MESSAGE TO EPHEDRINE USERS!!!!!!!

[MONSTER_TRICEPS]

An understanding of physiology here on getbig?
How wonderful to see that comprehension of human science is alive and well! 
AGB, why hast thou stayed quiet for so long?  This post should be force fed to all those attempting to speak with authoritarian tone on subjects they have no clue about.  I'd give you positive rep points if this site were lame enough to have them!

Go eat a dick bitch.

[I ETA PI]

81mg of aspirin has shown prophylactic effects against various cancers, and cardiovascular disease, many healthy people should take it. It has also shown effects against dementia and alzhemiers by reducing tau tangles, plauqes etc..

for one you can permently screw up your adrenal fucntion. exogenous application of eppies causes the adrenals to pump out more catecholamines, chronic use can cause damage. Also, eph is not selective in its beta agonism, thus you get the goodies, the fat loss with the bad stuff, such as increased heart rate, ateriole constriction, higher blood pressure all of this has a cumulative effect. the short burst of catecholamines is also bad for the psyche when coming down, similar to amphetamines.

beta receptor downregulation could occur, Hence the need for higher and higher doses, your body maintains homeostasis above all else, dont think there isnt consequences to those actions. The higher doses cause more cardiovascular issues. Not to mention that catecholamine release will inhibit the parasympathetic system via sympthomimetic action of eph., causing poor digestion among other things.

im not saying dont use it, im saying long term chronic use of any stim is dangerous, especially a shotgun stim like ephedrine.

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.

[I ETA PI]

Go eat a dick bitch.

Thank you for the compliment, I accept your apology. 

[KillerMonk]

I cannot believe no ones mentioned Cocaine as a stimulate for vicious training,The only time i used it was before a chest workout at my freind insistance i was lifting heavier and more endurance more reps and a incredible high and the most constructive workout i ever had.
Shit if i was ever going to get back into serious training again i would use it 3 to 4 times per week before serious training pity, it costs so much in OZ compared to the US

[Benny B]

you werent asking me, but no i have never had any negative sides. ive taken up to 100mg at one time.   

stupidasfuck

but no negative sides


or i just didnt feel any, cuz of the x and caffiene and weed running trough m at the same time

 

moron

[no one]

Thank you for the compliment, I accept your apology. 

don't pay any attention to MONSTER triceps- he claimed a little while back that hugh jackman had the ideal physique and that he strives to one day look like that.

all things considered then, i would say he's a bit of a nancy boy.

[MONSTER_TRICEPS]

BOOOOOOOOOOOOOOOOMMMM!!!!!!!! 

[candidizzle]

I cannot believe no ones mentioned Cocaine as a stimulate for vicious training,The only time i used it was before a chest workout at my freind insistance i was lifting heavier and more endurance more reps and a incredible high and the most constructive workout i ever had.
Shit if i was ever going to get back into serious training again i would use it 3 to 4 times per week before serious training pity, it costs so much in OZ compared to the US

yes and if you did that you would end up doing it 3-4 times a day


you cannot fuck around with cocaine like that. if your gonna do it you shouldnt use it before a workout...youll en up using it every workout.   and you should only use it occasionally on the weekends, and make sure to have some weed available for the come down..   or else youll be sad as fuck and desperate for more coke..


trust me.      i thought the exact same thing you did. and i did exactly what you said you would do.

[Brutal_1]

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...

LOL,

oh brother.... what is it with all these "MD triple MD" posters nowadays   

These guys are getting annoying....



Trying to ego-boost with pubmed searches and eloquent language is gayer than blaming advil 

[spinnis]

BOOOOOOOOOOOOOOOOMMMM!!!!!!!! 

Epic One Titted Gyno 

[The Coach]

No, adrenal insufficiency is Addison's disease, a REAL disease. 
A real disease that is NOT caused by stimulants.  Addison's disease is caused by a lack of production of cortisol and often aldosterone. 

Do you see the ignorance in your post?  Are you claiming that stimulants cause a DECREASE in cortisol production?
And if so, how is this related to the "crash" you wrote about earlier?



You must have shit where your brains should be. 

Background
Do not confuse acute adrenal crisis with Addison disease. In 1855, Thomas Addison described a syndrome of long-term adrenal insufficiency that develops over months to years, with weakness, fatigue, anorexia, weight loss, and hyperpigmentation as the primary symptoms. In contrast, an acute adrenal crisis can manifest with vomiting, abdominal pain, and hypovolemic shock.

