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The Dbol Main cycle ramp-off explained in detail: Article


Fonz
 Fonz
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Please try to keep this flame free. I have taken great pains to explain my(and others) reasoning in a clear and concise fashion.

The Dbol Main cycle ramp-off explained in detail: Article

The original Study:

Acta Endocrinol (Copenh) 1976 Dec;83(4):856-64 Related Articles, Links

Effect of an anabolic steroid (metandienon) on plasma LH-FSH, and testosterone and on the response to intravenous administration of LRH.

Holma P, Adlercreutz H.

Plasma levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as well as the response of LH and FSH to the intravenous administration of 100 mug of luteinizing hormone releasing hormone (LRH) were measured in 16 well-trained athletes (mean age 30 years) before and after 2 months of daily oral intake of 15 mg of metandienon, and anabolic steroid (Anabolin, 17 alpha-methyl-17beta-hydroxy-1,4-androstadien-3-one, Medica, Finland). All athletes continued to train regularly, just as they had done for several years. During administration of metandienon the mean plasma testosterone level fell 69%, from 29.4 +/- 11.6 nmol/1 to 9.1 +/- 7.5 nmol/1. The mean plasma levels of LH and FSH also fell significantly (P less than 0.001 and P less than 0.01, respectively), both about 50%. Because LH and FSH levels were low after administration of the steroid the maximum stimulation values after LRH administration were also lower than pre-treatment values although the mean increments did not differ significantly before and after administration of the anabolic steroid. However, after treatment, the FSH response curve had a biphasic pattern in most subjects, with peaks at 10 to 20 and 50 to 60 min after the iv injection of LRH. Administration of LRH after the treatment period had no effect on FSH secretion in two subjects and no effect on LH secretion in one. Our results show that administration of an anabolic steroid causes a pronounced lowering of plasma levels of testosterone, LH and FSH but causes no gross alteration in the response of LH secretion to stimulation by LRH. The reason for the biphasic response pattern of FSH to LRH administration in most subjects is not known.

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Ok, I'm making this flame-free so that no flame fests occurr and people get the right information, not all jumbled. It has actually been improved upon somewhat with the advent of some newer compounds and with the help of AF Vets.

This a more streamlined version, that should work for almost everybody.(Even those who almost always crash):

First, it was decided that the last 4 weeks, of the 8 week ramp-off should be 5mg instead of 10mg, as your HPTA should be recovered by some degree by that time.

The 10mg time/correlation:

Now, for 10mg.

10mg ------- 5mg --------- 2.5mg --------1.25mg ---------0.625mg

Half-lives = 3.4 * 4 = 13.6hrs(to 1mg)

13.6/16.0 = 85% or 0.85(As compared to 15mg)

Test decrease + LH Decrease

Normal(15mg) = 69% 50%
10mg = 58.7% 42.5%

Thats w/o Arimidex

W/ arimidex(Increases Test by an average of 58% in controlled trails, and reduces estrogen by about 90%):

10mg becomes: 58.7*(1-0.58)= 24.65% Test decrease
LH is reduction is reduced from 50% to 42.5%

(These numbers do not include the addition of clomid and HCG)

This is 5mg time/concentration correlation:

5mg ------- 2.5mg --------1.25mg ------ 0.625mg

Half-lives = 2.4 * 4 = 9.6hrs(to 1mg)

(Compared to 10mg)

9.6/13.6 = 70.59% or 0.7059

Test decrease + LH Decrease

Normal(15mg) = 69% 50%
10mg = 58.7%(-10.3%) 42.5%(-7.5%)
5mg = 41.43%(-27.57%) 30%(-12.5%)

Thats w/o arimidex

W/ arimidex:

5mg becomes: 41.43*(1-0.58)= 17.4% Test decrease
And LH, decreases to only a 30% decrease

(These numbers do not include the addition of Clomid or HCG)

Finalizing(W/arimidex included):

Testosterone decrease + LH Decrease

15mg == 69% 50%(Study)

10mg == 24.65% 42.5%(This for you weeks 1-4)

5mg == 17.4% 30%(This for you weeks 5-8)

(These numbers are in comparison to the 15mg dosage and do not include the addition of Clomid or HCG or other compounds which both stimulate LH, FSH and endo test)

End(Finalized Ramp-off):

(6-8 weeks) before end of Main cycle: Start 25mg proviron

End Main Cycle.

