Advanced Fat Loss Discussion (alpha/beta receptors)

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    Advanced Fat Loss Discussion (alpha/beta receptors)


    Below is a quote (editted) from an article I was reading that best discribes what I wanted to discuss.

    "Ephedrine stimulates all three beta-receptors. Beta-1 sends fat-mobilisation signals to the fat-cells. Beta-2 and 3 signal the mitochondria to use more fatty acids to produce heat. With this beta-team responding to ephedrine, fat gets burnt.

    However, the alpha receptor is not ephedrine-cooperative. As nutrionist-cum-bodybuilder Dan Duchane says, "You'd think ephedrine would mobilise lower-body fat, but in real life, things just don't work out so neatly.'' The problem: lower-body fat has nine times alphas as compared to betas. That's why, the hips and thighs remain plump, grudgingly conceding just a few millimetres. In fact, consuming ephedrine has a reverse effect on the alpha receptors. When the hormones stimulate the alpha, it digs its heels in. Result: the fat cells block the fatty-acid mobilisation out of the cells. Simultaneously, noradrenaline generation from the nerve-endings reduces and this lowers body temperature.

    Can this picture get worse? Yes. An ultra low-calorie diet increases the number of alpha receptors and reduces noradrenaline levels. To stem the alpha receptors' stubborn response, an alpha-blocker called yohimbine is given. So, in effect, the person who wants instant weight-loss ends up taking ephedrine, an agonist (stimulator) and yohimbine, an antagonist (blocker)!"
    I completely understand this and have for some time. I have used alternate methods (outlined below) with success. I wanted to discuss further and in more depth strategies to work around this issue.

    Once one gets to a leanness that leaves all but the stubborn lower body fat which of the choices does one make:

    • Add oral Y to the oral E to counter the alpha antagonism of E.
    • Drop the oral E and replace it with oral Y.
    • Add transdermal Y to the oral E.
    • Drop the oral E and replace it with transdermal Y.


    Of course there are many products out there that may very well suit my startegies but I am not looking for products but rather actives both orally and/or transdermally. What other actives can do what Y does to counter the antogonist effect that E has on alpha receptors? Or inversely, what can one do to replace E so as not to antagonize alpha receptors but yet still get the beta receptor agonist that E provides?

    Like I said in the title I would like to have some advanced discussion on the topic rather than just some "take this product" hype.

    Thanks in advance.

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    Well as suspected my research is leading me to products.

    Synepherine is an alpha 1 agonist.
    Phenylpropanolamine(PPA), epinephrine and norepinephrineis are alpha agonist.

    GTE is a COMT and may increase the alpha 2 receptor agonist of Y
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    this is an excellent topic, unfortunately its a bit over my head but I'm really looking forward to hearing some responses and educating myself on the topic

    Maybe something to give me a game plan to strip some fat off my girl's lower body She's great evidence that ultra low cal diets increase numbers of alpha receptors
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    Wow...

    The alpha- and beta-adrenoceptors are further subdivided into 9 subtypes (alpha1A, alpha1B, alpha1D, alpha2A, alpha2B, alpha2C, beta1, beta2, and beta3). Two other candidates (alpha1L and beta4) may simply be conformational states of alpha1A- and beta1-adrenoceptors, respectively. The classification of alpha-adrenoceptors does not include an alpha1C-receptor, because the original alpha1C-receptor was later determined not to be unique and it was reclassified as an alpha1A-receptor.
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    A little more information on Y and confirmation on what I have already been doing (fasted cardio with Y). As well it does include common sides and safety concerns.
    Synthesized yohimbine and its isomer rauwolscine have been used as pharmacological tools to differentiate the alpha-ARs due to their selectivity as antagonists for the a 2-AR. Another isomer, corynanthine, is used for its selectivity for the a 1-AR. They have served as probes for classification of AR types and to assess a 2 adrenergic functions in man for several decades. Herbal preparations from plant parts, however, have been used as aphrodisiacs and euphorics for centuries. Recently, yohimbine has been promoted as a dietary supplement to enhance athletic performance and fat loss. This and various clinical applications will be examined in this article.