Pathophysiology
The adrenal cortex produces 3 steroid hormones: glucocorticoids (cortisol), mineralocorticoids (aldosterone, 11-deoxycorticosterone), and androgens (dehydroepiandrosterone). The androgens are relatively unimportant in adults, and 11-deoxycorticosterone is a fairly weak mineralocorticoid in comparison to aldosterone. The primary hormone of importance in acute adrenal crisis is cortisol; adrenal aldosterone production is relatively minor.

Cortisol enhances gluconeogenesis and provides substrate through proteolysis, protein synthesis inhibition, fatty acid mobilization, and enhanced hepatic amino acid uptake. Cortisol indirectly induces insulin secretion to counterbalance hyperglycemia but also decreases insulin sensitivity. Cortisol also has a significant anti-inflammatory effect through stabilizing lysosomes, reducing leukocytic responses, and blocking cytokine production. Phagocytic activity is preserved, but cell-mediated immunity is diminished in situations of cortisol deficiency. Finally, cortisol facilitates free water clearance, enhances appetite, and suppresses adrenocorticotropic hormone (ACTH) synthesis.

Aldosterone is released in response to angiotensin II stimulation via the renin-angiotensin-aldosterone system, hyperkalemia, hyponatremia, and dopamine antagonists. Its effect on its primary target organ, the kidney, is to promote reabsorption of sodium and secretion of potassium and hydrogen. The mechanism of action is unclear; an increase in the sodium- and potassium-activated adenosine triphosphatase (Na+/K+ ATPase) enzyme responsible for sodium transport, as well as increased carbonic anhydrase activity, has been suggested. The net effect is to increase intravascular volume. The renin-angiotensin-aldosterone system is unaffected by exogenous glucocorticoids, and ACTH deficiency has a relatively minor effect on aldosterone levels.

Adrenocortical hormone deficiency results in the reverse of these hormonal effects, producing the clinical findings of adrenal crisis.

Primary adrenocortical insufficiency occurs when the adrenal glands fail to release adequate amounts of these hormones to meet physiologic needs, despite release of ACTH from the pituitary. Infiltrative or autoimmune disorders are the most common cause, but adrenal exhaustion from severe chronic illness also may occur.

Secondary adrenocortical insufficiency occurs when exogenous steroids have suppressed the hypothalamic-pituitary-adrenal (HPA) axis. Too rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands' ability to respond immediately. In acute illness, a normal cortisol level may actually reflect adrenal insufficiency because the cortisol level should be quite elevated.

Bilateral massive adrenal hemorrhage (BMAH) occurs under severe physiologic stress (eg, myocardial infarction, septic shock, complicated pregnancy) or with concomitant coagulopathy or thromboembolic disorders.


http://www.emedicine.com/med/TOPIC65.HTM

[The Coach]

Addisons Disease


Background
Thomas Addison first described the clinical presentation of primary adrenocortical insufficiency (Addison disease) in 1855 in his classic paper, On the Constitutional and Local Effects of Disease of the Supra-Renal Capsules.

Pathophysiology
Addison disease is adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex. It affects both glucocorticoid and mineralocorticoid function. The onset of disease usually occurs when 90% or more of both adrenal cortices are dysfunctional or destroyed.

http://www.emedicine.com/med/topic42.htm

[I ETA PI]

Background
Do not confuse acute adrenal crisis with Addison disease. In 1855, Thomas Addison described a syndrome of long-term adrenal insufficiency that develops over months to years, with weakness, fatigue, anorexia, weight loss, and hyperpigmentation as the primary symptoms. In contrast, an acute adrenal crisis can manifest with vomiting, abdominal pain, and hypovolemic shock.

Pathophysiology
The adrenal cortex produces 3 steroid hormones: glucocorticoids (cortisol), mineralocorticoids (aldosterone, 11-deoxycorticosterone), and androgens (dehydroepiandrosterone). The androgens are relatively unimportant in adults, and 11-deoxycorticosterone is a fairly weak mineralocorticoid in comparison to aldosterone. The primary hormone of importance in acute adrenal crisis is cortisol; adrenal aldosterone production is relatively minor.

Cortisol enhances gluconeogenesis and provides substrate through proteolysis, protein synthesis inhibition, fatty acid mobilization, and enhanced hepatic amino acid uptake. Cortisol indirectly induces insulin secretion to counterbalance hyperglycemia but also decreases insulin sensitivity. Cortisol also has a significant anti-inflammatory effect through stabilizing lysosomes, reducing leukocytic responses, and blocking cytokine production. Phagocytic activity is preserved, but cell-mediated immunity is diminished in situations of cortisol deficiency. Finally, cortisol facilitates free water clearance, enhances appetite, and suppresses adrenocorticotropic hormone (ACTH) synthesis.

