Talk:ECA stack

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Ephedrine acts to increase energy by its actions as a symptomimetic amine. It increases dopamine and noradrenaline levels in the brain, and also serves as a dopamine reuptake inhibitor.

Is ephedrine really a dopamine reuptake inhibitor?

-- Yes, AFAIK, all phenethylamines are due to the related uptake action for dopamine, adrenaline, and noradrenaline. As ephedrine binds at noradrenaline receptors that also transport dopamine, the effect is less than cocaine or amphetamine, but still seems to be present. I've included two references that should help clarify this.

--- (76.98.177.253 06:27, 31 October 2007 (UTC)) Ephedrine is not a reuptake inhibitor in the manner of cocaine or methylphenidate; rather it releases catecholamines by reversing the norepinephrine (NE) uptake pump (NET). It has little affinity for the dopamine (DA) uptake pump (DAT), but like amphetamine (which only moderate DAT affinity, but high NET affinity) it can release ectopic dopamine from noradrenergic terminals. The NET actually has a higher affinity for DA than it does for NE, so free-floating extrasynaptic DA can be uptaken and accumulate over time in noradrenergic terminals. Methamphetamine releases DA directly from dopaminergic terminals by reversing DAT. Of course, both amphetamine and ephedrine release relatively more NE than DA. Amphetamine releases less NE at the same dopaminergic potency because of its moderate affinity for DAT, which ephedrine does not significantly bind to. Methamphetamine has even less noradrenergic load at the same dopaminergic potency, and causes the least amount of sympathetic side-effects, but also the least amount of thermogenesis.[reply]

But unlike amphetamines & cocaine, ephedrine also has potent direct agonist action at the beta adrenoceptors; depletion of NA does not interfere with its pressor action: [1] The tolerance to thermogenic and anorectic effects that develops after prolonged release of NE & DA is a result of stimulation of the alpha-2 adrenoceptors. These are feedback autoreceptors/heteroreceptors that decreases synthesis of catecholamines. Secondly prolonged activation of central D2 dopamine and adrenoceptors in the hypothalamus results in their desensitization. The direct agonist effects of ephedrine (on the beta-3 adrenoceptor) and the nonsteroidal anabolic clenbuterol (on the beta-2 adrenoceptor) is independent of NE & DA levels, so their thermogenic effects last much longer than the anorectic & thermogenic effects of amphetamines and other diet drugs.

Yohimbine, an alpha-2 adrenoceptor antagonist is sometimes used to prolong and enhance the thermogenic effects of NE and adrenaline (AD), which can be released by ephedrine, pseudoephedrine, an amphetamine, or naturally from the sympathetic ganglia during intense exercise. However, blocking the sole manner in which the sympathetic nervous system inhibits its own feedback can result in malignant hyperthermia if you overdose on thermogenics.

Well written points about reuptake inhibition with phenethylamines; however, my understanding of tolerance was it was mediated via beta-receptor downregulation, which is histamine mediated and essentially consists of the receptor sinking into the cell membrane further; in fact, I think that study was about clen specifically, and also covered an antihistamine being used to slow the tolerance (which I think is dumb, but hey). Can you point to any significant studies showing the role of alpha-2 receptors in the desensitization process? I just find it hard to believe clen would slow this down, rather than speeding it up. Further, aren't D2 receptors in the hypothalamus typically inhibitory? I also read one study that implicated tolerance to amphetamine's anorectic effect was due to suppression of the kappa opioid system, which isn't too far of a logical leap given the connections between DA and dynorphin, but I'm not sure how that applies to ephedrine (which has similar anorectic and tolerance to amphetamine which far less effects on DA). More confusing are studies showing infusion of kappa opioid agonists producing an anorectic effect; in rats, at least. Anyway, there are so many downstream effects of these drugs I think it's hard to say for certain at some point.

Ok, answered my own questions here. The thermogenic effect is ultimately due to the action of the noradrenaline, rather than any direct effect of the ephedrine on beta-3 receptors, as l-ephedrine, the kind sold OTC, has little beta-3 agonist activity.