AM Dbol off-ramp: 8 weeks

#1.Start ramp-off at 10mg Dbol in the AM upon
waking up.(Weeks 1-4) and 5mgs(Weeks 5-8)
#2 Make damn sure you take the 10mg Dbol(Weeks 1-4) at the
same damn time every day. As soon as you wake up. This
wake up time (if 8 or 9 or 10 AM) must be used for the rest of
the ramp-off(8 weeks)(Circadian Rhythm is VERY important to
the success of the ramp-off) Same with the 5mg dose(Weeks
5-8).
#3 Proviron at 25mgs/day(LH booster)(Weeks 1-8)
#4 Arimidex at 1mg ED or more.(2mg is as high as I would go).
(Also on weeks 1-8)
#5 HCG at 5000IU�s 2X/week on Weeks 5,6,7,8
(Endo Test Booster)
#6 Clomid at 300mgs Day 1, and then 100mgs/day from then on
until the end of the bridge(LH and FSH Booster)

Weeks 1-4: Are designed to reduce androgen levels(10mg Dbol here) and stimulate the HPTA to start its own endo test production, and increase FSH, and LH levels.

10mg == 24.65% 42.5%(This for you weeks 1-4)

Your HPTA will be pretty much zero at the beginning off the ramp-off, and a combination of compounds that only decrease normal test levels by 24.65% and substances that increase LH and FSH and stimulate endo test(Clomid and Proviron) will let your HPTA recover by some margin.

Weeks 5-8: Are designed to reduce androgen levels even further(Only 5mg Dbol here), due to the fact that they are not needed because your HPTA has partially recovered in Weeks 1-4.

5mg == 17.4% 30%(This for you weeks 5-8)

With the reduction of androgens from 10mg to 5mg, you have changed the Test decrease to only 17.4% and let LH reduction only be 30%. Again, you will be on Clomid and Proviron, and these two will help you boost LH levels and increase test levels further. But now comes the interesting part. The introduction of HCG. HCG is probably the best booster of endo test at your disposal for short periods of time, via the stimulation of the Leydig Cells in the testes. HCG at the specified dosage will boost endo test levels back to the normal pre-main cycle range.
(Remember that 5mg Dbol only causes a 17.4% decrease in Test).
HCG should help nullify that.

And after those 8 weeks of the ramp-off, you come off.
Both Test and LH levels should be within the normal range, and you will not crash or suffer muscle loss like pretty much all post-cycle recovery methods.

Special thanks goes to the guys who helped me put all this into
a clear and concise article. You know who you are.

NEW:

As an addition: Androgel might be of definate use in Weeks 5-8 as it roughly doubles Test levels, w/o any decrease in LH. Which will further boost ending ramp-off test levels. If you have the time, this preparation shows great promise for further enhancing the ramp-off.

References:

(Thanks to Mr. Nobody and got Wood)

1. Swerdloff, RS, and Wang, C., et al., Long-term pharmacokinetics of transdermal testosterone gel in hypogonadal men., J Clin Endocrinol Metab. 2000 Dec;85(12):4500-10.

The intend of agel in the recovery program is for libido purposes, and may delay overall recovery a bit. However, its not just about fast recovery but achieving homeostasis in a managable manner, without slipping into depression and muscle loss while you wait for endo test to come back. The same goes for morning dbol.
As everyone knows already, only time will recover you completely.

from Gotwood:

testo gel lowered LH but not too much

Got Wood? note : these men ranged from 22-65. Testo enanthate (inj) lowered LH too much - to subnormal values. Testo gel lowered LH to normal, but not beyond to a subnormal range. This is evidence that the testo gel may not lower the LH too much, thereby inhibiting recovery. however again these are hypogonadal men.
============================
J Clin Endocrinol Metab 1999 Oct;84(10):3469-78

Pharmacokinetics, efficacy, and safety of a permeation-enhanced testosterone transdermal system in comparison with bi-weekly injections of Testosterone Enanthate for the treatment of hypogonadal men.

Dobs AS, Meikle AW, Arver S, Sanders SW, Caramelli KE, Mazer NA.