Aldosterone is released in response to angiotensin II stimulation via the renin-angiotensin-aldosterone system, hyperkalemia, hyponatremia, and dopamine antagonists. Its effect on its primary target organ, the kidney, is to promote reabsorption of sodium and secretion of potassium and hydrogen. The mechanism of action is unclear; an increase in the sodium- and potassium-activated adenosine triphosphatase (Na+/K+ ATPase) enzyme responsible for sodium transport, as well as increased carbonic anhydrase activity, has been suggested. The net effect is to increase intravascular volume. The renin-angiotensin-aldosterone system is unaffected by exogenous glucocorticoids, and ACTH deficiency has a relatively minor effect on aldosterone levels.

Adrenocortical hormone deficiency results in the reverse of these hormonal effects, producing the clinical findings of adrenal crisis.

Primary adrenocortical insufficiency occurs when the adrenal glands fail to release adequate amounts of these hormones to meet physiologic needs, despite release of ACTH from the pituitary. Infiltrative or autoimmune disorders are the most common cause, but adrenal exhaustion from severe chronic illness also may occur.

Secondary adrenocortical insufficiency occurs when exogenous steroids have suppressed the hypothalamic-pituitary-adrenal (HPA) axis. Too rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands' ability to respond immediately. In acute illness, a normal cortisol level may actually reflect adrenal insufficiency because the cortisol level should be quite elevated.

Bilateral massive adrenal hemorrhage (BMAH) occurs under severe physiologic stress (eg, myocardial infarction, septic shock, complicated pregnancy) or with concomitant coagulopathy or thromboembolic disorders.

There is no medical diagnosable term of "adrenal fatigue."  The Mayo Clinic is adament about this fact, feeling strongly enough about the general misunderstanding of this phenomenon to include articles stating this fact.  


The most humorous aspect in all of this is that you continue to COPY and PASTE articles that REFUTE your claims.  

Adrenal fatigue is not a REAL medical diagnosis, that is 100% clear.  But, what is even more funny is that the QUACKS claiming adrenal fatigue treatments use STIMULANTS as treatment for the "illness."

So, even if adrenal fatigue was accepted by the medical community, it would NOT be caused by stimulant intake.  
You saw another ignorant idiot mention adrenal fatigue somewhere and thanks to your total lack of knowledge in all things relating to science, you decided to spout off incorrectly about an illness that isn't even a real diagnosis.  






In case you can't follow what that says.....You just copy and pasted an article that states adrenal fatigue is a LACK of cortisol production.....all the while claiming that stimulants (those little thingies that can raise cortisol levels) cause adrenal fatigue.

According to coach: increased cortisol = lack of cortisol.   (which is entirely moot as there is no such thing as adrenal fatigue)

[I ETA PI]

Addisons Disease


Background
Thomas Addison first described the clinical presentation of primary adrenocortical insufficiency (Addison disease) in 1855 in his classic paper, On the Constitutional and Local Effects of Disease of the Supra-Renal Capsules.

Pathophysiology
Addison disease is adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex. It affects both glucocorticoid and mineralocorticoid function. The onset of disease usually occurs when 90% or more of both adrenal cortices are dysfunctional or destroyed.

http://www.emedicine.com/med/topic42.htm

Now you have me confused. 
I stated initially that Addison's disease is a "real" adrenal gland disorder.  This is NOT adrenal fatigue. 
Addison's disease involves deficiencies in Cortisol and Aldosterone, primarily.  This has NOTHING to do with any level of over-stimulation of the sympathetic nervous system. 

I no longer have any level of doubt that you're a moron, now I'm beginning to wonder if you can even read. 

[The Coach]

Hey, your the one who said it was addisons, im just making the comparison. I also never said it was a disease or a medical diagnosis.....those were your words. And yes, i saw that article from the Mayo a couple of months ago.

[The Coach]

Joeloco, put that motherfvcker in his place !

i eta pi = HUGE douchebag.




NT

Yeah, the dude definately lacks in people skills.

[The Coach]

Now you have me confused. 
  This is NOT adrenal fatigue. 
Addison's disease involves deficiencies in Cortisol and Aldosterone, primarily.  This has NOTHING to do with any level of over-stimulation of the sympathetic nervous system. 

