MESSAGE TO EPHEDRINE USERS!!!!!!!

[The Coach]

Nuerotoxin, you are so right. Im not saying drugs do not have a place, they surely do, but most doctors rely on them so much, not only because they get kickbacks but most don't know how to treat without them. I have NUMEROUS people to either cut back or eliminate meds but from weight reduction and proper food combinations. They got off the meds with their doctors approval of course.

[I ETA PI]

you are ignorant of the schooling naturopathic doctors receive. 4 years, nplexs and 100 000 dollars later is more like it with a undergrad degree preferred.

bastyr is a good school.

you have no idea about anything your talking about.

Never realized!
Makes 4 years of pre-med, 4 years of med school, 3 years of internal medicine, 3 years of cardiology, and a year of interventional cardiology seem like a cake walk!  

Who would have thought?

[The Squadfather]

Never realized!
Makes 4 years of pre-med, 4 years of med school, 3 years of internal medicine, 3 years of cardiology, and a year of interventional cardiology seem like a cake walk!  

Who would have thought?

[Necrosis]

The ASA helps prolong the effects (along with caffeine) by lowering prostaglandin production.  The combo elevates cAMP levels for a longer period.  
ASA can also raise serotonin levels by freeing up L-tryptophan.  Serotonin essentially works opposite of the "adrenaline neurotransmitters," but anyone taking MDMA will see that some positive mood correlations can come from elevated production or inhibited re-uptake of the mono-amine neurotransmitters.


I doubt there is any significant digestive issues with the level of stimulation from ECA.  Patients are frequently loaded up with various stimulants for ADHD in levels that would raise CA higher than a normal ECA cycle.  A decrease in salivation, appetite, and gastric clearance rates may/will be noticed, but anyone in the midst of a contest prep diet will know that leptin/ghrelin eventually trumps all in the end.

"The ASA helps prolong the effects (along with caffeine) by lowering prostaglandin production.  The combo elevates cAMP levels for a longer period"

so? PDE inhibition via caffeine and the adenosine agonism via competitve inhibition is not what we are talking about, caffiene has many beneficial properties, as does aspirin, ephderine is not a good drug imo for the stated reasons. Also, they do not elevate cAMP but prevent breakdown similar to licorice preventing coritisol degradation. Your not elevating cellular production but preventing breakdown via PDE. All of the purine alkaloids like theophylline work with this method of action, but why are we talking about that? are you just looking for somewhere to present your subpar knowledge? PDE inhibition is only relevant at high doses, and addition of other methylxanthines might induce more of an effect as the GRAS is actually quite low. One way to increase cAMP is via histiminergic receptors and induction of specific cytokines prevelant in disorders of low cellular cAMP.

again, eppies suck.


"ASA can also raise serotonin levels by freeing up L-tryptophan."

bwhahah if only life where this simple, this would make the user feel tired. Many factors are at play here.

[I ETA PI]

does modern medicine cure MS ? 



NT

No!  Which is why we need to switch to lecithin and fatty acid therapy!

[Necrosis]

Never realized!
Makes 4 years of pre-med, 4 years of med school, 3 years of internal medicine, 3 years of cardiology, and a year of interventional cardiology seem like a cake walk!  

Who would have thought?

ive done 4 years of pre med as would naturopathic doctor, then 4 years of naturopathic med school, then residence for two years, then med school.

are you claiming to be a doctor? i sure hope not. A gp and ND have the same schooling. IF you specialize you have more schooling, just like if you specialize in other fields.

im not discounting MD's, I will be one, im just saying your mockery of ND's is not required, and you should perhaps follow in the footsteps of andrew weil and offer better treatment strategies.

[I ETA PI]

"The ASA helps prolong the effects (along with caffeine) by lowering prostaglandin production.  The combo elevates cAMP levels for a longer period"

so? PDE inhibition via caffeine and the adenosine agonism via competitve inhibition is not what we are talking about, caffiene has many beneficial properties, as does aspirin, ephderine is not a good drug imo for the stated reasons. Also, they do not elevate cAMP but prevent breakdown similar to licorice preventing coritisol degradation. Your not elevating cellular production but preventing breakdown via PDE. All of the purine alkaloids like theophylline work with this method of action, but why are we talking about that? are you just looking for somewhere to present your subpar knowledge? PDE inhibition is only relevant at high doses, and addition of other methylxanthines might induce more of an effect as the GRAS is actually quite low. One way to increase cAMP is via histiminergic receptors and induction of specific cytokines prevelant in disorders of low cellular cAMP.

again, eppies suck.


