Do you always need the "A" in the ECA?

[cat]

Is it always necessary in the ECA stack to have the A?

Is it as efficient without the A?

[KZRSOIZE]

ive never heard of a "EC" stack ....

[Bryan Hildebrand]

taking the aspirin thins the blood which reduces viscosity

[apex23]

The A is not necessary.

[Gunners]

Is it always necessary in the ECA stack to have the A?

Is it as efficient without the A?

i's more efficeint, the aspirin is outdated and counterproductive.

[claymore1]

The A is not necessary.

Agreed

[•P®øD¶G¥•]

If you take it 3 times a day, take 81mg with each dose, that's 250mg or so ED, only thing you'll get is benefit.

[Bryan Hildebrand]

do you know why the A was added in the first place? answer that question and you will understand the purpose of adding aspirin far more oftne than not.

[mr intensity]

The third component of the ECA combination, aspirin, enhances the peripheral actions of ephedrine and
caffeine by inhibiting prostaglandin (PG) synthesis. PGs, like adenosine, have been implicated in inhibiting
NE release from the post-synaptic nerve terminal, and in inhibiting the lipolytic actions of sympathetic
stimulants.

[cat]

Thank you for your responses. I have difficulty with aspirin due to gastric problems [ulcers, etc.] which are exacerbated by the caffeine. Even the 'baby aspirin' doses gave me difficulty so I was looking for a way to avoid the Aspirin.

[cat]

ive never heard of a "EC" stack ....


i's more efficeint, the aspirin is outdated and counterproductive.

Could you explain how it is more efficient to eliminate it? Also, in what way is it counterproductive?

[Bryan Hildebrand]

as explained above, it is far from counterprodcutive.
additionally, and in leymans terms, if you are on AAS and want to add ECA while cutting, aspirin provides a degree of reduced clotting and increased viscosity. if you are using one of many AAS that produce an increase in red blood cells, RBC's, the aspirin helps ensure reduced potential for heart attack, DVT and stroke while in a dehydrated and tachycardic state both while training and during your rest periods. rest relative to your neurogenic stimulated state.

also, they make an "esoteric" coated aspirin that releases further in the gut thus reducing gastric issues. you can also try taking zantac, 150mg with it. zantac induces gastric emptying which will get your stomach contents out faster.

[Gunners]

yes , it's a prostaglandin inhibitor, welcome when taking strong simulants but only weakly. But the lesser secrection od muscle prostaglandin will increase insulin resistance, contributing to a smaller, fatter version of urself. i've found noticeable muscle growth after discontinuing aspirin.

[THE-DET-OAK]

i have to agree with gunners ive seen a few studies claiming NSAIDS inhibit muscle growth

[barbellbarbie]

i use the ecy stack there have been studies that show that ECA is better on extremely obese people where as the Yohimbe works on leaner people..

[Nitro Fueled Barbie/Mel Marx]

The third component of the ECA combination, aspirin, enhances the peripheral actions of ephedrine and
caffeine by inhibiting prostaglandin (PG) synthesis. PGs, like adenosine, have been implicated in inhibiting
NE release from the post-synaptic nerve terminal, and in inhibiting the lipolytic actions of sympathetic
stimulants.

agreed....the A really makes a difference for me.:yep:

[cat]

i use the ecy stack there have been studies that show that ECA is better on extremely obese people where as the Yohimbe works on leaner people..

That probably is the strongest combo, but I think I might jump right of my skin from the 3 together from the jitters.

I will try a small dose of the enteric 'coated' aspirin as a compromise and to save my gut.

Is there a standard ratio of E to C to A?
Does the dosing change if the A is omitted?

[Warped]

All the components helps making it the ECA stack. Removing either the E,C or A makes it less effective.

[ypmm5]

i's more efficeint, the aspirin is outdated and counterproductive.
I asked Dave P this a while back and he stated the same thing. It is out dated and no need for it.
Remember, with ephedra you get a thermogenic effect. Hence, your body temp will be slightly elevated. Hence, you body is burning calories. What do people take when they have a fever i.e. cold or flu, ASA or at least some aspirin product such NSAIDS or tylenol.
Do not take the ASA.