I emailled Dr. Wellman, author of the study comparing various stimulants' thermogenic properties in human BAT. Unfortunately, while this study is not fully available online (just the abstract), he told me the results were that d-pseudoephedrine had three times less thermogenic activity as l-ephedrine.

I assume that ephedrine increases the body temperature by 2 degrees Fahrenheit, but shouldn't this be spelled out?

Ephedrine was NEVER banned in the United States, Ephedra was. I think it is important to make this distinction in the article. The stack was most commonly "built" with Ma Hung or similar standardized for 25mg ephedrine alkaloids. The ban was for supplements on dietary supplements containing ephedrine alkaloids. Volksgeist 14:47, 26 March 2006 (UTC)[reply]

I've made a couple small changes to the page. Ephedrine was never banned and can legally be purchased with (or without) an expectorant. For example D&E Pharm sells pure Ephedrine HCL, although you must show ID to purchase. Ephedrine has always been able to be legally purchased OTC in products such as Bronchaid. Many companies that sell "bodybuilding" products started selling Ephedrine HCL (with an expectorant) -- such as VasoPro and BioTek. Although the ephedra ban was lifted I've seen very few products still being sold that contain ephedra alkaloids (most likely because of the fear of lawsuits). Volksgeist 14:54, 26 March 2006 (UTC)[reply]

You guys sure? AFAIK the regulatory change was just to prohibit marketing ephedrine (or ephedra) as a weight loss / performance supplement (as its uses for asthma kept it on the market), but it's been a while since I read the FDA ruling. Some states have more intrusive bans, such as mine which requires ephedrine to be sold with guaifenesin.

fahrenheit/celsius?

I assume that ephedrine increases the body temperature by 2 degrees Fahrenheit, but shouldn't this be spelled out?

pseudoephedrine

The article states: "ephedra (an herb which contains both ephedrine and pseudoephedrine)..."

I do not believe the herb ephedra contains pseudoephedrine. As its "pseudo" name would imply, I believe that, by definition, pseudoephedrine is a synthetic version of the naturally occuring substance ephedrine, and does not occur naturally in any substance, herbal or otherwise. —The preceding unsigned comment was added by 68.199.66.14 (talk) 16:03, 31 March 2007 (UTC).[reply]

No, ephedra contains ephedrine, pseudoephedrine and N-methylephedrine as it's main alkaloids. The pseudo- prefix has nothing to do with whether something is synthetic or not. In chemisty, pseudo is used to denote a stereoisomer of a substance that has no trivial name. Pseudoephedrine is a stereoisomer of ephedrine (the threo isomer, ephedrine is the erytho isomer). There is no such thing as a "synthetic version" as both a natural substance and the same substance made synthetically are chemically identical. 1.1.1 01:50, 3 April 2007 (UTC)[reply]

^^^Correct. The pseudo part is just related to shape of the molecule. It is made commercially in bioreactors using yeast cultures, which produce L-Pac; the precursor. They use this method, rather than extracting the plant, because large amounts of it are sold in the form of controlled cough medicine (you need to speak to the pharmacist not the server and, if you're in the US, sign a book). There are limits on the sale quantities and pharmacists watch for repeat customers, as it is a well known precursor to meth.

See this that I added to the Thermogenics article.

Themogenics is also the practice of deliberately exposing the body to very cold temperatures to raise Basal Metabolic Rate (BMR). This is usually done by soaking the body in icy cold water until a person can not tolerate it any longer almost to the point of inducing hypothermia. This then causes a release of thyroxine from the thyroid gland by means of the sympathetic nervous system thus raising BMR resulting in an overall increase in body temperature. The ancient Vikings used to practice this method of thermogenics. This method of thermogenics combinded with the ECA Stack mentioned above will produce a very powerful thermogenic responce. Dr CareBear 07:13, 12 July 2007 (UTC)[reply]

Reliable sources? MastCell ^Talk 16:51, 12 July 2007 (UTC)[reply]