Johns Hopkins Medical Center, Baltimore, Maryland 21287, USA. [email protected]

The pharmacokinetics, efficacy, and safety of the Androderm testosterone (T) transdermal system (TTD) and intramuscular T enanthate injections (i.m.) for the treatment of male hypogonadism were compared in a 24-week multicenter, randomized, parallel-group study. Sixty-six adult hypogonadal men (22-65 years of age) were withdrawn from prior i.m. treatment for 4-6 weeks and then randomly assigned to treatment with TTD (two 2.5-mg systems applied nightly) or i.m. (200 mg injected every 2 weeks); there were 33 patients per group. Twenty-six patients in the TTD group and 32 in the i.m. group completed the study. TTD treatment produced circadian variations in the levels of total T, bioavailable T, dihydrotestosterone, and estradiol within the normal physiological ranges. i.m. treatment produced supraphysiological levels of T, bioavailable T, and estradiol (but not dihydrotestosterone) for several days after each injection. Mean morning sex hormone levels were within the normal range in greater proportions of TTD patients (range, 77-100%) than i.m. patients (range, 19-84%). Both treatments normalized LH levels in approximately 50% of patients with primary hypogonadism; however, LH levels were suppressed to the subnormal range in 31% of i.m. patients vs. 0% of TTD patients. Both treatments maintained sexual function (assessed by questionnaire and Rigiscan) and mood (Beck Depression Inventory) at the prior treatment levels. Prostate-specific antigen levels, prostate volumes, and lipid and serum chemistry parameters were comparable in both treatment groups. Transient skin irritation from the patches was reported by 60% of the TTD patients, but caused only three patients (9%) to discontinue treatment. i.m. treatment produced local reactions in 33% of patients and was associated with significantly more abnormal hematocrit elevations (43.8% of patients) compared with TTD treatment (15.4% of patients). Gynecomastia resolved more frequently during TTD treatment (4 of 10 patients) than with i.m. treatment (1 of 9 patients). Although both treatments seem to be efficacious for replacing T in hypogonadal men, the more physiological sex hormone levels and profiles associated with TTD may offer possible advantages over i.m. in minimizing excessive stimulation of erythropoiesis, preventing/ameliorating gynecomastia, and not over-suppressing gonadotropins.

Hope some of you guys like it. If you guys want to try it be my guest. If you disagree w/ the article then simply don't try it. Pretty simple really.

Fonz

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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Blade
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I have some reservations about getting into this...but alright.

You're not accounting for the fact that you are coming off a cycle of AAS where full inhibition of the HPTA has been the situation for many, many weeks. Extrapolating from studies where a certain %age of suppression is observed from a baseline situation don't transfer well to the post-cycle situation. You're just delaying recovery, period. Androgen levels (and estrogen levels) need to approach a lower threshold for HPTA recovery to initiate. Your theory is based on the premise that you know what this lower threshold is.

Whether you can achieve some % of baseline T by artificial means (Androgel, HCG etc) is irrelevant, all your bloodtests would have to account for this fact, i.e. what is endogenously driven and what is exogenously driven? You should also be more concerned about what will happen once you go off all of these ancillaries, i.e. that your endocrinal system is able to maintain baseline hormone levels. Were these bloodtests you speak of performed e.g. 1-2 weeks upon cessation of all drugs?

You are essentially saying that the old practice of "tapering" is good after all, then - even though it has been abandoned years ago?


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Fonz
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Posted by: Blade
I have some reservations about getting into this...but alright.

You're not accounting for the fact that you are coming off a cycle of AAS where full inhibition of the HPTA has been the situation for many, many weeks. Extrapolating from studies where a certain %age of suppression is observed from a baseline situation don't transfer well to the post-cycle situation. You're just delaying recovery, period. Androgen levels (and estrogen levels) need to approach a lower threshold for HPTA recovery to initiate. Your theory is based on the premise that you know what this lower threshold is.

Whether you can achieve some % of baseline T by artificial means (Androgel, HCG etc) is irrelevant, all your bloodtests would have to account for this fact, i.e. what is endogenously driven and what is exogenously driven? You should also be more concerned about what will happen once you go off all of these ancillaries, i.e. that your endocrinal system is able to maintain baseline hormone levels. Were these bloodtests you speak of performed e.g. 1-2 weeks upon cessation of all drugs?

You are essentially saying that the old practice of "tapering" is good after all, then - even though it has been abandoned years ago?

No. Old tapering always used injectables.

And thats why it never worked.

The half-life was just too long.

With Dbol, you have a short half-life and thats what makes the ramp-off possible.

It would be impossible, with lets say winstrol.

Fonz

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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omnibus
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quote:


With Dbol, you have a short half-life and thats what makes the ramp-off possible.


How long will the d-bol and it's metabolites sit on the receptor once they are latched on to it?Won't the activated receptors cause supression even if blood levels are low?

I think Nandi has said androgens act directly on the hypothalamus,shutting you down.


