Aspirin, Coffee combination

[teamfatboy]

In this thead Nate said something that got me thinking:

(When doing cardio! :grin: ) I do the same as TFB, more because morning cardio is convenient and coffee helps push my low HR.

The coffee and aspirin thing TFB refers to comes from the old EFA stack, in which I am led to believe the caffeine, ephedrine & aspirin work synergistically to stimulate the CNS, giving more energy use thus increased fat loss. I'm not so sure it works without the ephedrine (which is now a prescription only item), but I'm happy to be proved wrong?

So, what IS the actual value of aspirin and caffeine without the ephedrine? Does the aspirin actually have any utility at all ? I've tried some googling, but the bro'science is thick out there today :roll:

[rose]

Are you at risk of CVD? My quick skim in relation to aspirin is best summed up by:

further studies are needed with a longer duration of therapy

(i.e. inconclusive results). Interested why you're taking it if you don't know why? Personally I'd just stick with caffeine.

[teamfatboy]

Are you at risk of CVD?

Short answer: originally, yes. Having been a bloater of immense proportions til about 5 years ago, there was a higher likelihood of CVD. Now, maybe not so much.

My quick skim in relation to aspirin is best summed up by:

further studies are needed with a longer duration of therapy

(i.e. inconclusive results). Interested why you're taking it if you don't know why? Personally I'd just stick with caffeine.

It was at trainer's suggestion, both for CVD mitigation and for the old ACE econo-fatburner.

[nate225]

Are you at risk of CVD? My quick skim in relation to aspirin is best summed up by:

further studies are needed with a longer duration of therapy

(i.e. inconclusive results). Interested why you're taking it if you don't know why? Personally I'd just stick with caffeine.

Good point.

I always took aspirin as a cheap life insurance policy, to reduce chance of clotting and CV event. However my Doc told me recently that another recent study showed negligible effect, in his words more studies were needed before any benefit could be shown (as per Rose's comment). I'm fairly sure the benefit shown in earlier studies were limited to those that had already suffered a CV event (although I'm not 100% on this). That aside he said keep taking it! :pfft:

However back to TFB's take, if I'm right it was more in reference to enhanced stimulant effect (as with the 'synergistic' 1+1+1 = 4 type deal alleged to occur with ephedrine, caffiene & aspirin)?

I've never seen any research (or even claims really) to suggest aspirin enhances caffiene's effect on the metabolism, however thats not to say it doesn't, I just haven't heard this before. Keen to see any research if it exists??

Nate

[rose]

I always took aspirin as a cheap life insurance policy, to reduce chance of clotting and CV event. However my Doc told me recently that another recent study showed negligible effect, in his words more studies were needed before any benefit could be shown (as per Rose's comment). I'm fairly sure the benefit shown in earlier studies were limited to those that had already suffered a CV event (although I'm not 100% on this). That aside he said keep taking it! :pfft:

That's what I was hinting at re studies in relation to CVD. The studies I found focussed on aspirin as an antiplatelet agent for prevention of CVD, but the study results were inconclusive and results negligible, thus:

further studies are needed with a longer duration of therapy

However back to TFB's take, if I'm right it was more in reference to enhanced stimulant effect (as with the 'synergistic' 1+1+1 = 4 type deal alleged to occur with ephedrine, caffiene & aspirin)?

I've never seen any research (or even claims really) to suggest aspirin enhances caffiene's effect on the metabolism, however thats not to say it doesn't, I just haven't heard this before. Keen to see any research if it exists??

I think it's meant to be the other way around. Caffeine is said to enhance the effect of aspirin. I thought that was the whole point of panadol with caffeine.

http://jcp.sagepub.com/cgi/content/abstract/47/6/715

Caffeine Accelerates Absorption and Enhances the Analgesic Effect of Acetaminophen

http://www.ncbi.nlm.nih.gov/pubmed/9373807

Caffeine did not enhance the analgesic effect of aspirin

:roll:

Boils down to why you're taking it. If professionally prescribed for CVD prevention and you trust your GP's advice then continue taking it. I don't believe it'd have any fat loss benefits. Anything that mentions aspirin and fat loss seems to be based on the ECA stack.

I'd probably look to other things like fish oil for CVD. Gotta wonder what effect regular aspirin intake has on your digestive system.

[nate225]

Good point re: GI tract impact of aspirin. Can give some peeps ulcers etc, although enteric coating stuff is usually presscribed for CVD patients.

Is there solid evidence re: ECA over straight EC? Or is it another myth I've taken for granted?