Quick question

Could someone please explain to me why aspirin is used in the stack in place of other NSAIDS/COX inhibitors such as Ibuprofen and acetominophen? I realize that aspirin is an irreversible inhibitor of COX, and would mostly like work longer because more enzymes would have to be made to reverse its effects, but by the logic presented in the article, couldn't other reversible inhibitors contribute the same effect? Would a regimen of aspirin staggered out with tylenol and ibuprofen increase the thermogenic effect? It is nearly impossible to find good information online, because everyone has their own anecdotal evidence with NO FACTS to ever back it up. -wamerocity

I will say only that acetaminophen is neither an NSAID nor a COX inhibitor. Beyond that, you might want to try the reference desk. MastCell ^Talk 00:45, 15 February 2009 (UTC)[reply]

I would bet that a fair number of people who experimented and developed this stack were also using oral anabolic steroids and prohormones that put alot of stress on the liver. The use of ibuprofen or acetominophen would be out of the question. —Preceding unsigned comment added by 68.188.247.232 (talk) 20:24, 2 May 2009 (UTC)[reply]

Well, ibuprofen doesn't "stress the liver"; its side-effect profile differs significantly from that of acetaminophen. Again, try the reference desk, or consider looking for a useful source for the article. MastCell ^Talk 18:32, 4 May 2009 (UTC)[reply]

Factual Accuracy?

What, exactly, is up for debate here?

What is lacking factual accuracy?

Greggor88 (talk) 16:56, 4 May 2009 (UTC)[reply]

Recent edits

I searched around and it seems like there are a hundred studies of caffeine/ephedrine or caffeine/ephedra but very very few studies that even include an aspirin component. And of those, fewer still compare ECA to EC to see how much effect the aspirin has or vary the amount of aspirin or try aspirin substitutes. It's safe to say ECA is proven to work well, but based on the two relevant studies I was able to find, it is *not* safe to say that ECA works better than EC. If we go outside the medical literature and look at discussions in the forums, it seems like people nowadays are recommending the Aspirin either be skipped altogether or minimized. I've updated the article to include some of this. --Blogjack (talk) 03:00, 2 August 2009 (UTC)[reply]

I have a major problem with these edits. You're citing isolated studies from the primary literature to argue that ECA is safe, when the general consensus at present is otherwise. Notice that virtually all of the studies you're citing are from the 1990s? These studies were conducted before the health risks of ephedra were fully recognized or understood. When it became apparent that ephedra was killing people, and the supplement was banned, research on ECA dropped off somewhat. It seems misguided (not to mention a violation of our sourcing guideliens) to cite this dated and obsolete literature in isolation, without acknowledging that ephedra was subsequently found to be extremely dangerous.

The best example of the problem with this approach is your citation of the dexfenfluramine study. You approvingly cite a study suggesting that dexfenfluramine boosts weight loss, from the 1990s. Perhaps you're unaware that dexfenfluramine was later found to cause valvular damage and death, and was withdrawn from the US market. Yet here we're presenting research from the 1990s in isolation, without acknowledging a key intervening event, which creates a misleading and dangerous article. See, if I selected a few citations from the 1990s, I could write a Wikipedia article claiming that dexfenfluramine was the greatest thing since sliced bread, and was highly effective for weight loss. Those studies exist. But it would be wrong, because we need to reflect reality in the form of subsequent knowledge of the dangers of these drugs. MastCell ^Talk 05:06, 2 August 2009 (UTC)[reply]

This article *does* in its current state acknowledge the dangers, repeatedly. I even improved and extended the risk section to reference a peer-reviewed study (from 2000) that summarized the risk factors which led to the ephedra ban. Currently this is reference #9, titled Adverse Cardiovascular and Central Nervous System Events Associated with Dietary Supplements Containing Ephedra Alkaloids.

I want the article on ECA to answer, with suitable references: (1) What is ECA, (2) what claims have been made for it? (3) What claims have been made against it? (5) what's the current legal status? The current article does that while the previous version did not - in your enthusiasm to emphasize the dangers you were needlessly vague about the claims and supporting evidence on *both* sides. This is an encyclopedia article, not a prescription.