    Early investigations demonstrate the activity of yohimbine as an a 2-antagonist that increases NE release and induces a hyperadrenergic state (33). Pharmaceutical studies show that yohimbine has high selectivity for the a 2-AR and weak affinity for the a 1-receptors. Its isomer rauwolscine has higher selectivity for the a 2-AR with little or no selectivity for the a 1 type. Later tissue and cells studies explained the mechanisms of various effects of yohimbine when administered to humans and other species by revealing the presence of a 2-AR and their functions at several sites within the body. Differential affinity of yohimbine and its isomers for the a 2-AR subtypes may also explain variability in tissue-specific responses.

    Clinically, yohimbine has been administered to induce anxiety in psychiatric patients, orthostatic hypotension and other autonomic failure conditions, adjunct therapy for opiate withdrawal, and male organic impotence (15,34). It is widely used by veterinarians to reverse sedation or anesthesia in animals. Other therapeutical applications currently under research are as a glucose-dispersal agent for treatment of non-insulin dependent diabetes and to treat adverse effects of anti-depressants.

    Yohimbine and Fat Loss

    Since a 2-ARs are present on adipose tissue and inhibit lipolysis, yohimbine has been proposed as a pharmaceutical approach to fat loss. In vitro results demonstrated that E, a non-selective agonist for a /b -ARs, produced less lipolysis than a selective beta-agonist (33). However, when an a 2-antagonist, such as yohimbine, was added, E induced the same rate of lipolysis as the beta-agonist. Clinical investigations report yohimbine administration (0.2 mg/kg total body weight) increases plasma levels of NEFAs and glycerol in obese and non-obese women as well as in men (26,35,36). Yohimbine increased weight loss when used with hypocaloric diets in several studies by preventing an adaptive lowering of the SNS that usually occurs with most calorie-restriction (37). Resting energy expenditure did not change in a group of obese and lean women when administered yohimbine (38). However, exercise energy expenditure in same subjects was significantly potentiated along with accompanying parameter of lipolysis

    Results from many studies conclude that the primary lipid-mobilizing effect of yohimbine is stimulation of the SNS (26,34,35). A beta-antagonist was administered to non-obese and obese subjects 60 minutes before yohimbine. This suppressed the b -AR effect of lipolysis induced by increases in NE levels. Plasma NEFA levels decreased, but plasma levels of NE were unchanged (34). However, yohimbine still had a transient lipid mobilizing effect evidenced by increased levels of NEFA after b -AR blockage (34,35). These results indicate that only a minor part of the lipid-mobilizing effect of yohimbine is attributed to direct blockage of the lipolysis inhibiting a 2-ARs on adipose tissue.

    Discrepancies exist in methodology used in yohimbine and weight loss research. Considering that increases in NE levels after oral yohimbine is dose dependant (39), most studies have shown optimal dosage to be 0.2 mg/kg (8). Some studies have used much smaller dosages with less significant results. Another cause of discrepancy is timing of yohimbine administration. The lipid-mobilizing effects of yohimbine are completely negated when administered with or after a meal (35). Administration of a 2-antagonists such as yohimbine increases insulin secretion during glucose stimulation. This is attributable to the blockage of the a 2-ARs on pancreatic beta-cells and to concomitant stimulation of the pancreatic beta-ARs. Yohimbine was administered to test subjects in earlier studies which caused increased insulin secretion to blunt its lipid mobilizing effects (40). However, in fasting conditions, yohimbine does not increase insulin levels. These results demonstrate the importance of nutritional status when administering a 2-antagonists as lipid-mobilizing agents.

