estimate the nadir concentration of testosterone resulting from maximal suppression of testosterone synthesis by nandrolone and of a slope parameter describing the steepness of the relationship between the nandrolone concentration and the testosterone output rate significantly improved the model. Figure 4 shows the predicted testosterone concentrations for the same individuals as shown in figure 2. These predictions were calculated using the Bayesian estimates of the individual's nandrolone pharmacokinetic parameters and testosterone pharmacodynamic parameters.




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TABLE 7
Population pharmacodynamic models for testosterone and inhibin







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Fig. 4. Observed and model-predicted time course of plasma testosterone concentrations in four healthy men over 32 days after i.m. injection of 100 mg of nandrolone ester. The four men were the same individuals as illustrated in figure 2, who were originally selected from each of the treatment groups according to the median predicted error of nandrolone concentrations, so that they were most representative of that group. , observed data; , individual Bayesian predictions.




No statistically significant covariates were detected in the GAM analysis for the inhibin pharmacodynamic model (figs. 5 and 6; table 7). Unlike testosterone, the inclusion of a parameter to estimate the nadir inhibin concentration did not improve the model, although a slope parameter did significantly improve the model fit. Figure 6 shows the predicted inhibin concentrations for the same individuals as shown in figure 2. Plasma inhibin was not assayed after nandrolone phenylpropionate (group 1) injection. These predictions were calculated using the Bayesian estimates of the individual's nandrolone pharmacokinetic and inhibin pharmacodynamic parameters.



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Fig. 5. Time course of plasma inhibin concentrations in 23 healthy men over 32 days after i.m. injection of 100 mg of nandrolone decanoate into the gluteal muscle in 4 ml of arachis oil vehicle (group 2) (), into the gluteal muscle in 1 ml of arachis oil vehicle (group 3) () or into the deltoid muscle in 1 ml of arachis oil vehicle (group 4) (). Results are expressed as mean and S.E.M. unless the S.E. is smaller than the symbol.







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Fig. 6. Observed and model-predicted time course of plasma inhibin concentrations in three healthy men over 32 days after i.m. injection of 100 mg of nandrolone decanoate. No inhibin data were available for the group that received nandrolone phenylpropionate injections. The three men were selected from three of the four treatment groups according to the median predicted error, so that they were most representative of that group. , observed data; , individual Bayesian predictions.
http://jpet.aspetjournals.org/cgi/content/full/281/1/93



Discussion
Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
The present study demonstrates that, in addition to the chemistry of the side-chain ester, both injection site and volume can systematically influence blood nandrolone levels after i.m. injection of nandrolone esters in an oil vehicle formulation. Corresponding to the patterns of blood nandrolone concentrations, pharmacodynamic indices reflecting androgen-induced inhibition of pituitary-testicular function, namely blood testosterone and inhibin concentrations, are also systematically influenced by these factors. Crucially, the mixed-effects pharmacodynamic modeling demonstrated that essentially all of the pharmacodynamic variability in plasma testosterone and inhibin concentrations was accounted for by the variability between esters and the site and volume of injection of the nandrolone injections. The present study extends knowledge of the clinical pharmacokinetics of nandrolone esters, which were reported in two previous studies concerning nandrolone decanoate kinetics in humans (Belkien et al., 1985; Wijnand et al., 1985); there are no reports of the pharmacokinetics of the phenylpropionate ester.

One feature of this study is the use of the population pharmacokinetic approach to integrating pharmacokinetic and pharmacodynamic data. Whereas the global statistical analysis indicates the significance of some key variables, a structural model allows more physiological interpretation of the findings, especially identifying the relationships between the pharmacokinetic and pharmacodynamic effects. We have used an indirect response model (Dayneka et al., 1993), which allows for more physiologically meaningful models, more realistic interpretation of derived estimates and statistically valid testing for categorical covariables, while more efficiently using all of the experimental data (Jusko and Ko, 1994). The indirect physiological model-based approach also readily allows incorporation, into a general model, of data from different subpopulations where the kinetics and dynamics had differing shapes for the effective dose-response relationships. It is a striking validation of the model-based estimates that the nadir concentrations of testosterone and inhibin correspond very accurately to the known concentrations of these hormones in castrated men (1-3 nM and 0 pg/ml, respectively) (McLachlan et al., 1990; Handelsman, 1994).

