You must shop very smart if you only spend 100$ a week.
MESO-Rx
Anabolic Steroids
Thenewera is taking over
- Thread starter Wunderpus
- Start date
ironwill1951
New Member
do you mean some of you guys are just realizing he is an egotist,
probably in the top 5 percent in the world.
probably in the top 5 percent in the world.
I didn't say I was top 5% in the world ... what?
Genetics wise I feel I'm superior in many ways, yes. But I also say that in the most humbling way possible. By no means am I claiming to be the best, just trying to create the best structure I can of myself. The shopping is definitely done smart. Kroger plus and when you come on Wednesday all meat goes on sale because of exproarion dates.
@ironwill1951 what now?
@Eman It is what it is, a public board. If that's how feels then by all means, that's what I am in his eyes. But I know where I stand in my own, so I'll handle where I go from there'.
weighted chinup
Member
I love lamp.
Subb'd.
Subb'd.
weighted chinup
Member
Is GH a possibility here gentlemen?
The reason I ask is because anecdotally the only time I've seen advanced guys add large amounts of stage weight in a single off season, both growth and insulin were being used.
Also, anecdotally, something I've observed is that very few people are capable of adding large amounts of stage weight with just anabolics without blasting for years and years. I understand insulin is involved, I'm wondering if we are throttling size by not including GH as a possible synergy. I get the cost component is always an issue.
The reason I ask is because anecdotally the only time I've seen advanced guys add large amounts of stage weight in a single off season, both growth and insulin were being used.
Also, anecdotally, something I've observed is that very few people are capable of adding large amounts of stage weight with just anabolics without blasting for years and years. I understand insulin is involved, I'm wondering if we are throttling size by not including GH as a possible synergy. I get the cost component is always an issue.
weighted chinup
Member
I've tampered with his omega beam, I've frequently used his methods along with my training as well. I've read some of your writeups as well, and we all kind of use that same style to some degree.
HGH is not a factor in this years showing.
1. Money
2. I'm OCD and haven't studied it for a year straight and don't find myself knowledgeable enough about the compound.. it will definitely be hindered results without it. But that's known already.. I wish I was 100% knoweldable and funds wasn't an issue. But, that's the way it has to roll.
Here are some posts I made on another forum
J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
Affiliation
Erratum in
J Clin Endocrinol Metab. 2004 Feb;89(2):732.
Abstract
Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14-26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P <or= 0.002); 50 mg, 32% (P <or= 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P <or= 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 +/- 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.
PMID 14671195
Clinical Pharmacology
All three drugs (anastrozole, letrozole, and exemestane) are given p.o. as once-daily doses. The recommended daily doses are as follows: for anastrozole, 1 mg; for letrozole, 2.5 mg; and for exemestane, 25 mg. The time needed to reach maximal E2 suppression is 2–4 days for anastrozole and letrozole and 7 days for exemestane (15 , 16) . In the exemestane study, these measurements were done every 7 days, and it is not known whether maximal estrogen suppression after exemestane may have occurred earlier. Anastrozole and exemestane achieve a steady-state drug level by 7 days (17) . In contrast, letrozole has been reported to take 60 days to achieve plasma steady-state levels, which may be reflective of the accumulation that occurs with letrozole over long-term dosing (18) . These data suggested a nonlinear relationship after repeated dose administration of letrozole. The half-lives of anastrozole and exemestane are 41 and 27 h (19 , 20) , respectively, and for letrozole, the half-life has been reported to be up to 4 days (21) . All three AIs effectively reduce E2, E1, and E1S: anastrozole by 81–94% (22 , 23) ; letrozole by 88–98% (23) ; and exemestane by 52–72% (17 , 24) . In one prospective study, a comparative evaluation was carried out to determine the extent of plasma E1, E1S, and E2 suppression after 6 weeks of treatment with either anastrozole or letrozole in postmenopausal women with metastatic disease (23) . There were no significant differences in reduction of plasma E2 by either agent (84.9% and 87.8%, respectively, for anastrozole and letrozole). Anastrozole and letrozole reduced E1 levels by 81.0% and 84.3%, respectively; the extent of this suppression was significantly greater in the letrozole group (P = 0.019). Letrozole reduced plasma E1S levels significantly more than anastrozole (98% versus 93.5%, P = 0.019). The clinical significance of this additional suppression of estrogen by letrozole remains to be defined. There are no comparative studies evaluating exemestane in relation to other agents, but in individual studies, E2 levels were suppressed by 65% with exemestane (17) .