[Bryan Hildebrand]

and I disagree. sure, I completely understand the potenital antithermogenic effect, however, at 82mg (which is all you should be taking) that effect will only last, at most, 2 hours. however, it will provide the anticoagulative effect for 24 hours.

safeguard against stroke or heartattack while on neurostimulants and AAS in a dehyrated state? i'll take missing out on 2 hours of thermogenic effect.

[cat]

I asked Dave P this a while back and he stated the same thing. It is out dated and no need for it.
Remember, with ephedra you get a thermogenic effect. Hence, your body temp will be slightly elevated. Hence, you body is burning calories. What do people take when they have a fever i.e. cold or flu, ASA or at least some aspirin product such NSAIDS or tylenol.
Do not take the ASA.


Does the dosing change if the A is omitted?

[Bryan Hildebrand]

nope.

[cat]

I asked Dave P this a while back and he stated the same thing. It is out dated and no need for it.
Remember, with ephedra you get a thermogenic effect. Hence, your body temp will be slightly elevated. Hence, you body is burning calories. What do people take when they have a fever i.e. cold or flu, ASA or at least some aspirin product such NSAIDS or tylenol.
Do not take the ASA.

I think this is the science behind the "no aspirin" concept:
Effects of Aspirin on Nitric Oxide Formation and De Novo Protein Synthesis by RINm5F Cells and Rat Islets



Guim Kwon (http://molpharm.aspetjournals.org/search?author1=Guim+Kwon&sortspec=date&submit=Submit),
Jeanette R. Hill (http://molpharm.aspetjournals.org/search?author1=Jeanette+R.+Hill&sortspec=date&submit=Submit),
John A. Corbett (http://molpharm.aspetjournals.org/search?author1=John+A.+Corbett&sortspec=date&submit=Submit)1 (http://molpharm.aspetjournals.org/content/52/3/398.full#fn-2) and
Michael L. McDaniel (http://molpharm.aspetjournals.org/search?author1=Michael+L.+McDaniel&sortspec=date&submit=Submit)

+ (http://molpharm.aspetjournals.org/content/52/3/398.full#) Author Affiliations


Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110


[/URL]

Abstract

Aspirin and aspirin-like drugs are the most commonly indicated agents for the treatment of inflammation. Mechanisms of action for these drugs, however, are not clearly understood. In this study, we examined the effects of aspirin on production of nitric oxide (NO), a proinflammatory mediator, and show that aspirin inhibits NO production by transformed pancreatic β cells (RINm5F) and rat islets in a concentration-dependent manner with an IC50 value of ∼3 mm. Therapeutic concentrations of aspirin (1–5 mm) that block NO production affected neither nuclear factor-κB activation nor inducible NO synthase (iNOS) mRNA transcription but potently inhibited iNOS protein expression by both RINm5F cells and rat islets. The effects of aspirin on islet function were examined by measuring glucose-stimulated insulin secretion in the presence of various concentrations of aspirin. Aspirin (1–5 mm) did not affect insulin secretion at basal or glucose-stimulated conditions, whereas higher concentrations of aspirin (10–20 mm) significantly increased basal insulin secretion. Aspirin at high concentrations of 10 and 20 mminhibited de novo protein synthesis as demonstrated by inhibition of [35S]methionine incorporation into total islet protein and by inhibition of rabbit reticulocyte expression by Brome mosaic virus mRNA, suggesting that inhibition of iNOS expression at these high concentrations of aspirin may be due to the impairment of the translational machinery. These findings indicate that inhibition of iNOS expression and NO production may explain, in part, the beneficial effects of aspirin as an anti-inflammatory agent at therapeutic concentrations, whereas inhibition of de novo protein synthesis may possibly explain clinical and side effects of aspirin in the inflamed tissues and organs such as stomach and kidney that may accumulate high concentrations of aspirin.

