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Thread: ECA Stack?

  1. #13
    Elite MS1605's Avatar
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    Quote Originally Posted by GearGoddess View Post
    You're confusing ECA with Clen protocol
    You don't need to do that with ECA. You don't lose its efficiency/potency over time. Your body doesn't adapt to it like that.

    This has been posted on several different sites, I dont know the OG author to give credit.

    What Is It?
    Ketotifen is a very safe antihistamine used extensively in Europe to treat bronchial asthma and allergies. It is also being studied as a treatment for colitis. When used for asthma, weight gain and an increase in appetite are among the most frequent side effects. Ketotifen also protects the cells in the stomach, small intestine and perhaps the rest of the gut from a number of toxins. A number of case studies suggest that it may be helpful treating skin problems such as acne. Ketotifen also reduces edema (swelling and puffiness caused by water retention) around sores.

    The mean elimination half life is 12 hours

    Off-Label Use

    Ketotifen is used to up-regulate beta-2 adrenergic receptors down-regulated by beta-2 adrenergic agonists. It upregulates adrenergic receptors due to its phosphodiesterase inhibition, since a phosphodiesterase enzyme is involved in their feedback/homeostatic pathway.

    Ketotifen and Clen
    Clenbuterol is a beta 2 agonist which has a limited anabolic effect during its first few days of use and afterwards is normally used to fight fat. At higher doses, however, it can be catabolic to muscle and it must be cycled on a 2 week on, 2 week off basis or the beta 2 receptors that clen binds to become saturated and down regulate.

    Ketotifen’s magic is that it upregulates the beta-receptors including the beta 2s that clen uses. As long as you are taking ketotifen, it will continue to clean these receptors, never allowing them to downregulate – even while on a heavy clen cycle. That means you can continue to take clen indefinitely without having to cycle off to regenerate the receptors. 2-3mg ED can upregulate even severely shut down receptors within a week.

    It also means that you don’t need as much clen to get the same results. It seems you can take about 30-40% less clen and it will be equally as effective. Ketotifen also seems to lessen the sides of clen including the jitters.

    Ketotifen and ECA
    Perhaps an even better use for ketotifen is taking it with the ECA stack. While the thermogenic effect of ephedrine is not as potent as clen because it doesn't have a high receptor affinity, and it is not limited to beta-2 receptors. In fact it seems to have a good effect on beta 3 receptors as well, which act as a type of thermogenic messenger and over half of ephedrine effect is from beta-3 stimulation. Clen has almost no effect on beta 3 however. So by keeping the beta 2 receptors up, ketotifen can allow the benefits of continuous beta 2 and beta 3 stimulation from ephedrine.

    "Ephedrine is believed to have some direct effect on both alpha adrenoceptors and beta adrenoceptors, but AT THERAPEUTIC DOSES, ephedrine exerts its thermogenic effect almost entirely via stimulating noradrenaline release from the sympathetic nerve terminals [endings] . . . at least 40% of the [thermogenic] response is mediated by an atypical receptor, which is presumed to be the beta 3-adrenoceptor."

    No studies have been done to find the most effective dose but German researchers used 4 mg ED. Dan Duchaine who discovered ketotifen for bodybuilding suggested 10mg ED but this is not the norm and would result in constant drowsiness. Much higher doses have been shown to be quite safe with no adverse affects other than increased drowsiness and appetite – it will make you hungry for solid foods.

    3-4mg ED seems ideal and many people go by 1-2mg ED. It is best taken before bed due to its' drowsiness inducing effects.

    Ketotifen Studies
    German researchers have published data showing that ketotifen lowers tnf-alpha in the test tube. One study used ketotifen in combination with oxymethadone, a steroid like Megace that helps people gain weight, so it is hard to gauge what effect ketotifen had (the study notes a 14% reduction in TNF-alpha levels and weight gains of 11-12 pounds in less than four weeks). A larger placebo controlled study of this combination is underway. The other study used ketotifen by itself in eight patients with elevated TNF-alpha, (but no wasting). Taking ketotifen for 12 weeks, these patients gained an average of six pounds, had increases in their body cell mass and reductions in their TNF-alpha levels.