About the suicidal properties:
Estrogen rebound does NOT exist so why are suicdal properties any better than competitive binding inhibition? E2 will always return to baseline whenever you stop using an AI regardless of its its adex or asin. I challenge anyone to post bloodwork showing significantly higher E2 levels after cessation of adex or letro use and/or clinical manifestations of such levels.
The AIs are classified into two types: (a) type I, suicidal or noncompetitive inhibitors; and (b) type II, competitive inhibitors (13 , 14) . Type I inhibitors are steroidal compounds, and type II inhibitors are nonsteroidal drugs. Both types mimic normal substrates (androgens), competing with the substrate for access to the binding site on the enzyme. After initial binding, the next step differs for the two types: once a noncompetitive inhibitor has bound, the enzyme initiates its typical sequence of hydroxylation, but hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Enzyme activity is thus permanently blocked; even if all unattached inhibitor is removed, enzyme activity can only be restored by new enzyme synthesis. Competitive inhibitors reversibly bind to the active enzyme site, and either no enzyme activity is triggered, or it is without effect. The inhibitor can disassociate from the binding site, allowing renewed competition between the inhibitor and the substrate for binding to the site. As a result, the effectiveness of competitive inhibitors depends on the relative concentrations and affinities of the inhibitor and the substrate. Continued activity requires constant presence of inhibitor.
To compete for binding to the active site, both competitive and noncompetitive inhibitors must necessarily share important structural features with the endogenous substrate. Noncompetitive inhibitors must also share structural features with androgens, allowing them to interact with the catalytic residual on the enzyme protein. This renders them inherently selective. By contrast, most competitive inhibitors interact with the heme iron, a common feature of all cytochrome P450 enzymes. Some may also bind to the highly conserved oxygen binding site in addition to the substrate binding site. Thus, unless the specificity of a competitive inhibitor is reinforced through other structural features, it may block the activity of a variety of cytochrome P450 enzymes, as does aminoglutethimide.
Both anastrozole and letrozole are type II nonsteroidal AIs, whereas exemestane has a steroidal structure and is classified as a type I AI, also known as an aromatase inactivator because it irreversibly binds with and permanently inactivates the enzyme. The clinical relevance of these differences in mechanism of action, if any, remains to be established.
Look at how even with aromasin estrogen levels come back quickly after cessation.
J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
Pharmacokinetics and dose finding of a potent aromatase inhibitor, aromasin (exemestane), in young males.[/QUOTE]
Estrogen rebound does NOT exist so why are suicdal properties any better than competitive binding inhibition? E2 will always return to baseline whenever you stop using an AI regardless of its its adex or asin. I challenge anyone to post bloodwork showing significantly higher E2 levels after cessation of adex or letro use and/or clinical manifestations of such levels.
The AIs are classified into two types: (a) type I, suicidal or noncompetitive inhibitors; and (b) type II, competitive inhibitors (13 , 14) . Type I inhibitors are steroidal compounds, and type II inhibitors are nonsteroidal drugs. Both types mimic normal substrates (androgens), competing with the substrate for access to the binding site on the enzyme. After initial binding, the next step differs for the two types: once a noncompetitive inhibitor has bound, the enzyme initiates its typical sequence of hydroxylation, but hydroxylation produces an unbreakable covalent bond between the inhibitor and the enzyme protein. Enzyme activity is thus permanently blocked; even if all unattached inhibitor is removed, enzyme activity can only be restored by new enzyme synthesis. Competitive inhibitors reversibly bind to the active enzyme site, and either no enzyme activity is triggered, or it is without effect. The inhibitor can disassociate from the binding site, allowing renewed competition between the inhibitor and the substrate for binding to the site. As a result, the effectiveness of competitive inhibitors depends on the relative concentrations and affinities of the inhibitor and the substrate. Continued activity requires constant presence of inhibitor.