An interesting feature of this analysis of testosterone suppression is that the first-order rate constant for the response compartment (kout) does not correspond to the metabolic clearance rate for testosterone. Using either bolus injection or steady-state infusion, the metabolic clearance rate for testosterone in men is ~540 liters/m2/day (Gandy, 1977) and the volume of distribution is 10 to 20 liters, which is similar to the 11.5 liters estimated in this study for nandrolone, a molecule almost identical to testosterone. These estimates would indicate a kout value of ~50 day1, whereas our observed estimate for kout was 0.708 day1; the latter is consistent with a much slower rate (half-time, ~1 day). This discrepancy is attributable to the fact that the overall kinetics of suppression of testosterone are dominated by the slow negative feedback system, rather than the much faster metabolic clearance of testosterone. This negative feedback is mediated via inhibition of pulsatile gonadotropin-releasing hormone secretion from hypothalamic neurons into the pituitary portal system and then pituitary LH secretion from gonadotropes. For example, a highly potent and specific gonadotropin-releasing hormone antagonist that causes immediate cessation of gonadotropin-releasing hormone action leads to castrate testosterone concentrations within 12 hr (Behre et al., 1992), compared with 5 to 10 days in this study. This illustrates the need for physiological insight when interpreting indirect pharmacodynamic models because, in this instance, the relationship between circulating nandrolone concentration and the input function to the model may itself be indirect. Our paradigm exemplifies a paradigm where the kout parameter may accurately predict the time course of overall behavior of a system without corresponding to the metabolic clearance rate of the drug or the pharmacodynamic endpoint under study.

In the present study we have used specific radioimmunoassays to measure the nandrolone, testosterone and inhibin concentrations, with the latter two representing effective markers of endogenous pituitary gonadotropin (LH and FSH, respectively) secretion. This reflects the physiological fact that pituitary LH acts exclusively upon testicular Leydig cells, due to their unique expression of cell surface membrane LH receptors. In healthy men, virtually all circulating testosterone originates from Leydig cells, with an absolute requirement for trophic influence from LH derived from the bloodstream. Similarly, pituitary FSH acts exclusively upon testicular Sertoli cells, which uniquely express FSH receptors on their cell surface membranes, and virtually all circulating immunoreactive inhibin originates from the gonads (Burger, 1992). As a result, blood levels of these two hormones are useful integrated bioassay indicators of endogenous pituitary gonadotropin secretion, as reflected by the testicular hormonal response to ambient blood LH and FSH levels. In the present study, these two pharmacodynamic indices showed physiologically meaningful distinctions between the esters and the effects of injection site and volume.

