The Dbol bridge... By Fonz... and, I want to hear your bridge experience...

[psychedout]

This is an old post By Fonz... but a very good one.
-------------------------------------------------

I've been reading some of the posts regarding this
bridge and some of them are truly from left-field.
First of, this is a BRIDGE. OK? a B-R-I-D-G-E.

Your LH function and Test levels are supposed
to RECOVER.

Ok, now having said that.
Here's the pharmo-kinetics behind Methandrostenelone,
brand name Dianabol.

10mg taken at once will increase your average testosterone level by 5 times and decrease your endogeneous cosrtisone
by 50-70%.

The reason why dianabol is a good choice for a bridge is that
its VERY anti-catabolic. It also dopaminergic. Giving you the
benefits of increased CNS strength modulation by
its androgenic mode of action.
Androgens, in case you don't know, increase neuro-muscular
function, thus STRENGTH.

OK. Now, lets delve into the metabolic chemistry behind
dianabol's choice as a bridging agent.

When are testosterone levels highest?

Answer: In the AM, thats when.

Your body releases a tesosterone spike in the morning.
This is when tesosterone levels are highest.

When are Insulin levels lowest?

Answer: In the AM thats when.

Low insulin levels=increased protein used as fuel.
(Also fat, but protein is also being converted
to glucose via glucogenesis)

OK, here is where dball's short half-life works for us
(Its 3.2-4.5 hrs btw)

Lets take Subject X.

He's in bridging mode.
He has just woken up.
The body is about to release tesosterone, thus
creating a spike.
His insulin levels are low.
His LH and test levels are very low.



He pops 10mgs of dianabol.

Here is where things get interesting.

The 10mgs of dianabol will cause a testosterone
spike WHICH COINCIDES WITH the testosterone
released ENDOGENEOUSLY in the AM by the testes.

The body will be partially fooled.
It will not entirely detect the increased levels of testosterone
(above the normal test sipke), thus LH function WILL
REMAIN only partially(Very little actually) suppressed.

In other words, he is "piggy-backing" an extra dose of testosterone on top of the endogeneously reduced one,
thus creating an "inflated" test spike.

Henceforth, LH levels WILL BE ALLOWED TO SLOWLY
RECOVER over time.
Also, dballs anti-catabolic effect will help curb protein-loss
in the morning from low insulogenic levels.

HOWEVER, and here is where almost all of you go wrong.

You CANNOT GO PAST 10mg of dianabol in the AM
for this bridge to work!!!!

Why? Because of the blood levels of dianabol you would generate.

10mg in the AM will be broken down to 5mg in about 4 hrs
(Probably less)

5mg of dianabol, is not enough to cause another rise
in testosterone levels after the precceeding one. Thus,
LH function is allowed to up-regulate.

Anything more(Say 20mgs), will cause a SEDCONDARY
testosterone spike which WILL inhibit LH function further,
thus not allowing LH function to recover.

Oh yeah...100mgs? ROTLMFAO!! Fat chance.

The difference between 20mgs and 10mgs means the difference
between allowing LH to recover slowly and not allowing it to.

So, here's the scenario summed up:

Beginning: LOW LH and test.

Adding the 10mgs dball.

LH is allowed to SLOWLY RECOVER over time as
testosterone levels are kept at a level which
will not cause muscle-loss. Also, dball's anti-catabolic effects
will reduce protein degradation.(Via cortisone
reduction)

This is what i call a double positive. You have managed to
INCREASE anabolism(Test levels) and DECREASE
catabolism(cortisone), during a bridge to boot!!

The bridge should last 8 weeks, NO LESS.
I also have to say, that it WILL NOT restore
complete LH function. It'll get you 80-90%
of the way there but the only way you're going
to get your full LH function back is if you go OFF
completely.
Anavar WILL NOT restore LH completely either btw.
(In case anybody is wondering.)
The difference is that with anavar you can take it
throughout the day and with dball it HAS TO BE
once in the AM.

Hope that clears the air.

---------------------------------------------
And at last I would like to here how your experience went with the dbol bridge?

Cheers.

 

[THEEGAME2544]

So does this mean that I can pop my clomid and nolva for PCT and still become just about fully restored while having the dbol in the AM to help with catabolism after coming off a long cycle?

 

[Ulter]

I have used the dbol bridge many times over the years. It works great.

 

[Big Moose]

So does this mean that I can pop my clomid and nolva for PCT and still become just about fully restored while having the dbol in the AM to help with catabolism after coming off a long cycle?

Interested in this as well. Nolva/HCG and the a.m. d-bol.

 

[psychedout]

I think it means you can use clomid/nolva in the am to help recovery. Fonz would know.

Notice you only 80-90% recover though.

Bump.