    Studies suggest yohimbine may increase vasodilation in adipose tissue. Subjects administered yohimbine showed significantly increased levels of plasma NEFA when they changed from a supine position to an upright position (26). The increase in NEFA levels observed were probably due to b -AR stimulation of lipolysis and possibly an increase in net outflow of NEFA from adipose tissue due to yohimbine-induced decrease in local vasoconstriction. When nitroprusside, a vasodilator, was infused by microdialysis, extracellular glycerol concentrations decreased and escape of ethanol increased in adipose tissue (20,24). This suggests that the escape of glycerol from the extracellular spaces in adipose tissue can be accelerated by increased blood flow. The peripheral vasodilation effects of many a a-antagonists are known. However, the direct vasodilation effects in adipose tissue by yohimbine will need to be conclusively assessed by techniques such as microdialysis.

    Increased peripheral vasodilation by blockage of the blood vessel wall a 2-ARs may increase systemic distribution of lipolysis by-products. Submaximal-intensity exercise could enhance net lipolysis in combination with yohimbine administration. Microdialysis studies suggest that NEFAs accumulate within adipose tissue during strenuous exercise due to limited transport into systemic blood supply (13). Recall that exercise-induced increases in blood flow does not rise in proportion to NEFA production (41,42). Therefore, the rate of systemic NEFA delivery does not increase simultaneously with increasing intensity of exercise. Accumulation of NEFA in adipose extracellular spaces may possibly exert a feedback inhibition on lipolysis. As well, vasoconstriction may be induced by high concentrations of NEFA or high sympathetic stimulation (43). Increased peripheral vasodilation in adipose tissue effected by a 2-antagonists may enhance removal of lipolysis by-products during low- to moderate-intensity exercise. Additionally, higher systemic transport of NEFA may increase their uptake into working muscles.

    Considering the research that is available thus far, it is conceivable that the optimal plan for administrating yohimbine as a lipid-mobilizing agent would be early mornings after an overnight fast and several hours before breakfast. The relatively low levels of plasma glucose would not stimulate a yohimbine-potentiated increase in insulin that would otherwise negate its lipolytic effects. Utilization of body fat stores would be optimal with low insulin levels and lipid-mobilizing stimulation of the SNS. Conceivably, yohimbine administration could be followed in two to three hours by ingestion of a high-protein, high-fat meal. Protein ingestion will cause only a transient rise in plasma glucose levels with a concomitant rise in insulin secretion. Accompanying dietary fat will slow digestion and absorption of protein in the same meal. Therefore, the resulting insulin spike will only transiently blunt lipolysis.

    Most of the studies with yohimbine as adjunct treatment for weight loss report very few side effects in subjects. However, whatever the therapeutic use, side effects will occur due to the blockage of a 2-ARs on other tissues. Dosage, nutritional status, and general physiological condition of the individual can modify these side effects. Side effects may consist of skin flushing, headaches, and excitement. Men may experience an increase in or prolonged erections possibly due to increase in vasodilation in the penile tissue, which has a high density of a -ARs.

    Few study subjects experienced changes in blood pressure or rise in heart rate. This may be explained by blockage of both vascular a 1/a 2-ARs and minimizes the vascular responses induced by catecholamine release (15,33,44). However, vascular changes have been reported when yohimbine administration is accompanied by exercise. Anecdotally, many people dosing with yohimbine report rapid increase in heart rate during cardiovascular (aerobic) activity. It is wise to monitor heart rate closely when combining the two.

    Some individuals experience profuse sweating and increased salivation at higher doses (45,46). Yohimbine will block the a 2-ARs mediating acetylcholine and effect the cholinergic system as mentioned in the beginning of this article installment. Other side effects may include water retention and increased colon excretion (47).

    Most studies reported that subjects experienced little or no side effects with single oral dosages ranging from 5-20 mg. Those studies basing dosages on bodyweight (0.2mg/kg) also reported few problems with side effects. Yohimbine administration to subjects in psychiatric research induced episodes of anxiety in individuals with pre-diagnosed anxiety disorder (48). Control subjects did not experience similar effects. Central nervous system effects are dose dependent. High oral dosages (40 mg ) and intravenous administration may significantly increase plasma E levels with resulting increase in heart rate and blood pressure (49,50).