"ASA can also raise serotonin levels by freeing up L-tryptophan."

bwhahah if only life where this simple, this would make the user feel tired. Many factors are at play here.

Did you say adenosine AGONISM?  I didn't feel the need to read after that....

[Necrosis]

Did you say adenosine AGONISM?  I didn't feel the need to read after that....

competitive inhibition is agonism, your not a doctor obviously.

caffeine and adenosine share a similar structure, hence caf binds to the receptor competitively inhibint adenosine binding and stimulating its actions making it, geuss what, an agonist.


keep googling.

[The Coach]

You would think with all of that education he would be able to carry on any intelligent conversation without name calling. People might listen a little more and learn something, but when he comes off they way he does he instantly loses credibility. I would rather learn from usmokepole, he can teach without putting someone down.

[I ETA PI]

ive done 4 years of pre med as would naturopathic doctor, then 4 years of naturopathic med school, then residence for two years, then med school.

are you claiming to be a doctor? i sure hope not. A gp and ND have the same schooling. IF you specialize you have more schooling, just like if you specialize in other fields.

im not discounting MD's, I will be one, im just saying your mockery of ND's is not required, and you should perhaps follow in the footsteps of andrew weil and offer better treatment strategies.

It is quite obvious to see you haven't completed med school.

Get back to me after 4 years of brainwashing and the Hippocratic oath, you'll be mocking ND's, talking down to patients, refusing to answer your pager, and making the fellows do all your work just like everyone else.  

You must have taken the MCAT if you've finished 4 years of med school.  
Don't worry....you no longer need to apply for permission to take the test more than 3 times!  

[I ETA PI]

You would think with all of that education he would be able to carry on any intelligent conversation without name calling. People might listen a little more and learn something, but when he comes off they way he does he instantly loses credibility. I would rather learn from usmokepole, he can teach without putting someone down.

He can teach because you have so much to learn. 

An empty mind is like a sponge, it is up to YOU to add the water!

[benz]

Never realized!
Makes 4 years of pre-med, 4 years of med school, 3 years of internal medicine, 3 years of cardiology, and a year of interventional cardiology seem like a cake walk! 

Who would have thought?

15 years or hard study to come here and get owned by bums - PRICELESS

[Necrosis]

It is quite obvious to see you haven't completed med school.

Get back to me after 4 years of brainwashing and the Hippocratic oath, you'll be mocking ND's, talking down to patients, refusing to answer your pager, and making the fellows do all your work just like everyone else.  

You must have taken the MCAT if you've finished 4 years of med school.  
Don't worry....you no longer need to apply for permission to take the test more than 3 times!  

great rebuttal you never responded to anything i said.

[I ETA PI]

Say what you want about Squad, but he tells it like it is.  
Exaggerate your lifts, and you'll be caught.
Put up big numbers, and you'll get respect.  

Same thing in this thread.

[I ETA PI]

competitive inhibition is agonism, your not a doctor obviously.

caffeine and adenosine share a similar structure, hence caf binds to the receptor competitively inhibint adenosine binding and stimulating its actions making it, geuss what, an agonist.


keep googling.

Antagonists have affinity but no efficacy for their receptors and binding will disrupt the interaction and inhibit the function of an agonist or inverse agonist at receptors.  

Agonists bind to the receptor and triggers a response.  


Binding to a receptor is not agonism unless it triggers a responce in that cell.  
At least look this stuff up before you post.  



I can just imagine you in Trauma....
"Doc, he's hypotensive!"

"Give him some diovan, that'll get his BP up.  It's an Angiotensin II receptor antagonist, so it's really an agonist!  Trust me, I know this stuff."  
haha

[The Coach]

Dude's on here so much flamming me he must either can't get patients or cant get a job!

[benz]

Antagonists have affinity but no efficacy for their receptors and binding will disrupt the interaction and inhibit the function of an agonist or inverse agonist at receptors. 

Agonists bind to the receptor and triggers a response. 


Binding to a receptor is not agonism unless it triggers a responce in that cell. 
At least look this stuff up before you post. 



I can just imagine you in Trauma....
"Doc, he's hypotensive!"

"Give him some diovan, that'll get his BP up.  It's an Angiotensin II receptor antagonist, so it's really an agonist!  Trust me, I know this stuff." 
haha

Ok doc, 15 years studying to waste your time here? Are you serios about being a doc?

[I ETA PI]

Dude's on here so much flamming me he must either can't get patients or cant get a job!