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Blade
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Yes, and this is what happened in the study where 2.5mg of Anavar led to HPTA suppression. Although the half-life is longer (probably twice that of Dbol), the dosage used was 1/4th of this proposed 10mg Dbol strategy. And with an oral which doesn't aromatize.

You can't say that the Anavar study is irrelevant since we're talking about Dbol either, when you consider those two facts (dosage and aromatization).

I'm still curious about the details of those blood-tests, though.


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Bobo
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Posted by: Blade
Yes, and this is what happened in the study where 2.5mg of Anavar led to HPTA suppression. Although the half-life is longer (probably twice that of Dbol), the dosage used was 1/4th of this proposed 10mg Dbol strategy. And with an oral which doesn't aromatize.

You can't say that the Anavar study is irrelevant since we're talking about Dbol either, when you consider those two facts (dosage and aromatization).

Thats what we've been trying to say. D-bol aromtizes into 17-methyl E2 which half-life is 2 days. This in itself is suppressive. Also the HPTA is suppressed through different pathways with estrogen. Arimidex will not elleviate this and will still keep you suppressed to an extent.


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Bobo
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Aromatase inhibition in the human male reveals a hypothalamic site of estrogen feedback.

Hayes FJ, Seminara SB, Decruz S, Boepple PA, Crowley WF Jr.

Department of Medicine and National Center for Infertility Research, Massachusetts General Hospital, Boston 02114, USA. [email protected]

The preponderance of evidence states that, in adult men, estradiol (E2) inhibits LH secretion by decreasing pulse amplitude and responsiveness to GnRH consistent with a pituitary site of action. However, this conclusion is based on studies that employed pharmacologic doses of sex steroids, used nonselective aromatase inhibitors, and/or were performed in normal (NL) men, a model in which endogenous counterregulatory adaptations to physiologic perturbations confound interpretation of the results. In addition, studies in which estrogen antagonists were administered to NL men demonstrated an increase in LH pulse frequency, suggesting a potential additional hypothalamic site of E2 feedback. To reconcile these conflicting data, we used a selective aromatase inhibitor, anastrozole, to examine the impact of E2 suppression on the hypothalamic-pituitary axis in the male. Parallel studies of NL men and men with idiopathic hypogonadotropic hypogonadism (IHH), whose pituitary-gonadal axis had been normalized with long-term GnRH therapy, were performed to permit precise localization of the site of E2 feedback. In this so-called tandem model, a hypothalamic site of action of sex steroids can thus be inferred whenever there is a difference in the gonadotropin responses of NL and IHH men to alterations in their sex steroid milieu. A selective GnRH antagonist was also used to provide a semiquantitative estimate of endogenous GnRH secretion before and after E2 suppression. Fourteen NL men and seven IHH men were studied. In Exp 1, nine NL and seven IHH men received Anastrozole(10 mg/day po x 7 days). Blood samples were drawn daily between 0800 and 1000 h in the NL men and immediately before a GnRH bolus dose in the IHH men. In Exp 2, blood was drawn (every 10 min x 12 h) from nine NL men at baseline and on day 7 of anastrozole. In a subset of five NL men, 5 microg/kg of the Nal-Glu GnRH antagonist was administered on completion of frequent blood sampling, then sampling continued every 20 min for a further 8 h. Anastrozole suppressed E2 equivalently in the NL (136 +/- 10 to 52 +/-2 pmol/L, P < 0.005) and IHH men (118 +/- 23 to 60 +/- 5 pmol/L, P < 0.005). Testosterone levels rose significantly (P < 0.005), with a mean increase of 53 +/- 6% in NL vs. 56 +/- 7% in IHH men. Despite these similar changes in sex steroids, the increase in gonadotropins was greater in NL than in IHH men (100 +/- 9 vs. 58 +/- 6% for LH, P = 0.07; and 85 +/- 6 vs. 41 +/- 4% for FSH, P < 0.002). Frequent sampling studies in the NL men demonstrated that this rise in mean LH levels, after aromatase blockade, reflected an increase in both LH pulse frequency (10.2 +/- 0.9 to 14.0 +/- 1.0 pulses/24 h, P < 0.05) and pulse amplitude (5.7 +/- 0.7 to 8.4 +/- 0.7 IU/L, P < 0.001). Percent LH inhibition after acute GnRH receptor blockade was similar at baseline and after E2 suppression (69.2 +/- 2.4 vs. 70 +/- 1.9%), suggesting that there was no change in the quantity of endogenous GnRH secreted. From these data, we conclude that in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease responsiveness to GnRH


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Fonz
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Posted by: Blade
Yes, and this is what happened in the study where 2.5mg of Anavar led to HPTA suppression. Although the half-life is longer (probably twice that of Dbol), the dosage used was 1/4th of this proposed 10mg Dbol strategy. And with an oral which doesn't aromatize.