    Several contraindications exist that individuals should be aware of when considering dosing with yohimbine. As with most any a 2-antagonist, yohimbine can acutely increase blood pressure in hypertensive patients. It should also not be combined with other drugs that are known to inhibit neuronal uptake or metabolism of NE, such as some anti-depressants. Individuals should also consider the tendency of yohimbine to evoke psychiatric reactions in those who are predisposed to anxiety or panic episodes (51). Yohimbine will act synergistically with ethanol to increase alcohol intoxication by increasing NE turnover albeit through different mechanisms (52).
    This may be basic stuff but people far too often just take a supplement and get the results they want. I prefer to understand what I want to achieve and then choose my supplementation accordingly.

    I cannot seperate the brain from the brawn. As a matter of fact, for me, they are synergystic.
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    Thanks for posting that study, B! Like you said, it confirms what I already thought, but it also explains how and why, which I never knew before. Great thread!
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    Man B, I had no idea on all that...This has me taken a bit back, I had to rethink my plan
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    Y helps me to start taping into the lower ab/oblique fat that we all hate. Whether oral or trans, it helps out immensely when trying to get into the single digit BF%.
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    Rodja,

    I am with you on the Y. The issue can be that using effective doses of Y orally can be quite high and not pleasant. I really enjoy and find much success with Lipo (recently Napalm) but at time sthey can be inconvenient or cost prohibitive. Either or it does provide the results I need when I get to a point where more E, cardio and a deficit is not an option. In the past I used to restric calories even more and my LBM would suffer. I don't enjoy more cardio when I am starving.
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    I have been using Leviathan lately and I can definitely feel some jitters from it. I am not sensitive to stims either, so I know for some that it is way too much. When I was using the Lipo-U/Clen combo, I dropped an insane amount of fat on it. It is a pain in the ass to apply though.
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    Quote Originally Posted by Rodja View Post
    I have been using Leviathan lately and I can definitely feel some jitters from it. I am not sensitive to stims either, so I know for some that it is way too much. When I was using the Lipo-U/Clen combo, I dropped an insane amount of fat on it. It is a pain in the ass to apply though.
    Yeah- clen is a potent beta-3 agonist, but unfortunately these receptors down regulate fairly fast, within two weeks usually (unless you use something like ketotifen, seems to attenuate this)- plus with the Lipo-U you get good alpha stimulation....

    I like everything when it comes to fat loss- yohimbe, e, c, synephrine, but you REALLY have to be careful with what you use as far as mixing and matching as far as chronotropic effects, etc. Know your body and your response to these things- and monitor your bp and body temp frequently when taking any of these compounds.....

    The best LEGAL (imho) fat loss plan I can think of involves high polyphenol green tea, L-tyrosine, ECA, and topical yohimbe, some sort of herbal anabolic, along with morning fasted cardio over an 8 week period, along with cycling in some type of forskolin, bacopa, or gugglesterone for thyroid support....Diet should be clean, w/ LOTS of H20....

    Best illegal (also imho) fat loss plan- clen/T3/GH/Win (or epi, superdrol, or any "dry" ph) along with morning fasted cardio - this protocol is anabolic and anti-catabolic- BUT the clen will need to be rotated with eca, or ketotifen needs to be taken with it to attenuate down-regulation.....
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    I should have elaborated and said to rotate the Lipo-U every 7 days.
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    i'm doing clen/ketotifen right now with leviathan and dropping fat rapidly, especially my core, adding in reset ad as soon as it gets here to keep my adrenals healthy.
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    Quote Originally Posted by Rodja View Post
    I have been using Leviathan lately and I can definitely feel some jitters from it. I am not sensitive to stims either, so I know for some that it is way too much. When I was using the Lipo-U/Clen combo, I dropped an insane amount of fat on it. It is a pain in the ass to apply though.
    did you use cap cream as well? And were you finding site specific fatloss? If so where were you applying it? And did you still get the shakes from the clen?
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    I tracked down a very informative post of an old acquaintance of mine that some of you may know.

    Note: these doses are daily totals.