 

[needsize]

I had different results with the dbol bridge, I found it didnt help keep much size and I felt shut down all the way through, I have much better results with var

 

[majutsu]

What's really interesting about dbol/winny/anadrol etc is their non-anabolic receptor action. They do not compete well with testosterone for testosterone receptors in the muscle, whereas, of course, anabolics like tren/deca/primo/eq/&test all compete for the testosterone receptors in the muscle, listed in order of strength. So how does winny/dbol/etc work? Well new research shows (like said above) that these pharmaceuticals compete for the glucorticoid receptors. They are really anti-catabolic therefore (anti-wasting), and not truly anabolic. But when you work out hard, there is a big spike in cortisol, which negates any growth you might create. So these non-AR drugs as they're called lower cortisol a great deal, as noted, and therefore certainly lead to muscle growth. The old-school approach of mixing an anabolic (like deca or primo) with a non-AR medicine (like dbol or winny), using both pro-anabolic (promoting protein synthesis) and anti-cabolic (preventing cortisol buildup and wasting) means at the same time, therefore makes alot of sense. Needsize, I would imagine any of the anti-cortisol drugs would work as a bridge, but maybe with your mass compared to Fonz, you might need a higher dose like 15 or 20. But if that turned out not to work, though, I guess it's possible that you might need anavar's anabolic properties (without suppression at low doses) coupled with anti-catabolic properties. Maybe at a certain mass, dbol alone doesn't bridge, but maybe primo light+dbol or anavar is required. I don't know, but it's interesting stuff. I find dbol makes a great bridge at 10 for my stats. Below is the study I reworded into regular words. The original abstract is below. This lab has alot of papers on this. Another one may indicate how growth hormone is "cutting" through means of glucocorticoid receptors.

Endocrinology. 1994 Mar;134(3):1401-8. Related Articles, Links


Stanozolol and danazol, unlike natural androgens, interact with the low affinity glucocorticoid-binding sites from male rat liver microsomes.

Fernandez L, Chirino R, Boada LD, Navarro D, Cabrera N, del Rio I, Diaz-Chico BN.

Departamento de Endocrinologia Celular, Facultad de Ciencias Medicas, Universidad de Las Palmas de Gran Canaria, Canary Islands, Spain.

Some 17 alpha-alkylated androgens used as anabolic agents, such as stanozolol (ST) and danazol (DA), have specific effects on the liver that are not exerted by testosterone. This gives rise to the possibility that a steroid-binding protein, other than the androgen receptor, could modulate the intracellular actions of these agents. Male rat liver microsomes contain a homogeneous population of [3H]dexamethasone ([3H]DEX)-binding sites which we have denominated low affinity glucocorticoid-binding sites (LAGS). Because glucocorticoids, progestagens, and the synthetic estrogen ethynyl estradiol compete with [3H]DEX for binding to the LAGS, we aimed to study the possible interactions between androgens and the LAGS. To investigate whether several androgens had the capability of interacting with the LAGS, we performed competition experiments. The LAGS had no affinity for testosterone or methyltrienolone (R1881). However, some 17 alpha-alkylated androgens (DA (IC50, 116 nM) > ST >> fluoxymesterone > mestaline > methandriol >> methandrostenolone > methyltestosterone) were able to compete with [3H]DEX binding to liver microsomes. ST and DA were potent inhibitors of [3H]DEX binding to liver microsomes. They decreased both the affinity and the number of [3H]DEX-binding sites, increased the dissociation rate of [3H]DEX from the LAGS, and provoked a time- and dose-dependent inactivation of the [3H]DEX-binding site. These results strongly suggest that ST and DA exert a negative allosteric modulation on [3H]DEX binding to the LAGS. The in vivo administration of ST (but not other androgens) to male rats provoked a time- and dose-dependent decrease in the LAGS level. Full recovery of the LAGS concentration required at least 8 h and was blocked by protein synthesis inhibitors. Such results suggest that ST irreversibly inactivates the [3H]DEX-binding site in vivo as it does in vitro. Taken together, these observations are indicative of an irreversible interaction between some 17 alpha-alkylated androgens and the LAGS both in vitro and in vivo and suggest that ST may be an important pharmacological tool that can be used in the elucidation of the molecular structure of the LAGS. These results also mean that the LAGS are a steroid-binding entity able to distinguish between natural androgens and 17 alpha-alkylated testosterone derivatives used as anabolic agents.

 

[The Terminator]

I found the dbol bridge was good for keeping muscle gains, but poor for sex drive...Not worth the trade off imo...

 

[THEEGAME2544]

Bump for an answer to my above post.

And,

also whether dbol being 17aa will have that much effect on liver values at 10mg in the AM?

 

[str8cubano]

I have used the dbol bridge many times over the years. It works great.

Ulter, i thought you didn't come off test all year round?