I no longer have any level of doubt that you're a moron, now I'm beginning to wonder if you can even read. 

I never said Addison's was adrenal fatigue, you in fact posted that Addison's was adrenal insuffieniency, I posted those two articles to show that it was not the same thing as you claim.  Also, you don't have to give the definition of Addison's.........I already posted it! In case you missed it, here's the link again.

http://www.emedicine.com/med/topic42.htm

[The Coach]

Your the only who called it a "disease", from what I understand it's a syndrome and yes there is a correlation related to Addisons but it could also be called non-Addison's hypoadrenia, neurasthenia and adrenal neurasthenia....I understand that adrenal fatigue is probably the laymans term for it.
Shortly because I am just starting to learn about this, unlike you who seems to be a doctor and me just a trainer who enjoys learning, reading and doing research because I didn't have privilege of finishing college..........but.... .from what I have learned so far is that when a person is stressed, the body reacts a stress response through the sympathetic nervous system. When this happends epinephrine is secreted through the adrenal medulla and the hypothalamus pituitary releases ACTH which in turns causes the adrenal cortex to increase the production of cortisol.

When we have a high stress situation the production of cortisol is increased to such a high level that the can become exhausted and at that time DHEA is will start to decrease with stress. But with chronic stress there is a decompensation of DHEA at the same time cortisol levels are rising.


I'm not done...I'm leaving work right now and will finish my thought when I get home, but I have more. Dude, like I said, I may not have the formal schooling you have but I am damn well willing to learn and you trying to belittle someone just shows your true character, I hope to God your not a Dr. but don't put someone down just because you might know more.

He apparently missed this part that I wrote.

[I ETA PI]

I never said Addison's was adrenal fatigue, you in fact posted that Addison's was adrenal insuffieniency, I posted those two articles to show that it was not the same thing as you claim.  Also, you don't have to give the definition of Addison's.........I already posted it! In case you missed it, here's the link again.

http://www.emedicine.com/med/topic42.htm

Addison's is also known as chronic adrenal insufficiency. 
So, yes, Addison's is adrenal insufficiency. 


Adrenal fatigue is a made up term obtuse trainers like to talk about. 


Your reading comprehension is on par with small children, Viriginian mountain men, and trees. 
It is quite surreal to be explaining this to someone that is too ignorant to even realize how moronic he is. 

Remember, when tying your shoes, the rabbit goes AROUND the tree. 

[I ETA PI]

STFU !

Neurotoxin my man! 
Are you familiar with the paradoxical nature of glutamate?

[I ETA PI]

joeloco, medicine's diagnostic model is wait until it's a full blown disorder.....then put a fancy name on it. subclinical disorders ? haha

complimentary medicine is designed to keep the public out of this HUGE douchebags office. (assuming he's a douchebag "dr")

go through any Merck Manual....lots of "BIG FANCY WORDS" with few cures.


I ETA PI knows a lot.... about nothing.  


NT

Of course the most brilliant minds in the world are dead wrong.  Surely a few naturopathic idiots with a 6 week training course know best!

Q. What did the naturopathic "doc" get on his MCAT?

A. Drool

[The Coach]

 


Adrenal fatigue is a made up term obtuse trainers like to talk about. 


 

You obviously have me confused with "trainers" who just count reps and collect their money. The difference between other "trainers" and me is I take my business seriously enough to constantly research ways to continue to help people. You.....well, I don't know what you do, but you sound like a blow hard.

[The Coach]

Of course the most brilliant minds in the world are dead wrong.  Surely a few naturopathic idiots with a 6 week training course know best!

Again, you must have me confused with someone who just did a "6 week training course"

[I ETA PI]

why...can you cure ALS ? (rhetorical question)





NT

No, but I've read "A Brief History of Time" and "the Universe in a Nutshell."
Does that count? 

I'm assuming the link with my post on the Glutamate paradox (glutamate as neurotransmitter and neurotoxin) is why you mention ALS. 

Are you going to claim that a "hypothesis" is also scientific fact? 
Why not make the stretch on the glutamate hypothesis if we're going to make the stretch to giving fairy tale symptoms a "real" disease association? 

Perhaps we can cure MS with some eggs and fish oil.....

[Necrosis]

Of course the most brilliant minds in the world are dead wrong.  Surely a few naturopathic idiots with a 6 week training course know best!

Q. What did the naturopathic "doc" get on his MCAT?

A. Drool

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.