The evidence *for* ECA is that we have lots and lots and lots of controlled studies that found it safe and effective with minimal side effects. I have been unable to find even *one* controlled study that found otherwise, and not for lack of searching. If you can find one, please add it. The main limitation of the evidence *for* is that the longest controlled studies are for 6 months; it's still conceivable the positive effects would wane or negative effect would show up if taken for many years. (though the Denmark prescription study suggests not).

The evidence *against* ECA is that among a vast pool of consumers who were self-medicating using an unknown combination of drugs in unknown quantities, some of which were of unknown purity, there were a significant number of health issues reported to the FDA as plausibly related to ephedrine or ephedra overdose. The main limitation of the evidence against is that it wasn't controlled. We *can* say from that evidence that when you let manufacturers put whatever they want in a pill and make whatever claims they want about it in a health-food store, some people will probably overdose and die. But we *can't* attribute those deaths to any particular formulation or dosage regime. So we know enough to be concerned, but not nearly enough to be certain that the prior studies were wrong. --Blogjack (talk) 15:21, 2 August 2009 (UTC)[reply]

As per your suggestion and the sourcing guidelines I have replaced all but one of the abstract-only 1990s study references with references to more recent (post-2000) full-text articles which generally cover the earlier ones as part of their review. The most important new ref I've added is probably this Danish one: http://aje.oxfordjournals.org/cgi/content/full/168/8/966 Fully aware of the prior controversy, based on a huge case-control study, the study authors concluded: Our main finding was that prescription of an ephedrine/caffeine product was not associated with adverse cardiovascular outcomes. This was found across a wide range of patient subgroups, different cardiovascular outcomes, different assumptions about exposure, and different utilization patterns. They later criticize drawing strong conclusions from "spontaneous reporting schemes" and add - this is in 2008, mind you - that The few controlled clinical studies that have been conducted—including ours—have failed to demonstrate any cardiovascular toxicity of ephedrine. It doesn't matter whether you look at studies from the 1990s or from the 2000s, the conclusion is the same. As a drug, ECA is quite plausibly a great one for a great many people; as an uncontrolled supplement, FDA was within their rights to decide it was problematic. Why can't the article say both of those things? --Blogjack (talk) 17:31, 2 August 2009 (UTC)[reply]

another of the new studies I've added (from 2002: http://www.nature.com/ijo/journal/v26/n5/full/0802023a.html) tries to reconcile their findings like so: How can the absence of treatment-related adverse events in this and two previous clinical trials of ephedra combinations (334 subjects in total) be reconciled with the adverse event reports collected by the FDA from users of these products? Possible explanations include coincidence, pre-existing pathology, non-recommended usage and increased individual sensitivity. --Blogjack (talk) 19:13, 2 August 2009 (UTC)[reply]

Dude. We do *not* need to mention the ban and alleged risk of death in every single section of the article. One or two places should suffice. And there's nothing wrong with mentioning that ephedrine is legally available for other purposes. It's only illegal in a very limited context. It's illegal as a supplement; it's still legal as a drug, both prescribed and unprescribed, and that's something people who come read this article might want to know. --Blogjack (talk) 17:42, 2 August 2009 (UTC)[reply]

How risky is ECA, exactly?

Check my math on this. the NEJM estimates 12 million Americans used Ephedra supplements in 1999. If the risk of any reportable adverse effect were as high as 1 in 10,000, we'd expect that much use to produce 1,200 adverse effects per year of which they expect ~15% would actually get reported to the FDA. So we'd expect to see 180 adverse events reported to the FDA per year. The actual number of adverse events recorded was 140 over 21 months = 80/year, suggesting my initial 1-in-10k estimate is too high by about a factor of 2.25. Thus, the chance of a reportable adverse event is closer to 1 in 22,500. ~20% of the actually reported adverse events resulted in death or permanent impairment, so the risk of death-or-disability is: 1 in 112,500, aka 0.0008%. And your risk of specifically being killed from taking ephedra supplement is half of that, or roughly equivalent to the risk of being hit in your home by a crashing airplane. Is that about right? --Blogjack (talk) 18:01, 4 August 2009 (UTC)[reply]