You can't say that the Anavar study is irrelevant since we're talking about Dbol either, when you consider those two facts (dosage and aromatization).

I'm still curious about the details of those blood-tests, though.

Approximately 9 hours.(The half-life of oxandrolone)

Fonz

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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macro
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while not commenting on the positives or negative of bridging...

anavar is bi-phasic.. it has a half life of apprx 90min... it primary metabolite.. has a half life of apprx 11hrs

femara is probably a better choice with dbol

it is strongly aromatic, why exactly?? though perhaps related to liver impact..

agree with bobo, its E2 metabolite is VERY potent.. it may be that even small amounts of conversion leaves a potent estrogenic effect..

as to why anavar is suppressive ??? it should not be, if it is non aromatic and binds solely to the AR...


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Nandi12
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quote:


as to why anavar is suppressive ??? it should not be, if it is non aromatic and binds solely to the AR...


Androgens that don't aromatize are thought to be suppressive via two mechanisms. First, they act directly on the hypothalamus to alter GnRH pulse frequency (1). This altered signal from the brain to the pituitary interferes with LH secretion.

Second, nonaromatizing androgens are thought to act directly on the pituitary to interfere with the transcription of the gene for LH production. So this reduces the amount of LH produced by the pituitary (2)

(1) Acta Endocrinol (Copenh) 1983 Apr;102(4):499-504

Androgenic and oestrogenic steroid participation in feedback control of luteinizing hormone secretion in male sheep.

D'Occhio MJ, Schanbacher BD, Kinder JE.

(2) Mol Endocrinol 2001 Nov;15(11):1906-17

Androgen suppression of GnRH-stimulated rat LHbeta gene transcription occurs through Sp1 sites in the distal GnRH-responsive promoter region.

Curtin D, Jenkins S, Farmer N, Anderson AC, Haisenleder DJ, Rissman E, Wilson EM, Shupnik MA.


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macro
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those are study findings are good "guesses" but thats really all they are

will have to look at the second study..

but the fact that the first is from 83 (are there any subsequent with similar?) seems odd and most recent study seem to find solely E related suppression...


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Nandi12
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Well, Einstein published his theory of special relativity in 1905 and it has never been refuted...

I just pulled this one on DHT out of my files.

"Since DHT is a nonaromatizable androgen, and neither DHT nor DHT-hp binds readily to the estrogen receptor, suppression of LH and FSH secretion by this drug probably occurs via an androgen-dependent mechanism" (1)

I've reproduced figures from this DHT study as well showing drops in T, LH, and FSH.

http://jcem.endojournals.org/cgi/content/full/86/9/4078

Suppression from non aromatizing steroids is real.

One can always say, and any responsible author would, that the results of any study "suggest" or "provide evidence" for a theory, rather than prove something to be true. Nobody likes to eat crow.

(1) J Clin Endocrinol Metab 1987 Mar;64(3):557-62

Dihydrotestosterone heptanoate: synthesis, pharmacokinetics, and effects on hypothalamic-pituitary-testicular function.

Keenan BS, Eberle AJ, Sparrow JT, Greger NG, Panko WB


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Fonz
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Posted by: Nandi12
Well, Einstein published his theory of special relativity in 1905 and it has never been refuted...

Bad comparison.

You're comparing a theory that encompassed INVENTING three-dimensional space geometry + waiting for an eclipse.

Yes, an eclipse. It was not until the eclipse experiment that his theories was FINALIZED.

This is a simple E suppression study.

Lets not get patronizing OK?

Fonz

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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Nandi12
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The eclipse was the first experimental verification of General Relativity, not Special Relativity.

My point is 1983 is not that long ago.


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Fonz
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Posted by: Nandi12
The eclipse was the first experimental verification of General Relativity, not Special Relativity.

My point is 1983 is not that long ago.

Special is simplistic. General is what made him famous in physics circles. People just comprehend special better b/c its simple.

But OK. I do get your point.

Fonz

If I want to add flavor to my cooking. . . . . . . I just burn it

There is NO such thing as over training just under EATING. ~ Trey Brewer


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