[Bobsta]

From what i was always told and understood in laymans terms, Asprin was added to the stack as it prolonged the effects of ephedrine and caffeine by increasing body's tolorance to heat, now as i said thats a real basic explanation and it doesnt make much sense to me but here's a little something that might explain it a bit better:

ECA Supplement Stack For Muscle Growth and Fat Loss

by Stimulating the ß-Agonist System - The Role of Ephedrine,

Caffeine, and Aspirin

By Michael C. Prevost Ph.D.

The role of the ß-agonist (beta agonist) pathway in controlling

the body's fat stores, muscle hypertrophy (growth), the body's

response to exercise and even muscle fiber type has been

brought to light in the last 10 years through the efforts of

hundreds of scientists with literally thousands of papers

being published on the subject. Clearly, the ß-agonist pathway

is one of the most important signalling pathways in the body.

To understand how the ß-agonist pathway works and what role

Caffeine, Ephedrine and Aspirin plays in the system one must

first understand what a ß-agonist is and what they do.

On the surfaces of many of the cells of the body (for our

purposes the most important tissues are muscle and fat cells)

are located b receptors. These b receptors bind b-agonists

(adrenaline and noradrenaline). When a ß-agonist is bound

to a b receptor, the receptor initiates a series of chemical

reactions that results in the production of a chemical

messenger called C-AMP. This C-AMP then activates

enzymes that phosphorylate proteins. Why is thisimportant?

Well, many of these proteins are enzymes and

phosphorylation activates some enzymes and de-acitvates

others. In fat cells enzymes are activated that induce

lipolysis (fat breakdown). In muscle cells enzymes are

activated that increase metabolism and cause a host of

other important reactions which control muscle growth, fiber

type and enzyme concentration. So, how do ephedrine,

caffeine and aspirin fit into this pathway? Ephedrine

enhances ß-agonist production and even acts as a

ß-agonist itself. Caffeine inhibits the breakdown of C-AMP.

Aspirin inhibits the negative feedback loop that would

reduce ß-agonist production. So taken together these

agents enhance three to four different steps in the ß-agonist

pathway.

Ephedrine's role as a lipolytic agent (one that breaks down

body fat to be used as energy) has been known for some

time. It has been shown that ephedrine when taken in

therapeutic doses is mildly effective in the management

of obesity. The problem was that the initial lipolytic effects

of ephedrine were soon diminished as other steps in the

pathway were reduced in a negative feedback cycle. In an

effort to enhance these steps that were being

downregulated due to negative feedback, scientists added

caffeine and aspirin to the regime. The result was a very

effective combination in the management of obesity

(dosages given were 20mg ephedrine, 300mg caffeine, and

80mg aspirin, roughly equivalent to one typical ephedrine

tablet, a cup of coffee and one aspirin). In fact, not only

did the results (lipolysis) not decrease over time as with

most drugs, but they actually increased with time. The

effects of the combination of ephedrine, caffeine and

aspirin were categorized into desirable and undesirable

effects. The desirable effects were lipolysis and protein

sparing (subjects on the drug combination retained

more muscle mass while dieting than the subjects on

placebo). Again, these desirable effects did not diminish

over time. The undesirable effects, increased heart rate

and muscle tremors, lasted only a few days and never

returned. In fact, after 1 year of supplementation subjects

were experiencing no side effects but were still

experiencing the desired effects of lipolysis and protein

sparing. To date it has not been determined if the ephedrine,

caffeine and aspirin combination can enhance muscle

growth and fat loss in healthy, exercising adults. However,

based on what we know about the ß-agonist system, it is

certainly possible. It is important to note, however, that a

small handful of subjects among the large subject pool

had to drop out of the study due to an intolerance to the

supplementation regime. So it appears that most

people can use the ephedrine, caffeine and aspirin

combination with no problems, while a small handful of

people may be intolerant. A consultation with a

physician is suggested before beginning this ECA

supplement regime.

The ß-agonist pathway may effect processes other than

muscle sparing and fat loss. In fact in chickens ß-agonists

were shown to be stronger growth promoting agents than

steroids (believe it or not but poultry science folks are

doing a lot of research trying to produce more muscular

chickens since the muscle is the meat that we eat). In fact

ß-agonists seem to produce muscle growth without the

stimulus of exercise, something steroids have failed to

do. However ß-agonists are not as effective in rats and

the effects on humans is unknown. The ß-agonist

clenbuterol can cause slow twitch muscle fibers to

be converted to fast twitch fibers. It can also prevent

muscle atrophy due to disuse. Other studies have shown

that b-antagonists (agents that block b-receptors and

prevent them from functioning) cause muscles to shift

from fast twitch to slow twitch and cause muscle atrophy

(muscle wasting or breakdown). These studies indicate

that ß-agonists might play an important role in the

maintenance of fast twitch muscle fibers and in maintaining

and perhaps increasing muscle mass. It may be no

coincidence then that large amounts of ß-agonists

(adrenaline and noradrenaline) are produced during

high intensity training sessions. Perhaps these

ß-agonists are necessary in initiating the muscle growth

stimulus.