    Quote Originally Posted by Dante
    1) Classic ECA stack
    a) 60 mgs ephedrine (herbal or sythetic)
    b) 600 mgs caffeine (herbal or sythetic)

    2) Adipo-alternative stack ( it is my guess that the reformulated Adipo,called Beta-3, will use the bitter orange alkaloid Octopamine, while keeping the caffeine and the yohimbine the same, just a guess though).
    a) 60 mgs synephrine (herbal or sythetic)
    b) 600 mgs caffeine
    c) 18-20 mgs of yohimbine hcl (pure only- you do not want to screw around with yohimbe extracts which are not quantified and accounted for).

    3) Advanced ECA stack
    a) 60 mgs ephedrine (herbal or syntheitic)
    b) 600 mgs caffeine (herbal or synthitic)
    c) 30-60mgs synephrine (herbal or syntheic)- I have used high amounts of synephrine with ECA stacks before, with minimal disturbance in the process of doing so. However, if you are to do this, I suggest that you take a more conservative approach at first.

    4) Hardcore ECA stack
    a) 60mgs of ephedrine (herbal or syntheic)
    b) 600 mgs of caffeine (herbal or synthetic)
    c) 10-20 mgs of yohimbine hcl (pure only)
    This is not a stack that you can mess around with, this is only for those those that know their tolerance to ECA itself. Add the yohimbine gradually, or if you wish, you can lower the ephedrine dose, to increase the yohimbine dose.

    5) Extreme ECA stack
    a) 60mgs of ephedrine (herbal or synthetic)
    b) 600mgs of caffeine (herbal or syntheic)
    c) 10-20 mgs of yohimbine hcl (pure)
    d) 15-45 mgs of synephrine (herbal or sythetic)
    As the warning above, for the hardcore stack holds true, it is even more relevant for this stack. Do not touch this, unless you are certain of your toleranc to ECA alone.


    Lipoderm-Y may be added to any of the aformentioned stacks, to enchance the site-specific, Alpha -2 negative feedback disinhibition of transdermal yohimbine hcl. If you are to do this, perhaps it would be best to add it to stacks 1,2, or 3. As for stacks 4, and 5, I would wait to see the toleranc of them first, before that it is that you add something else to further your efforts.

    Dante...........
    If one has a tolerance to stimulants and can handle it ECY is pretty damn potent fat burner. I imagine that the ECYS would knock your socks off
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    What about something like HELIOS?
    Its an injectible Y HCL/Clen to be injected in stubborn areas, I have always been curious about it since its mention in Anabolics
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    Quote Originally Posted by B5150 View Post
    I tracked down a very informative post of an old acquaintance of mine that some of you may know.

    Note: these doses are daily totals.

    If one has a tolerance to stimulants and can handle it ECY is pretty damn potent fat burner. I imagine that the ECYS would knock your socks off
    Personally i prefer clenbuterol to ephedrine i hate how the eca stack makes me feel, i can't sleep i'm just wayyyyyyyy to wired, and isn't yohimbine hcl+ephedrine a no no? It's supposed to cause high blood pressure.
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    Quote Originally Posted by CHAPS View Post
    and isn't yohimbine hcl+ephedrine a no no? It's supposed to cause high blood pressure.
    Well not necessarily. We use it to stimulate both beta and alpha receptors. As stated in my previous posts the E is an antagonist of the alpha receptor and the Y is an agonist that counters the antagonist results from the E.

    As Dante stated and I will further state:
    As the warning above, for the hardcore stack holds true, it is even more relevant for this stack. Do not touch this, unless you are certain of your toleranc to ECA alone.
    It is a hardcore stack. It is not for those who do not have an very good tolerance for stimulants. As well, even those like myself with a high tolerance need be careful because it will elevate HR and BP. I use it for short periods of time because of this.