Your grasp of the written word is astounding.  

[I ETA PI]

Ok doc, 15 years studying to waste your time here? Are you serios about being a doc?

Hell no!
I'm a bodybuilder, through and through!
I'm just sitting her living off my girlfriend for now.  She knows it's worth it though.  Once I go pro and get a big contract, we'll all be on easy street. 

I've been trying to get in contact with Ed Connors or Lou Zwick to see if they can help me out. 
I've been emailing Irv Gelb about a shoot out in LA after my next show...gonna be a big spread in MuscleMag!

When you love something, you're willing to lay it all on the line for that one moment in the sun...all oiled up, dehydrated, almost naked....knowing your dreams are at your fingertips.

Beverly Nutrition sends me lots of pamphlets, so I know they're looking at sponsoring me.  Plus, some guy with a limp named Joe said he was going to make a movie of me as well.  I'm on my way baby...like I tell my girlfriend, if bodybuilders got paid for how hard they work, we'd make more than doctors!

[The Coach]

You and Zwick deserve each other!

[no one]

Your grasp of the written word is astounding. 

lol.

[The Coach]

Oh look, your first patient, if you can help him you can surely cure any disease!!

[Van_Bilderass]

It's not adrenal "damage" you have to worry about with prolonged, ongoing, high dose stimulant use. The adrenals will continue to work well, squeezing gluco-corticoid out with every exogenous stressor. This creates a chronic cortisol state and leads to peripheral insulin resistance. This is why many stimulant abusers of very pro-longed duration, who are concomitantly too fearful of weight regain to take drug holidays, are often left dissatisfied with their long term body composition. Mind you they recount superb results when they first began using stimulants, but now some report backsliding.

For astute followers of clinical endocrinology, you will notice that just about all of the stimulant based obesity medications either slow down, stop, or even revert the rate of weight loss they originally proffered. However, this is not because the stimulant has stopped working, quite the contrary the stimulant is still working, and working well-pumping out glucocorticoid that confers positive feedback on the CNS versus the more conventional negative feedback loop most couch scientists are aware of. And therein lies the quandary.

The weight loss dissatisfaction that is at times seen with long term, chronic, high dose users of stimulants that also constantly require dose escalation, is the result of an evolving metabolic millieu that does not favor body composition in the long run. With each dose they take after day #1 they begin traversing towards an insulin resistant state, which unlike the acute insulin resistance one gets from virginal rhGH use, will hamper fat to lean ration. In fact women who began prescription diet pills in the 70's and never took a break, often times show the same emotional, psychiatric, and physiologic signs and symptoms as those who require glucocorticoid therapy such as prednisone for autoimmune disorders. Even some homology can be drawn, albeit less patently with Cushing's.

Note all of the above specifically addresses those who 1) take stimulants for years and years  2) take ever increasing doses  3) never take drug holidays. Of course, this can all be obviated with judicious dosing, but more importantly, conservative frequency of use.

Now, if there were only some way to throw out the bath water without the baby...

I have heard this before and you could very well be right (have you posted on other boards under a different name?). However, do you have some hard data showing these negative bodycomposition changes in long term stimulant users?

What is the difference between acute and chronic insulin resistance you mention? Why does the insulin resistance from GH make you leaner but insulin resistance from stimulants eventually make you fatter?

[Necrosis]

Antagonists have affinity but no efficacy for their receptors and binding will disrupt the interaction and inhibit the function of an agonist or inverse agonist at receptors.  

Agonists bind to the receptor and triggers a response.  


Binding to a receptor is not agonism unless it triggers a responce in that cell.  
At least look this stuff up before you post.  



I can just imagine you in Trauma....
"Doc, he's hypotensive!"

"Give him some diovan, that'll get his BP up.  It's an Angiotensin II receptor antagonist, so it's really an agonist!  Trust me, I know this stuff."  
haha

your description of agonism fits caffeines adenosine receptor activation and your description of antogonists is plain wrong.

"Agonists bind to the receptor and triggers a response. "

what would you consider an adenosinemimetic then?

[I ETA PI]

You and Zwick deserve each other!

Sarcasm, my cerebral deprived friend.  
Written sarcasm is a bit harder to detect than spoken sarcasm, but that is not your fault.  Those with reading disabilities often learn to cope through better recognition of tone inflection and body language.  

If you believe in your heart that you can improve your reading comprehension, then I believe you can too.  

I'm going to be with you all the way, from day one.  Let's tackle this disabilty once and for all!