Variations in side-chain ester chemistry are important in the pharmacokinetics of androgen esters in oil vehicle (Behre et al., 1990). Experimental studies suggest that absorption rates are predicted by the oil/water partition coefficients (or hydrophobicity) and that the oil vehicle is absorbed more slowly than the androgen ester (Tanaka et al., 1974). In humans, the very short propionate (three-carbon aliphatic) ester of testosterone has distinctly shorter duration of action than esters with longer (seven- or eight-carbon) side-chains (Nieschlag et al., 1976; Schulte-Beerbuhl and Nieschlag, 1980; Schurmeyer and Nieschlag, 1984; Belkien et al., 1985; Fujioka et al., 1986). More subtle changes in side-chain ester structure have proven ineffective in altering human clinical pharmacokinetics, because substitution of a linear aliphatic side-chain of seven carbons (enanthate ) with either a saturated, cyclized, seven-carbon aliphatic chain (cyclohexanecarboxylate) (Schurmeyer and Nieschlag, 1984) or a linear, aliphatic, eight-carbon chain (cypionate ) (Schulte-Beerbuhl and Nieschlag, 1980) resulted in virtually unchanged kinetics. Wider variation in ester side-chain chemistry to include greater chain length and/or aromatic ring structures is a more effective determinant of ester pharmacokinetics, because nandrolone hexoxyphenylpropionate ester (aromatic ring with 18 carbons) had far better depot properties, with a prolonged and retarded release profile, compared with the decanoate (aliphatic chain with 10 carbons) (Belkien et al., 1985). The present study indicates that a side-chain ester consisting of a 10-carbon aliphatic chain has better depot properties than a nine-carbon chain including an aromatic ring. Because the vehicle (arachis oil) was unchanged during this study and because of the experimental observation that the oil vehicle influences local reaction to the oil injection (Brown et al., 1944), as well as androgen ester pharmacology (Ballard, 1980; Al-Hindawi et al., 1986), the present conclusions may be extrapolated to other vegetable oil injection vehicles only with caution.

Injection technique, including injection site, volume and concentration, as well as the nature of the vehicle, could theoretically be important for androgen ester release rate. Injection site may be important because of differences in tissue composition (Cockshott et al., 1982) and blood flow (Bederka et al., 1971); indeed, i.m. oil-based injections may more accurately be termed intermuscular (Ballard, 1968) or intralipomatous (Cockshott et al., 1982). The former reflects the tendency of oil vehicle to distribute along intermuscular fascial planes (Ballard, 1968), whereas the latter depends upon the amount of fat at the injection site (including systematic gender differences) (Modderman et al., 1983) together with needle geometry and anatomy of the injection depot. Intralipomatous deposition of injections with a larger vehicle volume may explain the slower release kinetics of nandrolone decanoate in the gluteal region, as well as the differences from the deltoid site, which has a lower fat content. The higher blood flow in the deltoid, compared with the gluteal, muscle (Evans et al., 1975) may also be important. Analogous site-dependent differences in absorption rate and physiological effects have been described for a variety of drugs in aqueous solution (Greenblatt and Koch-Weser, 1976). To our knowledge, there are no previous reports examining the systemic pharmacokinetic and pharmacodynamic effects of injection site and volume for androgen esters in oil vehicle in men.

One possible clinical impact of these observations may lie in recent observations of differences between population groups in the efficacy of regular i.m. injections of testosterone enanthate in an oil vehicle to suppress testicular function for male contraception (World Health Organization Task Force on Methods for the Regulation of Male Fertility, 1990). In that and related (World Health Organization Task Force on Methods for the Regulation of Male Fertility, 1993) studies, interethnic differences in susceptibility to androgen-induced azoospermia were not due to differences in overall body size or related differences (Handelsman et al., 1995). Evaluation of the possibility of ethnopharmacological differences, however, required a greater understanding of the rate-determining mechanisms of androgen release from androgen ester depots in oil vehicles. The present findings suggest that differences in absorption of androgen esters may contribute to such interethnic differences through possible local mechanical factors (e.g., exercise, compression and muscle and fat mass) at the injection site, and this issue warrants further study. Analogous variations in the pharmacokinetics of steroid esters have been reported among women from different countries using long-acting contraceptive steroids (Garza-Flores, 1994), although no explanation has been advanced. Further analysis of the present observations may facilitate such ethnopharmacological studies, as well as clinical applications of androgen esters in oil vehicle formulations.

http://jpet.aspetjournals.org/cgi/content/full/281/1/93

[one8nine]

youve got to be kidding ive seen that study before years ago
decas active life is about 15 days injecting once a week is at half the active life
injecting 1/4 way through the active life is much more effective
id much rather go between 100% to 75%, than 100% to 50% but you can do whatever you want

[LATS60]

youve got to be kidding ive seen that study before years ago
decas active life is about 15 days injecting once a week is at half the active life
injecting 1/4 way through the active life is much more effective
id much rather go between 100% to 75%, than 100% to 50% but you can do whatever you want

You may have, but you can't deny the facts and facts is what that study gives, amongst many other studies done by the likes of bhasan and behre and even neislag.