    Side Effects and Warnings

    Ketotifen is virtually non-toxic (although it is not advised for patients with epilepsy). People who took twenty times the recommended dose (in suicide attempts) suffered no serious consequences (other than embarrassment). Its primary side effects seem to be temporary drowsiness, dry mouth,(and other mucuos membranes) appetite stimulation and weight gain.

    Carcinogenesis, Mutagenesis, Impairment of Fertility
    Ketotifen fumarate was determined to be non-mutagenic in a battery of in vitro and in vivo mutagenicity assays including: Ames test, in vitro chromosomal aberration test with V79 Chinese hamster cells, in vivo micronucleus assay in mouse, and mouse dominant lethal test.

    Treatment of male rats with oral doses of ketotifen ≥ 10 mg/kg/day orally [6,667 times the maximum recommended human ocular dose of 0.0015 mg/kg/day on a mg/kg basis (MRHOD)] for 70 days prior to mating resulted in mortality and a decrease in fertility. Treatment with ketotifen did not impair fertility in female rats receiving up to 50 mg/kg/day of ketotifen orally (33,333 times the MRHOD) for 15 days prior to mating.

    Oral treatment of pregnant rabbits during organogenesis with 45 mg/kg/day of ketotifen (30,000 times the MRHOD) resulted in an increased incidence of retarded ossification of the sternebrae. However, no effects were observed in rabbits treated with up to 15 mg/kg/day (10,000 times the MRHOD). Similar treatment of rats during organogenesis with 100 mg/kg/day of ketotifen (66,667 times the MRHOD) did not reveal any biologically relevant effects.

    Oral treatment of pregnant rats (up to 100 mg/kg/day or 66,667 times the MRHOD) and rabbits (up to 45 mg/kg/day or 30,000 times the MRHOD) during organogenesis did not result in any biologically relevant embryofetal toxicity. In the offspring of the rats that received ketotifen orally from day 15 of pregnancy to day 21 post partum at 50 mg/kg/day (33,333 times the MRHOD), a maternally toxic treatment protocol, the incidence of postnatal mortality was slightly increased, and body weight gain during the first four days post partum was slightly decreased.

    Liu YL, Toubro S, Astrup A, Stock MJ Contribution of beta 3-adrenoceptor activation to ephedrine-induced thermogenesis in humans Int J Obes Relat Disord. Sep;19(9). 678-685

    Grahnén A; Lönnebo A, Beck O, Eckernäs SA, Dahlström B, Lindström B (May 1992). "Pharmacokinetics of ketotifen after oral administration to healthy male subjects". Biopharm Drug Dispos 13 (4): 255–62. doi:10.1002/bdd.2510130404. PMID 1600111."
    "What hurts more, Physical pain or Mental pain? What hurts more, getting punched in the face or getting your heart broken?" -Tashi, HCX MMA

  2. #14
    Veteran MrRippedZilla's Avatar
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    Quote Originally Posted by MS1605 View Post
    For years now I thought it was the beta 2 receptors that was down regulated by the ephedra and ketotifen upregulates beta 2 receptors?
    Ephedrine (not the same as ephedra, which is a "dirtier" version) binds weakly to the beta 2 receptors and is in/out of the system fairly quickly due to its half life, which is why there is no need to worry about upregulating the receptors - unlike something that its them hard & for ages like Clen.
    This is supported by the literature, which has never shown downregulation of any kind and actually suggests an enhanced effect the longer your run it, as can be seen here, here and a bunch of other places (there was a really cool study showing it to be effective even after 1yr of continued use that I can't located at the moment).

    Also, that article doesn't actually tell you why to use keto with just kinda says do it. In fact, the quote about ephedrine working primarily via noradrenaline release from the SNS is true and evidence for its weak binding affinity to beta 2 receptors so...
    Like I said, no need for keto
    Last edited by MrRippedZilla; 05-24-2017 at 07:55 AM.
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  4. #15
    Elite MS1605's Avatar
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    Thanks for the clarification zilla. Always learning something new from you.

    "What hurts more, Physical pain or Mental pain? What hurts more, getting punched in the face or getting your heart broken?" -Tashi, HCX MMA

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