It is important to note that some ß-agonists can be

dangerous (for example clenbuterol and cocaine) and

illegal and these substances are not recommended. Also,

as mentioned earlier, although the ß-agonist combination

of caffeine, ephedrine and aspirin appears to be safe a small number of people are intolerant and

consultation with a physician is suggested.

[rose]

Asprin was added to the stack as it prolonged the effects of ephedrine and caffeine by increasing body's tolorance to heat, now as i said thats a real basic explanation and it doesnt make much sense to me

Makes perfect sense. Aspirin is an antipyretic drug, i.e. used to reduce fever.

[Bobsta]

yea you're right, i just didnt quite understand how by doing so it would prolong the effects of ephedrine and caffein... but that article makes good sense to me

[nate225]

Cheers for that Bobsta!

From what i was always told and understood in laymans terms, Asprin was added to the stack as it prolonged the effects of ephedrine and caffeine by increasing body's tolorance to heat,

Ephedrine

enhances ß-agonist production and even acts as a

ß-agonist itself. Caffeine inhibits the breakdown of C-AMP.

Aspirin inhibits the negative feedback loop that would

reduce ß-agonist production. So taken together these

agents enhance three to four different steps in the ß-agonist

pathway.

That said it would appear that aspirin would still inhibit the -tive feedback while caffiene inhibits C-AMP breakdown without the ephredrine acting as a beta agonist.

So backl to TFB's oringinal question would this equate to aspirin & caffeine being more effective than caffeine on it's own as a 'fat burning' supplement?

[Nik Antunovich]

Correct me if I'm wrong but...

Going by the above article I understand that the aspirin was only used to stop the negative feedback loop that ephedrine had over a period of use by itself. Caffeine only inhibited C-AMP breakdown and did not seemingly interact with the other drugs.

So, caffeine is still going to inhibit C-AMP breakdown. Since aspirin was only used to counter the effects of ephedrine, assuming there are no other reasons for ß-agonist reduction or other effects of the asiprin, I would say there is no reason to stack aspirin with caffeine without stacking ephedrine also.

Therefore, caffeine by itself is likely to be as effective as stacking caffeine and aspirin in reducing body fat and inhibiting atrophy/maintaining protein sparing.

To answer the question, from the above deduction, caffeine and aspirin would not be more effective as taking caffeine by itself.

[rose]

I don't believe it'd have any fat loss benefits. Anything that mentions aspirin and fat loss seems to be based on the ECA stack.

from the above deduction, caffeine and aspirin would not be more effective as taking caffeine by itself.

That was my take on it, but you said it better.

So back to TFB's oringinal question

Scope kinda expanded to include CVD when TFB mentioned he was taking aspirin for that reason as well.

If you believe there are CVD prevention benefits then take it, but I wouldn't get hopes up re fat loss. If anything it probably makes you fat :shock:

[teamfatboy]

Wow - that's exactly the kind of discussion that makes this so valuable... thanks Rose, Nate, Bobsta and Nik.

Thanks to the clear way you put the facts, you've convinced me that the aspirin is not going to improve the effects of the caffeine, and since it's not required on other grounds, there's no reason to continue it. In fact, the risk of ulcers etc contra-indicates it, even before the effects of diminished analgesic response are considered.

Appreciate the time and assistance.

[nate225]

Correct me if I'm wrong but...

Going by the above article I understand that the aspirin was only used to stop the negative feedback loop that ephedrine had over a period of use by itself. Caffeine only inhibited C-AMP breakdown and did not seemingly interact with the other drugs.

So, caffeine is still going to inhibit C-AMP breakdown. Since aspirin was only used to counter the effects of ephedrine, assuming there are no other reasons for ß-agonist reduction or other effects of the asiprin, I would say there is no reason to stack aspirin with caffeine without stacking ephedrine also.

Therefore, caffeine by itself is likely to be as effective as stacking caffeine and aspirin in reducing body fat and inhibiting atrophy/maintaining protein sparing.

To answer the question, from the above deduction, caffeine and aspirin would not be more effective as taking caffeine by itself.

Yeah sounds about right, my take was more on using caffeine to inhibit C-AMP breakdown and whether this increased level of C-AMP (as compared to no caffiene use state) led to negative feedback in itself (and could justify aspirin use to somewhat negate) or the negative feedback was totally due to the actions of the ephedrine?