Deca 's HALF LIFE is about 15 days you mean, so i am injecting at a 1/4 way through the active life, thats why 1x wk is good enough.

[one8nine]

You may have, but you can't deny the facts and facts is what that study gives, amongst many other studies done by the likes of bhasan and behre and even neislag.

Deca's HALF LIFE is about 15 days you mean, so i am injecting at a 1/4 way through the active life, thats why 1x wk is good enough.

no i agree with the study 100%, i think that just proves my point even more
we just have opposing opinions on what stable blood levels should be

im sorry you are right, i meant half life, my mistake

cypionate has a 12 day half life, do you inject that once a week?

[MoNSTERoRBE]

very interesting arguement...considering its about my cycle! lol

still leaning towards 189's suggestion. if anything mostly bc id reduce the amount of pokes

[LATS60]

no i agree with the study 100%, i think that just proves my point even more
we just have opposing opinions on what stable blood levels should be

im sorry you are right, i meant half life, my mistake

cypionate has a 12 day half life, do you inject that once a week?

No of course not, half the half life will give stable enough serum levels to avoid unwanted sides, so i inject cyp E5D depending of course on the blast i'm on at the time, no disrespect and i respect your opinion, but don't go posting i give bad advice when i don't please, remember 189 you only need to keep levels fairly stable, supraphysiological effects will only manifest themselves towards the end of the active life, so as i said with the deca , my once wk makes for a 1/4 of the active life, giving stable enough levels without supraphysiological effects.

[LATS60]

very interesting arguement...considering its about my cycle! lol

still leaning towards 189's suggestion. if anything mostly bc id reduce the amount of pokes

Uh, my suggestion of shooting deca 1x wk instead of 189's 2 x wk reduces the pokes i think.

[one8nine]

No of course not, half the half life will give stable enough serum levels to avoid unwanted sides, so i inject cyp E5D depending of course on the blast i'm on at the time, no disrespect and i respect your opinion, but don't go posting i give bad advice when i don't please, remember 189 you only need to keep levels fairly stable, supraphysiological effects will only manifest themselves towards the end of the active life, so as i said with the deca, my once wk makes for a 1/4 of the active life, giving stable enough levels without supraphysiological effects.

you are right i could have been more polite about my opposing opinion

[one8nine]

Uh, my suggestion of shooting deca 1x wk instead of 189's 2 x wk reduces the pokes i think.

very interesting arguement...considering its about my cycle! lol

still leaning towards 189's suggestion. if anything mostly bc id reduce the amount of pokes

either way you gotta shoot 2x a week
i just say you do 1.5 every time, stay more stable, youre shooting anyway
he thinks you should inject 2ml, then 1ml, then 2ml, 1ml etc... and be less stable

either way your injection frequency is the same

[LATS60]

you are right i could have been more polite about my opposing opinion

Ok mate, we'll agree to disagree.
Hater of sustanon , well now then thats,,,,,,,,,,,,,,,,,,,,,,,,,,, just kidding lol.

[LATS60]

either way you gotta shoot 2x a week
i just say you do 1.5 every time, stay more stable, youre shooting anyway
he thinks you should inject 2ml, then 1ml, then 2ml, 1ml etc... and be less stable

either way your injection frequency is the same

LOL, in my first post on this thread i said it easier to put them in the same barrel and jab 2 x wk, jeez this is getting silly.

[one8nine]

LOL, in my first post on this thread i said it easier to put them in the same barrel and jab 2 x wk, jeez this is getting silly.

sorry you are right

so really we both agree 1.5ml 2x a week

so our arguement really doesnt relate to this thread ha ha

[MoNSTERoRBE]

1.5ml 2wice a week!! gotcha

thanks alot lat and 189

[MoNSTERoRBE]

btw..i start today..wish me luck ill keep u guys posted