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Mathematical look at frequency of injections

zig - the attack analogy is probably got merit, any thing the body sees is exogenous it tries to compensate for.
 
I follow your math and apart from the theory most guys who have tried more frequent injections have noticed better results = theory is backed by experiment .

I would do more frequent injections with my upcoming test enanthate/d-bol cycle but, honestly, I don't have the experience or comfort with injections.
 
I have always been under the impression that EOD injections were standard with an acetate bound anabolic... ?

I know daily injections would keep the levels more fluid, but what is the lifespan of that ester like exactly?




-Stew
 
According to Bill Roberts TA has a half life between 24-36 hrs. IS that what you meant?

Andy
 
Andy13 said:
According to Bill Roberts TA has a half life between 24-36 hrs. IS that what you meant?

Andy



No, I KNOW that EOD injections work good, and I know about all the he said/ she said mumbojumbo... I was just wondering if you'd ever seen a scientific evaluation of the acetate ester.




-Stew
 
Stew Meat said:




No, I KNOW that EOD injections work good, and I know about all the he said/ she said mumbojumbo... I was just wondering if you'd ever seen a scientific evaluation of the acetate ester.




-Stew

What exactly do you mean by "scientific evaluation of the acetate ester?"

Andy
 
My friend says..... my brother says.... my cousin says.... Bill Philips says... blah blah blah...


How long does it take esterase to break down all the carbon chains that compose the acetate ester maning no more ester... for instance, enthanate is about 10-14 days. So that would put the halfife around 7 days meaning it should be injected every 3.5 days to keep levels fluid. I'm wondering what the span of acetate is so I can judge the benefit of ED as opposed to EOD and I don't care if so and so had better results from ED... some also get better results from using sustonon (lol!) and some get hairloss blocked by saw palmetto (lol!).

I'm not suggesting that you should know the answer to what I was asking, I just didn't know if you'd ever come across anything.


-Stew
 
Stew Meat said:
My friend says..... my brother says.... my cousin says.... Bill Philips says... blah blah blah...


How long does it take esterase to break down all the carbon chains that compose the acetate ester maning no more ester... for instance, enthanate is about 10-14 days. So that would put the halfife around 7 days meaning it should be injected every 3.5 days to keep levels fluid. I'm wondering what the span of acetate is so I can judge the benefit of ED as opposed to EOD and I don't care if so and so had better results from ED... some also get better results from using sustonon (lol!) and some get hairloss blocked by saw palmetto (lol!).

I'm not suggesting that you should know the answer to what I was asking, I just didn't know if you'd ever come across anything.


-Stew

I'm still not sure what you mean be "break down all the carbon chains that compose the acetate ester meaning no more ester.."

Are you talking about the entire depot or a molecule? I don't understand what you mean by "enanthate takes 10 to 14 days, so the half life is 7 days..."

Just to clarify, I'm sure you mean "hydrolyze." But a lot of guys think the ester is "broken down." I guess they think the carbon atoms are removed like in beta oxidation or something. No. The ester is simply hydrolized to the parent steroid plus the coorisponding carboxylic acid. In the case of TA, it's acetic acid (vinegar hehe). And ester hydrolysis is instantaneous!

It certainly is reasonable to think that different parent steroids as well as different esters have more/less affinity for the esterase enzyme.. Perhaps this factors into release rate.

Incedentally, a member of another board who's opinion I hold in the highest regard feels that the rate limiter in de-esterification is the actual removal of the ester itself...

I'm curious as to how much blood concentrations affect the rate of hydrolosis of the ester... Meaning, mid-way through the cycle, would hydrolysis speed up since the blood concentration of steroid ester is increased?

BTW Stew... Damnit, when are you going to reply to my DNP thread?

Andy
 
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Stew Meat said:
I don't care if so and so had better results from ED... some also get better results from using sustonon (lol!) and some get hairloss blocked by saw palmetto (lol!).




-Stew

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Saw palmetto extracts for treatment of benign prostatic hyperplasia: a systematic review.

JAMA 1998 Nov 11;280(18):1604-9 (ISSN: 0098-7484)

Wilt TJ; Ishani A; Stark G; MacDonald R; Lau J; Mulrow C [Find other articles with these Authors]
Department of Veterans Affairs Coordinating Center of the Cochrane Collaborative Review Group in Prostatic Diseases and Urologic Malignancies, Minneapolis Veterans Affairs Medical Center, Minn 55417, USA. [email protected].

OBJECTIVE: To conduct a systematic review and, where possible, quantitative meta-analysis of the existing evidence regarding the therapeutic efficacy and safety of the saw palmetto plant extract, Serenoa repens, in men with symptomatic benign prostatic hyperplasia (BPH). DATA SOURCES: Studies were identified through the search of MEDLINE (1966-1997), EMBASE, Phytodok, the Cochrane Library, bibliographies of identified trials and review articles, and contact with relevant authors and drug companies. STUDY SELECTION: Randomized trials were included if participants had symptomatic BPH, the intervention was a preparation of S repens alone or in combination with other phytotherapeutic agents, a control group received placebo or other pharmacological therapies for BPH, and the treatment duration was at least 30 days. DATA EXTRACTION: Two investigators for each article (T.J.W., A.I., G.S., and R.M.) independently extracted key data on design features, subject characteristics, therapy allocation, and outcomes of the studies. DATA SYNTHESIS: A total of 18 randomized controlled trials involving 2939 men met inclusion criteria and were analyzed. Many studies did not report results in a method that permitted meta-analysis. Treatment allocation concealment was adequate in 9 studies; 16 were double-blinded. The mean study duration was 9 weeks (range, 4-48 weeks). As compared with men receiving placebo, men treated with S repens had decreased urinary tract symptom scores (weighted mean difference [WMD], -1.41 points [scale range, 0-19] [95% confidence interval (CI), -2.52 to -0.30] [n = 1 study]), nocturia (WMD, -0.76 times per evening [95% CI, -1.22 to -0.32] [n = 10 studies]), and improvement in self-rating of urinary tract symptoms; risk ratio for improvement (1.72 [95% CI, 1.21-2.44] [n = 6 studies]), and peak urine flow (WMD, 1.93 mL/s [95% CI, 0.72-3.14] [n = 8 studies]). Compared with men receiving finasteride, men treated with S repens had similar improvements in urinary tract symptom scores (WMD, 0.37 International Prostate Symptom Score points [scale range, 0-35] [95% CI, -0.45 to 1.19] [n = 2 studies]) and peak urine flow (WMD, -0.74 mL/s [95% CI, -1.66 to 0.18] [n = 2 studies]). Adverse effects due to S repens were mild and infrequent; erectile dysfunction was more frequent with finasteride (4.9%) than with S repens (1.1%; P<.001). Withdrawal rates in men assigned to placebo, S repens, or finasteride were 7%, 9%, and 11%, respectively. CONCLUSIONS: The existing literature on S repens for treatment of BPH is limited in terms of the short duration of studies and variability in study design, use of phytotherapeutic preparations, and reports of outcomes. However, the evidence suggests that S repens improves urologic symptoms and flow measures. Compared with finasteride, S repens produces similar improvement in urinary tract symptoms and urinary flow and was associated with fewer adverse treatment events. Further research is needed using standardized preparations of S repens to determine its long-term effectiveness and ability to prevent BPH complications.
 
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