Would be nice if someone could commit $50K to run a trial and finally answer the question! :grin: Alternately any up to speed biochemists might know more about this pathway and be able to finally put it to bed?

[Nik Antunovich]

Would be nice if someone could commit $50K to run a trial and finally answer the question! :grin: Alternately any up to speed biochemists might know more about this pathway and be able to finally put it to bed?

I've already given my 10c!

The only bio-chemists I know all have their head in DNA rather than anything remotely useful to what we do on here. They are f'n weido's for the most part, I'm just waiting for a US style shooting to happen here in NZ.

[nate225]

Would be nice if someone could commit $50K to run a trial and finally answer the question! :grin: Alternately any up to speed biochemists might know more about this pathway and be able to finally put it to bed?

I've already given my 10c!

The only bio-chemists I know all have their head in DNA rather than anything remotely useful to what we do on here. They are f'n weido's for the most part, I'm just waiting for a US style shooting to happen here in NZ.

LOL whats your background Nick?

I've done some undergrad organic biochemistry but it's all a bit of a blur nowdays! :grin:

[Nik Antunovich]

Noting special. Been through uni with a focus on the sciences. At uni now doing some postgrad stuff. Will probably finish my MSc next year, if I can be asked going without a wage for much longer. Focus has been on wine related chemistry, oenology. It's all very simple to that biochem stuff. Problem with biochem, especially parts of it like DNA rep, is that even though there is some good theory around it is often getting broken down every few years and re-written. In a living system things are so damn complex compared to a chemical solution. So many more variables. I really take most biochem tongue in cheek as I know and feel we'll have to unlearn it down the track at some point. Also, when genetic variables are thrown into the equation it becomes even worse.

[nate225]

Good to know Nik,

I'll add you to the list of people to annoy when I want a research article :grin: (as I no longer have access to the databases)!

Uni's a good time and learning new stuff in all fields is something I enjoy, however as you say there comes a time when paying bills gets in the way! :nod:

[Nik Antunovich]

Nate, annoy me any time. The gym is time out for me and an important part of my lifestyle. It's what I do to relax but I do take it fairly seriously so any learning to do with it is always a bonus. Hope I can help at some point.

[KRS1]

The goal of the ECA stack is to increase the levels of c-AMP.

Ephedrine does this by increasing the production of c-AMP.

Caffiene does it by inhibiting the break down of c-AMP.

Asprin prolongs the action of both drugs by preventing the body from realising it has elevated c-AMP levels.

The body likes homeostasis, keeping things the same. When drugs like ephedrine or caffiene cause an increase in c-AMP levels the body recognises this and takes steps to reduce c-AMP levels back to normal. This process is commonly refered to as a negative feed back loop. Asprin disrupts this feed back loop so the body does not attempt to fight the actions of ephedrine and caffiene.

As caffiene does raise c-AMP levels on its own, adding asprin will prolong its effects. Asprin should prolong the action of any drug that raises c-AMP.

On another note, as a legal alternative to ephedrine, try 1,2 dimethylamylamine. Also known as geranamine or DMAA it is a powerful stimulant of norepinephrine production (just as ephedrine is), norepinephrine will in turn cause the increase in c-AMP production.

[nate225]

The goal of the ECA stack is to increase the levels of c-AMP.

Ephedrine does this by increasing the production of c-AMP.

Caffiene does it by inhibiting the break down of c-AMP.

Asprin prolongs the action of both drugs by preventing the body from realising it has elevated c-AMP levels.

The body likes homeostasis, keeping things the same. When drugs like ephedrine or caffiene cause an increase in c-AMP levels the body recognises this and takes steps to reduce c-AMP levels back to normal. This process is commonly refered to as a negative feed back loop. Asprin disrupts this feed back loop so the body does not attempt to fight the actions of ephedrine and caffiene.

As caffiene does raise c-AMP levels on its own, adding asprin will prolong its effects. Asprin should prolong the action of any drug that raises c-AMP.

On another note, as a legal alternative to ephedrine, try 1,2 dimethylamylamine. Also known as geranamine or DMAA it is a powerful stimulant of norepinephrine production (just as ephedrine is), norepinephrine will in turn cause the increase in c-AMP production.

That was my chain of thought KRS1, maybe some value to using A with C but to a much lesser degree than when with EC or even E on its own.

Maybe a case of risk vs. reward (as Rose mentioned earlier many people find A hard on GI tract).

Re: the DMAA (I'm aware I'm going off point here), anecdotally this has shown some great results, however I'm unaware of contraindications yet. Seems to be a relatively new product in this arena, I'd say potentially good tool but buyer beware (and do some research!). Can't be worse than BZP! :pfft: