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Ideal ratio for the ephedrine/caffeine/aspirin combo?

Rhadam said:
False. Aspirin actually has some nice benefits.
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jswain34 said:
Its line 5 bucks for a **** ton of pills, why not just get them?

Prostaglandins (increase with EC) inhibits cAMP i believe, which will reduce the goal of lipolysis due to the role that cAMP plays in the mobilization and degredation of triacylglycerols -> diacylglycerols -> monoacylglycerols -> fatty acids that are moved into the mitochondria with the help of serum albumin (transport in blood) as well as carnitine (transport across mitochondrial membrane) to be oxidized for fuel.

The aspirin reduces the prostaglandins that reduce the cAMP activation.

Basically, the aspirin isn't useless. And with how cheap it is, why not just include it?
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Invalid Link Removed, if anything, for most of the members of this board.
 
Cinn said:
Invalid Link Removed, if anything, for most of the members of this board.
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Once again, with how cost to pill ratio being SO low...why not just use it and squeeze out any potential benefit?

Im not going to read that study right now, but thats my opinion at this point.
 
So do we have to use aspirin if using EC stack (or are there any benefits)? Been doing EC by itself the whole time...

EDIT: Oh nevermind, gotta read before posting...
 
Any point to dosing EC once a day if wanting to have the energy/ metabolism support while on lean bulk? I've recomped nicely on 2-3 servings a day but I feel like I can't really get the size I want on it. But don't wanna give it up entirely :D
 
chedapalooza said:
Any point to dosing EC once a day if wanting to have the energy/ metabolism support while on lean bulk? I've recomped nicely on 2-3 servings a day but I feel like I can't really get the size I want on it. But don't wanna give it up entirely :D
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Lots of powerlifters I know irl use a standard dose of EC preworkout. The only problem is that it might reduce your appetite and that might not be good if you have a hard time getting calories in.
 
jswain34 said:
Once again, with how cost to pill ratio being SO low...why not just use it and squeeze out any potential benefit?

Im not going to read that study right now, but thats my opinion at this point.
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Aspirin is not so benign as to be considering only the cost in one's decision to use it as part of an EC stack. Even at small doses there is a risk of GI problems such as ulcers and decreased small bowel blood flow, and it has an effect on platelet function.
 
Cinn said:
Aspirin is not so benign as to be considering only the cost in one's decision to use it as part of an EC stack. Even at small doses there is a risk of GI problems such as ulcers and decreased small bowel blood flow, and it has an effect on platelet function.
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I'd just use a baby aspirin.
 
For those who have used bronkaid as their E source, did you ever get shortness of breath between doses (6-8 hours post dose?) I'm currently only using 25mg (down from 50mg daily) to rebuild some tolerance. I think the absence of a second dose is causing shortness of breath. I cannot recall this happening when I came off last time (a year ago) Any thoughts? I've read that this is a normal reaction to lowering the dose/coming off
 
chedapalooza said:
For those who have used bronkaid as their E source, did you ever get shortness of breath between doses (6-8 hours post dose?) I'm currently only using 25mg (down from 50mg daily) to rebuild some tolerance. I think the absence of a second dose is causing shortness of breath. I cannot recall this happening when I came off last time (a year ago) Any thoughts? I've read that this is a normal reaction to lowering the dose/coming off
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Yes, the b2 adrenergic receptor downregulates in the trachea as a result of chronic stimulation. No big deal really
 
mr.cooper69 said:
Yes, the b2 adrenergic receptor downregulates in the trachea as a result of chronic stimulation. No big deal really
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Damn, should I go back to 50mg or cycle off for a week? It's odd, I can breathe fine working out, but when I'm at rest is actually when it's most noticeable.. Feels like I'm "forgetting" to breath

Edit addition:
I've been at 25mg bc I wanted to lower tolerance without coming off entirely (long hours w school and coaching and work and not trying to crash and burn) I was planning on staying at 25mg daily for all of September then kicking it back to 50mg daily to the end of December (24 weeks total) before taking several months off. Thoughts coop? I'm not opposed to coming off for 7-10 days if you think it will help. But I've read it's relatively pointless/not necessary to stop
Again, I am using bronk, not straight eph hcl
 
Bump: I decided I will cycle off for a week beig that I've been on 25mg for about 3 weeks. I will just come off entirely and hopefully when I start back on 50mg after a week I will feel better.
 