As with your inadvertent advocacy for dexfenfluramine, you're either intentionally or mistakenly omitting significant context which undercuts your argument. The NEJM paper was published in 2000, and summarized reports to the FDA from 1999. Subsequently, in 2002, Metabolife was compelled by the Justice Dept to turn over their adverse-event files. As it happens, they had collected over 15,000 adverse event reports, ranging from insomnia to death, which they withheld from the FDA. So the calculations in the NEJM article were major underestimates, as Metabolife had short-circuited the FDA reporting process by intercepting adverse-event reports and suppressing them. Do the calculations again, if you'd like, using the real numbers.

A more useful statistic is, of course, readily available - ephedra accounted for 64% of the herbal adverse events in the US, despite making up only 0.82% of herbal sales (PMID 12639079). Ephedra was dramatically riskier than other herbal supplements, which themselves have very checkered safety records (cf. kava). If you're interested in what reliable sources have to say, and in accurately representing relevant context rather than cherry-picking numbers that are well-known to be outdated and erroneous, then let's talk. It would be a more useful way to go rather than simply using this platform to claim that ephedra is safe. MastCell ^Talk 22:43, 4 August 2009 (UTC)[reply]

If House Report is accurate, Metabolife had 114 incidents that should have been reported to the FDA, including 3 new deaths, over 5 years. Reworking the figures as if the FDA saw all of those but leaving everything else the same produces an ephedra risk of "adverse events" of 1 in 13,592 (0.0073%) and ephedra risk of death of 1 in 285,068 (0.000035%) - so we're still in "hit by a crashing plane" territory. We may have to disagree on how useful the herbal supplement comparison stat is.

But to take this back out of OR: what source do you recommend that you think accurately calculates the *actual* risk of death and risk of adverse effects of ECA in its various forms? In terms of probability, I mean. I found a dozen articles that say "we didn't find anything serious but can't exclude the possibility of 1-in-a-thousand risks". I also found articles about the FDA reports but most of them were innumerate, just counting deaths and bad outcomes but not looking at them in proportion to the number of users or the magnitude of their likely net consumer surplus. You clearly think the risk is substantial, but the sources you point to as evidence of this don't really bear that out as far as I can tell. I'd especially like to see a criticism from "the other side" of that huge 2008 Denmark case-control study. I do want to accurately represent relevant context and I really appreciate the sources you've provided so far. It's been informative and the article is already the better for it. --Blogjack (talk) 05:54, 6 August 2009 (UTC)[reply]

Out of respect for the badly abused and battered talk page guidelines, let's agree to disagree, and go back to using this page for its intended purpose. You are free to take that as a complete and unmitigated concession to your correctness if it will move things along. I ask in return only that you read WP:NOT and cease using this page to advance your personal views on the safety of ephedra, and that we return to discussing reliable sources and their content rather than original research. MastCell ^Talk 04:23, 6 August 2009 (UTC)[reply]

Disappointment

How shall I express how infuriated I am with the changes you two have made to this article without compromising my reliability as an editor?

This is the article that I first laid eyes upon when I went in search of knowledge -- when I began researching ECA:

http://en.wikipedia.org/w/index.php?title=ECA_stack&diff=306630724&oldid=251342304

Look at the difference. You transformed an informative, well-written article into a page filled with legal information and a curt mention of ECA and its effects on the human body. You allowed your petty argument over the risks of ECA to utterly compromise your usefulness as editors and publishers of information that many people consult for knowledge.

This article is barren. It isn't even two pages long. A first-time reader would look at it and think the following:

I know what ECA stands for
It could kill me
It looks like it does it what it was designed for
It's vaguely legal? I can't really tell.

Please note that I actually called a passerby to my office to ask his initial reactions to the article. Where are the mentions of its mechanism of effect? How about symptoms and side-effects? Common dosage? Is there anything remotely useful that can be gleaned from the current article?