Aspirin and ALD are the most commonly indicated agents for treatment of inflammation. These drugs have an enormous range of effects, including reducing pain or fever, dissolving corns, inhibiting blood clotting, inducing peptic ulcers, and promoting uric acid loss and fluid retention by the kidneys ([URL="http://molpharm.aspetjournals.org/content/52/3/398.full#ref-1"]1 (http://molpharm.aspetjournals.org/content/52/3/398.full#sec-1)). The broad range of biological actions of aspirin have made it difficult to delineate its mechanisms of action. The most well accepted mechanism of action of aspirin is inhibition of prostaglandin biosynthesis (2 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-2)). This theory, however, has been challenged because of discrepancies in clinical efficacies of aspirin in the treatment of diseases such as rheumatic fever, gout, and rheumatoid arthritis, which require much higher doses of aspirin (4–8 g/day) than required to inhibit prostaglandin production (1 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-1), 3 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-3)). Moreover, salicylic acid, which is ineffective as a prostaglandin H synthase inhibitor, is nevertheless able to reduce inflammation at comparable doses to aspirin (1 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-1), 3 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-3)). As alternative mechanisms of action for aspirin and ALD, the interference of cellular signaling by binding to key regulatory proteins such as G proteins (1 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-1)) and inhibition of the transcriptional factor NF-κB (3 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-3)) have been proposed. Nonspecific effects of aspirin and ALD due to high concentrations accumulated in some organs have also been proposed to account for the clinical and side effects of these drugs (4 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-4)).
NO synthesized by iNOS has been implicated as a mediator of inflammation in rheumatic and autoimmune diseases (5-7 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-5)). We (8-10 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-8)) and others (11-13 (http://molpharm.aspetjournals.org/content/52/3/398.full#ref-11)) have previously shown that cytokine-mediated production of NO by pancreatic β cells plays a key role in dysfunction and destruction of β cells associated with autoimmune diabetes. In light of the possible role of NO in the pathogenesis of autoimmune diabetes, we sought to find agents that block NO production by pancreatic β cells. In this study, we report that aspirin blocks NO production by primary and transformed rat pancreatic β cells at therapeutic concentrations and inhibits total de novoprotein synthesis at higher concentrations, which may explain some of the clinical and toxic effects of aspirin.

[Bryan Hildebrand]

great find. thx for sharing.

[barbellbarbie]

That probably is the strongest combo, but I think I might jump right of my skin from the 3 together from the jitters.

I will try a small dose of the enteric 'coated' aspirin as a compromise and to save my gut.

Is there a standard ratio of E to C to A?
Does the dosing change if the A is omitted?
Ya the Y even makes me a little tweaky and im fairly immune to stimulants

i started with 25mg ephedra, 300mg caffeine and 1 extra strength Excedrin for eca then added 1 pill of the 500mg yohimbe.. i am basically immune to this dosing now and have to take a truck load but thats how i started

lipodrene (the oigional with ephedrine you can still get it online) which is 25mg ephedra 300mg caffeine the Excedrin then just got the yohimbe from the vit shop

[Shariff Abel]

it's like mr G without the "G" !! so Yes you must have the "A"

[barbellbarbie]

^^^mother of fuckin god!

[Warped]

^^^mother of fuckin god!
Lol.

[Gunners]

and I disagree. sure, I completely understand the potenital antithermogenic effect, however, at 82mg (which is all you should be taking) that effect will only last, at most, 2 hours. however, it will provide the anticoagulative effect for 24 hours.

safeguard against stroke or heartattack while on neurostimulants and AAS in a dehyrated state? i'll take missing out on 2 hours of thermogenic effect.

I tolerate ephedra well but, maybe i'll chuck it in this time, especially during this hot summer. Thanks for the warning ive heard of cases like this before.

[rj45]

Is it always necessary in the ECA stack to have the A?

Is it as efficient without the A?

You don't need the e or the C either. However, A helps by lowering BP temporarily.