Ephedrine sulfate is 77% ephedrine so 19.2 mg ephedrine per 25 mg tab the rest is sulfur obv (that's where the sulfate part of the name comes from). Forget the percent HCl is put but I think its like 20.5 mg ephedrine per 25 grams ephedrine hcl
 
chedapalooza said:
Bump: I decided I will cycle off for a week beig that I've been on 25mg for about 3 weeks. I will just come off entirely and hopefully when I start back on 50mg after a week I will feel better.
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You can also just take ketotifen to upregulate the b2 receptor
 
Ketotifen is a second-generation noncompetitive H1-antihistamine and mast cell stabilizer with a half life of around 12 hours. Due to its antihistiamine properties, it will bring down regulation of the beta receptors to a halt which we delve into more eventually. It is most commonly sold in as a salt of fumaric acid, ketotifen fumarate, and is available in two different deliveries. We as weekend warriors want to use its oral form, which is used to prevent asthma attacks. Side effects include drowsiness, weight gain, dry mouth, irritability, and increased nosebleeds, appetite, change, diarrhea, chills, increased sweating and insomnia. (Invalid Link Removed)
Ketotifen Inceases LBM

Individuals with wasting syndrome lose muscle aka lean body mass rather than body fat which is due to the lack of anabolic hormones in their body. Several possible alternatives to the approved drugs for AIDS-related wasting are discussed, one of them being Ketotifen. TNF inhibitors prevent inflammation from causing diseases such as Chron’s disease. As a reminder, inflammation is the biggest cause of all diseases. TNF-inhibitors also increase hunger as a decrease inflammation tends to lead in an increase in metabolic rate. This would make perfect sense since an elevated metabolic rate is associated with a healthy immune system. A study combining ketotifen and oxymetholone, the oral anabolic steroid, was presented at the Ninth International AIDS Conference. Preliminary data from a study combining ketotifen and oxymetholone showed that 18 out of 22 patients gained an average of 11.4 pounds after treatment of an average of 3.9 weeks. Sure it was not ketotifen alone, but considering their state of condition, it sure did not counter the effects of oxymetholone. (Smart T. GMHC Treat Issues. 1995 May;9(5):7-8, 12.)

Ketotifen may prove as another form of HRT

The aim of this study I came across was to identify the sites of the inhibitory action of TNF-alpha (tumor necrosis factor alpha) on LH/hCG injections-stimulated testosterone formation. By using cultured porcine Leydig cells as a model, TNF-alpha was shown to inhibit testosterone secretion when testicular cells were stimulated with hCG but not when incubated with 22R-hydroxycholesterol (a cholesterol substrate derivative that readily passes through cell and mitochondrial membranes). Such an observation suggested that the cytokine may affect cholesterol transport and even the availability to cytochrome P450scc in the mitochondria. Specifically, we report here that TNFalpha reduced in a dose- and time-dependent manner hCG-induced StAR (steroidogenic acute regulatory protein) levels. The maximal and half-maximal effects were obtained with 20 ng/ml and 1.6 ng/ml of TNFalpha, respectively. Maximal inhibitory effects of TNFalpha on StAR messenger RNA and protein levels were obtained after 48 h of treatment. Additionally, the presence of TNFalpha receptors P55 in terms of protein (identified through cross-linking experiments) and messenger RNA (identified through RT-PCR analysis) suggested that the effects of the cytokine are directly exerted on the testicular steroidogenic cell type. So in essence TNF alpha as it rises lowers levels of testosterone. Since, ketotifen is a TNF alpha inhibitor; it may indirectly increase testosterone levels quite substantially; especially if one may be at stake for waste syndrome. (Mauduit C, et.al Endocrinology 1998 Jun;139(6):2863-8)