In conclusion, I guess I can only express my disappointment. I have neither the skills nor the prestige to bring this article back to the useful page it used to be. I can only hope my words have some sort of impact. --Greggor88 (talk) 19:45, 24 August 2009 (UTC)[reply]

That "article you first laid eyes on" was almost entirely composed of unreferenced claims that would require a lot of specialized knowledge to verify so I'm not surprised it got cleaned out and reset. If you've got info you'd like to add to the current version, be bold and add it! Especially if you can give a reference - any reference - to justify what you're adding. I agree the current article is a bit of a mess. I've been meaning to improve it, but I kind of got burned out on the subject after doing a lot of work just to establish that it "looks like it does it what it was designed for" in the face of opposition. FWIW, my research convinced me to try it; I've lost 15 lbs in 3 months so far. --Blogjack (talk) 22:02, 31 August 2009 (UTC)[reply]

Thanks for the encouragement. I will get to work on the article as soon as I have some more free time. FWIW, my research (starting, but certainly not ending with the wiki page that I described) convinced me to also try it. I have lost 38lbs and 8% bodyfat since February by adding ECA, healthier foods, and running to my ordinary workout routine. Greggor88 (talk) 16:38, 2 September 2009 (UTC)[reply]

–––––––––––––––––––––––––– The changes in this article are sad. The changes have been petty and not in the spirit of being more informative. The original article was incredible informative. The edited version is utterly UNinformative. I think the editors need to step back, put the egos in check for the good of the community, and return this entry back to the original version. When I saw the original version months ago, I researched other sources that did not contradict the original version in any material way.JiggyFlyy (talk) 14:58, 21 September 2009 (UTC)USER:Jiggyflyy[reply]

Also Disappointed

The neutrality of this article is kind of botched. While I can say that the majority of articles out there will be politically correct, what about actual statistic for the folks who don't die instantly? Any article that has a "this is bad, mkay" approach will steer people who are going to do this regardless to an article that has no balanced information WITH warnings. —Preceding unsigned comment added by 167.211.190.10 (talk) 21:15, 14 January 2011 (UTC)[reply]

Just curious

as to why even basic information such as the ratio of ingredients in the ECA stack (20 mg ephedrine/200 mg caffeine/325 mg aspirin) is neglected in the article?

No criticism intended, you guys work hard on these articles, just curious as to the sparsity of information. —Preceding unsigned comment added by 69.227.94.182 (talk) 15:01, 11 September 2009 (UTC)[reply]

Beginning to Edit

As promised long ago, I'm beginning work on this page. It will mostly consist of adding information, since the article is really quite barren. First order of business - information on the mechanism of action of the Ephedrine, Caffeine, and Aspirin combination in particular. I hope no one objects if I pull relevant data from the Ephedrine page, Caffeine page, and Aspirin page? Greggor88 (talk) 19:53, 20 November 2009 (UTC)[reply]

History? Cites for claimed mechanism of action?

What's the history of this thing? Who first thought this was a good idea? - David Gerard (talk) 11:56, 13 June 2010 (UTC)[reply]

Also: I've looked at the article version linked above, the one with a detailed claimed mechanism but no references. I figured that we could reasonably put in a claimed mechanism of function, if we could find quality references for that, even if there's a remarkable lack of scientific evidence that the stack actually works. (Although I've found lots of claims that "it's scientifically proven!" without links to said science.)

I can find very little, and what I can find gives different mechanisms. And it's mostly terribly low-quality stuff on people's random web pages or eHow articles or FAQs that misspell "freqently"[sic]. The more I look into this, the more it appears to be made entirely of broscience.