To compete for binding to the active site, both competitive and noncompetitive inhibitors must necessarily share important structural features with the endogenous substrate. Noncompetitive inhibitors must also share structural features with androgens, allowing them to interact with the catalytic residual on the enzyme protein. This renders them inherently selective. By contrast, most competitive inhibitors interact with the heme iron, a common feature of all cytochrome P450 enzymes. Some may also bind to the highly conserved oxygen binding site in addition to the substrate binding site. Thus, unless the specificity of a competitive inhibitor is reinforced through other structural features, it may block the activity of a variety of cytochrome P450 enzymes, as does aminoglutethimide.
Both anastrozole and letrozole are type II nonsteroidal AIs, whereas exemestane has a steroidal structure and is classified as a type I AI, also known as an aromatase inactivator because it irreversibly binds with and permanently inactivates the enzyme. The clinical relevance of these differences in mechanism of action, if any, remains to be established.
Look at how even with aromasin estrogen levels come back quickly after cessation.
J Clin Endocrinol Metab. 2003 Dec;88(12):5951-6.
Pharmacokinetics and dose finding of a potent aromatase inhibitor, aromasin (exemestane), in young males.[/QUOTE]
If someone told me my arms look small that would be some serious motivation to put in work
D-max
Member
Several people have told you you act like a douche bag here but I've yet to see you put in serious work to change that.
We don't put up with that shit here. This is a community and this thread is your house, we don't just turn out eyes when someone comes in and shits in your house. He broke an unwritten rule.
@Just Fish where's your pictures?
My avi
Thats me after lifting 6 months natural. Fresh off not being able to lift for 3 years.
D-max
Member
Careful calling him out. He'll start a flurry of pm's calling you lots of naughty names. I just got another. Going to go cry again. Douche bag hurt my feelers.
Anyways.. hope everyone's day is off to a good start. Decided to let breakfast please me.
6 slices of bread (14g carbs/2 slices) .5g fat
2 whole eggs
Cinnamon
....okay I made French toast...sugar free syrup though..only 5g carb
+6 egg whites with .5cup light soymilk for a drink
Today I'm going to track my training weight for weight. I'll post below.
Chest shoulders. If anyone would like the workout for today let me know and we can do it together.
6 slices of bread (14g carbs/2 slices) .5g fat
2 whole eggs
Cinnamon
....okay I made French toast...sugar free syrup though..only 5g carb
+6 egg whites with .5cup light soymilk for a drink
Today I'm going to track my training weight for weight. I'll post below.
Chest shoulders. If anyone would like the workout for today let me know and we can do it together.
I dont condone statements like these in some ones log.
There is constructive criticism then theres this^^^
Doesnt really promote the kind of support for some ones journey in this section
Agreed
Thats why im out. I cant really get behind any of this
@Thenewera
Enjoy your journey
ironwill1951
New Member
I hope I wasn't taken wrong I think @Thenewera has a huge ego bigger than most,
I don't see that as a bad thing its the same as me saying he is very confident.
hell anybody that's good at what they do has a big ego . the two go together.
I don't see that as a bad thing its the same as me saying he is very confident.
hell anybody that's good at what they do has a big ego . the two go together.
While you youngins blast away , Im gonna keep pacing myself for the long run on my lil 600-750mg/wk blast of test . I still get results off these "small" amounts , why chance it with mega-doses ? (then I will have to commit to larger doses forever) too poor for that...~Ogh
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