I am going to take it one step further and show documentation of a study in which testosterone injections LOWERED levels of TNF alpha in hypogonadal men. Testosterone has immune-modulating properties, and current in vitro evidence suggests that testosterone may suppress the expression of the proinflammatory cytokines TNFalpha, IL-1beta, and IL-6 and potentiate the expression of the anti inflammatory cytokine IL-10. That is not to say that testosterone does not suppress the Immune system. When testosterone gets to high the body starts to produce less auto immune hormones to make more anabolic hormones. Back to the study; researchers reported a randomized, single-blind, placebo-controlled, crossover study of testosterone replacement in the form of Sustanon 100 vs. placebo in 27 men ranging in age from 53 to 71 years old with low levels of total and free testosterone. When the men were injected with testosterone, levels of TNF alpha and IL-1 beta dropped notably. Levels of cholesterol had also dropped significantly which shows the heart protective properties of keeping TNF-alpha under control. In conclusion, testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol. Twenty of these men had established coronary disease, and because total cholesterol is a cardiovascular risk factor, and pro inflammatory cytokines mediate the development and complications associated with atheromatous plaque, these properties may have particular relevance in men with overt vascular disease. Another reason why a study in the future should be done on Ketotifen and its affects on sex hormones, I predict good things to come from a study of that kind. If you ask me, I will tell you it’s one heck of a drug and should be used in pct, not only because of its positive effects on testosterone but also IGF-1 which we will get into next. (Malkin CJ et.al. J Clin Endocrinol Metab. 2004 Jul;89(7):3313-8.)
Ketotifen WILL AID IN LEAN MUSCLE GROWTH through IGF-1

In this study, Conscious rats were injected intravenously with recombinant human TNFalpha or vehicle for 24 h. TNFalpha decreased the concentration of both total and free IGF-I in the plasma by 30-40%. This change was associated with a reduction in IGF-I mRNA expression in liver by 39%, gastrocnemius by 73%, soleus by 46% and the heart by 63%, but a 2.5-fold increase in the whole kidney. What I found interesting was that TNFalpha did not alter IGF-II mRNA expression in skeletal muscle. TNFalpha also increased IGFBP-1 in the blood (4times-fold) and this response was associated with an increase in IGFBP-1 mRNA expression in both liver (3times-fold) and kidney (9times-fold). However, IGFBP-3 levels in the blood were reduced 38% in response to the injection of TNFalpha. This change was accompanied by a 60-80% reduction of IGFBP-3 mRNA in the liver and kidney but no significant change in muscle. Hepatic mRNA levels of the acid-labile subunit were also reduced by TNFalpha by 46%. Finally, tissue expression of mac25 (also referred to IGFBP-related protein-1) mRNA was increased in gastrocnemius by 50% but remained unchanged in the liver and kidney. These results more fully characterize the changes in various elements of the IGF system and, thereby, provide potential mechanisms for the alterations in the circulating IGF system as well as for changes in tissue metabolism observed during catabolic insults associated with increased TNFalpha expression. As you see the same applies to IGF-1, the more the TNF alpha the less available IGF one will have. When a TNF inhibitor is presented, IGF levels will rise. (Lang CH et.al Growth Horm IGF Res 2001 Aug;11(4):250-60)
Ketotifen may have anti-catabolic properties

When individuals train hard, TNF alpha has been shown to rise. Of course we know that if you were to take ketotifen post training it would not be as great as prior to training but that is still fine. Caffeine in moderate doses is shown to increase performance yet keep cortisol lower compared to those who train without it. I simply suggesting that taking Ketotifen prior to training like most do will still provide the intended anti-catabolic effects that I theorize about. As I mentioned before, we need more studies done with ketotifen especially regarding its effects on the endocrine system. (Pedersen BK et. al. Exerc Immunol Rev 2001;7:18-31)


Taking ketotifen with ephedrine is pretty synergistic, as ephedrine works highly upon beta 3 receptors, ketotifen upregulates those beta receptors, thus making it more potent. Plus the fact that it reduces the amount you need for these agents, will in turn reduce the amount of side effects. IF you have the experience and tolerance, stacking all three of these agents would be a tremendous thermogenic fat burning stack.
I recommend taking 1mg of ketotifen 30 minutes prior to a meal twice a day. Remember take it while on clen or ECA to keep the receptors clean and maximize those cycles.
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From another forum...
 
chedapalooza said:
Well that looks very promising.. What about when you cease use? How long can/should you stay on?
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That is the most glorified explanation of ketotifen ever lol. You don't need it, and it would probably be counterproductive since it causes morning grogginess secondary to H1 sedation and also increases appetite
 
mr.cooper69 said:
That is the most glorified explanation of ketotifen ever lol. You don't need it, and it would probably be counterproductive since it causes morning grogginess secondary to H1 sedation and also increases appetite
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Yea I saw that in further reading. This is one bandwagon I won't jump on.
 
Anyone know if I can take Claritin with ephedrine (not at same time) 4-5 hours after my last EC dose late at night. Killer sinus / allergy headaches
 
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