Is there any even slightly citable source for a claimed mechanism of action, even if scientifically unproven? At least we could inform the reader with that - David Gerard (talk) 13:12, 13 June 2010 (UTC)[reply]

No-one got anything, then? - David Gerard (talk) 17:50, 27 June 2010 (UTC)[reply]

[tumbleweeds.gif] - David Gerard (talk) 10:07, 1 August 2010 (UTC)[reply]

After two months of nothing, I've added to the article that there is no single mechanism claimed by proponents, let alone scientifically verified - David Gerard (talk) 09:56, 16 August 2010 (UTC)[reply]

I'm just reading The 4 Hour Body by Tim Ferriss. He claims the ECA stack is scientifically proven. His only citation? A link to that old version of this article, covered in "citation needed"! AAAAAAAA - David Gerard (talk) 23:49, 10 February 2011 (UTC)[reply]

How about this for a reference for a mechanism? It seems pretty well sourced in the references section: http://www.mesomorphosis.com/articles/haycock/ephedrine-and-beta-adrenergic-receptors.htm —Preceding unsigned comment added by 72.195.150.18 (talk) 12:49, 18 March 2011 (UTC)[reply]

David Gerard, I found a study discussing the mechanism of action of the stack in rats. http://escholarship.org/uc/item/6zh730fw#page-1 The author concludes that there appears to be some homology between the effect in rats and humans, but that it is controversial. I believe this is enough for us to include the mechanism of action description as provided in the old version of this page as long as we note that the mechanism is still disputed in humans.

As a side note, I may be misreading your comment on 11 February 2011, but I hope you're not trying to claim that the efficacy of the stack is unproven. There are numerous studies that conclude that EC(A) has a noteworthy effect on fat loss. Here is one such study: http://care.diabetesjournals.org/content/30/5/1179.abstract?cited-by=yes&legid=diacare;30/5/1179 The ECP group was taking 25mg Ephedrine HCl and 200mg Caffeine thrice daily and lost 6% body fat when compared to the placebo group. There are other references already sourced in the article. Please contact me directly if you have any questions or comments. I find it difficult to keep track of article discussion pages. Greggor88 (talk) 21:05, 9 November 2011 (UTC)[reply]

Athletic Performance

One thing missing from this page is the status of the drug wrt WADA. I believe it is a banned stimulant, which is not mentioned! — Preceding unsigned comment added by 178.111.197.37 (talk) 16:12, 5 January 2012 (UTC)[reply]

Anders Breivik

Should there be a mention that Anders Breivik used this stuff to give him a bit of a buzz during his killings? See: http://www.bbc.co.uk/news/world-europe-18282760

No. No there shouldn't. If we included every minor instance of somebody using X drug while doing Y, the articles for every drug would be a mile long. Greggor88 (talk) 00:40, 19 June 2012 (UTC)[reply]

Please cite these claims

There's a heck of a lot of uncited claims here, particularly around mechanism (where I see there's yet another uncited mechanism) and effectiveness (where there's uncited claims directly opposed by actual cited research). This article has had uncited claims of mechanism removed several times over the years - a different mechanism each time, to boot.

What it needs for mechanism claims is something that specifically addresses the claim that the ECA stack does what is claimed of it - not cites for each piece, these pieces then strung together as original research. That is, cites that specifically say they are about the ECA stack itself - David Gerard (talk) 20:43, 29 March 2013 (UTC)[reply]

I asked at WikiProject Medicine, and they concurred that no claim beats uncited or wrong claims. So I'm moving these here. Remember, the citations (to WP:MEDRS standards) need to actually be about the ECA stack itself, not cites for things that you could only put together into being about the ECA stack through original research:

===Mechanism===

Ephedrine indirectly stimulates the adrenergic receptor system, which is part of the sympathetic nervous system (SNS), by increasing the activity of noradrenaline at the post-synaptic α- and β-receptors. Noradrenaline affects parts of the brain, such as the amygdala, where attention and responses are controlled. Norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. It increases the brain's oxygen supply.^{[citation needed]}

Caffeine antagonizes the adenosine receptors nonselectively, along with the adenosine receptor A2a. The adenosine receptor A2a suppresses neurotransmitters such as glutamate, epinephrine, norepinephrine, dopamine, acetylcholine, and to a lesser extent, serotonin. Consumption of caffeine can increase these neurotransmitters. There has also been conclusive evidence that caffeine inhibits acetylcholinesterase, an enzyme that breaks down acetylcholine. For this reason, Caffeine enhances noradrenaline.^{[citation needed]}

One marketing claim made for the ECA stack was that it would increase athletic performance. Studies in the medical literature generally support this claim.^{[citation needed]} While a wide degree of variability exists as to the specific effects seen, preparations containing all three ingredients in the proper dosages have all shown positive effects on increasing workload and decreasing perceived exertion. Experts recommend taking a one week 'washout period' following ECA cycles.^{[citation needed]} but these are generally done with subjects who have already built up a tolerance to stimulants through the use of caffeine and/or caffeinated beverages.^{[citation needed]} To be successful, a washout week should contain no caffeine or ephedrine of any form in order to achieve best results.^{[citation needed]}

-David Gerard (talk) 14:46, 30 March 2013 (UTC)[reply]

Someone's just added some more claims as to the components, not the stack, plus a recipe which they say is "common knowledge". That would be relevant and useful if it is, so surely there should be verifiable citations that this is the recipe - David Gerard (talk) 08:27, 1 September 2013 (UTC)[reply]

Mechanism - original research again?

AlexEng added a claimed mechanism for the ECA stack here. This appears to be a series of studies about the components, and one about ephedrine combined with caffeine.

Notably, none of the references I could see are about the ECA stack itself. This looks very like original research.

This has been a problem plaguing this article, per the above discussion going back many years. I've found multiple claimed mechanisms for the stack, all in unreliable sources ... and all different!

AlexEng - where did you find this explanation of the stack? - David Gerard (talk) 10:50, 19 August 2022 (UTC)[reply]

@David Gerard: did you read the cited sources? I spent my spare time over the course of roughly three days back in January reading about a dozen studies and drafting that section based only on those facts that were supported in the peer-reviewed journals. Frankly, I don't remember all of the details of this project, as I didn't take very many notes. In particular, obtaining free and legal access to each of the studies (including ones I tossed that looked initially promising but were ultimately irrelevant to the subject matter) took a colossal amount of time, and I'm not eager to repeat the process. Please review the cited journals yourself before stating that they are 1) original research, and 2) unreliable sources. I'm happy to talk specifics regarding any issues you identify in your review.

Some of the cited sources describe the action of each component of the stack and some describe the interactions of the components and the effective action of the stack as a whole. In a section describing mechanism of action of a drug cocktail, it is appropriate to describe the salient parts of each component's action prior to describing the effects of the combination itself. If you have a better proposal, I would be happy to work together to improve the content.

One final note: I am rarely active on Wikipedia at this time due to pressure at work. Please be patient with me if further dialog is needed. The best way to draw my attention is by sending an email from the link in the note on my talk page. Even in that case, it might take up to a day to respond. Thank you, David! AlexEng^(TALK) 19:13, 19 August 2022 (UTC)[reply]

No, the "original research" is your synthesis of these papers. The actions you describe yourself taking are simply just WP:SYNTH, in Wikipedia terms - that you combine material from multiple sources to reach or imply a conclusion not explicitly stated by any source.

Could the section be written to make statements about the ECA stack - not its components, but the ECA stack as a whole - only in terms explicitly stated by any source?

You say some speak specifically of all three parts of ECA together in combination in the same place? If so, you didn't quote them or note those parts - David Gerard (talk) 22:05, 19 August 2022 (UTC)[reply]

I know what SYNTH is. This is not the case here. I'll again reiterate my request that you read the actual papers before claiming it's OR. All of the referenced content in the article is sourced to studies that discuss the stack. Even the parts that discuss the secondary components (Aspirin and Caffeine) are from studies that deal with their combined use with Ephedrine. Nowhere did I combine material to reach or imply a conclusion not stated by any source. If that's what you really think, then please point out what specific conclusion(s) you think are unsupported. Please use direct quotes from the article. AlexEng^(TALK) 03:04, 22 August 2022 (UTC)[reply]

.