    EDIT: Also at times I will cycle the E down to half the dose and go full dose with the Y to help minimize the HR and BP issues.
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    What do people here think of alpha-yohimibine as opposed to yohimbe in a fat loss stack?
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    Quote Originally Posted by CHAPS View Post
    did you use cap cream as well? And were you finding site specific fatloss? If so where were you applying it? And did you still get the shakes from the clen?
    No cap, but I did find site specific fat loss and without the systemic effects. I really can't do oral clen anymore because of the negative effects on VO2 max. I was applying it to my abdominals and I saw some great results. I would love to try this tactic with Napalm in the near future.
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    Rodja,

    Did you add clen in solution or powder to your LU?
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    Quote Originally Posted by B5150 View Post
    Rodja,

    Did you add clen in solution or powder to your LU?
    Clen in solution. I would never want to handle clen powder.
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    Next question, how many ml's did you add? I assume it was 100mcg/ml.
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    Quote Originally Posted by Urban Monk View Post
    What do people here think of alpha-yohimibine as opposed to yohimbe in a fat loss stack?
    Though I am a bit biased, I find Alpha-Yohimbine superior to Yohimbine.

    MUCH lower incidence of side effects, positive mental state, central adipostat control (as opposed to peripheral), and longer term effectiveness (IME).

    It also combines much better with things like E.
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    very good discussion so far, subb'd
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    Quote Originally Posted by B5150 View Post
    Next question, how many ml's did you add? I assume it was 100mcg/ml.
    30mL.
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    Quote Originally Posted by Rodja View Post
    30mL.
    I used Lipo-derm ultra with rasberry ketones, i think i mixed around 4g's of RK in their and did two bottles like that and i definitely noticed some site specific fatloss on chest, lower abs and obliques. I'd like to try the LPU+Clen+cap, i'm willing to put up with the pain. But right now i don't need anythign else 150mcg clen/ketotifen with 6 caps leviathan the core fat is dripping off. Tren E+Epistane is also in their to keep me anti-catabolic.
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    Quote Originally Posted by Rodja View Post
    30mL.
    30ml of solution into 120ml of LU?

    The 3mg (30ml of 100mcg) into 120ml of LU is about right from what my research has shown me. How was absorption with that much solution added to the Lipo carrier?
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    Quote Originally Posted by B5150 View Post
    30ml of solution into 120ml of LU?

    The 3mg (30ml of 100mcg) into 120ml of LU is about right from what my research has shown me. How was absorption with that much solution added to the Lipo carrier?
    Just make sure to shake the solution before applying. I still got a nice warming sensation from that solution.
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    Quote Originally Posted by B5150 View Post
    I tracked down a very informative post of an old acquaintance of mine that some of you may know.

    Note: these doses are daily totals.

    If one has a tolerance to stimulants and can handle it ECY is pretty damn potent fat burner. I imagine that the ECYS would knock your socks off
    *whew* - glad those are *daily* totals - my ass would be in orbit wa!! before lunch!

    I'm a little foggy @ the mo, so no science from me, just a general note:

    yohimbe/yohimbine can kick like a mule - a little too much, and you'll feel like you're under attack, like your heart's gonna explode - if you're already taking stims of various sorts, be careful!!

    GTE & forskholin are such natural partners for each other, I always combine them.
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    Anecdotally speaking, I can NOT combine E and Y. Even 3mg of Y with a standard E dose (25mg) makes me very uncomfortable. I started Leviathan recently with no E and I can tolerate a full dose of it with no problem.
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    subbed
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    wow, full of usefull info...why isnt anyone else responding...summer is here, lets get this fired up again!
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    well i only saw this bc of the other thread
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    me too, but after reading this, Im interested in the effects of Y...Aspirin isnt really mentioned in the discussion, why not? does this mean that A is better than Y? Im not going to use an anti-inflammatory when Im tearing down alot of muscle with my intense workouts. But I totally understand the purpose of messing with the doses of E & Y to compensate for the other (lowering E, raising Y)...is anyone going to keep up with this? Im about to start my 3rd week tomorrow of my ECY stack, increasing dosages to 3x ED (ECY), and I need advice
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    good ole yohimbine.. the poor mans viagra..

    I need to read this but at the time but I am in full blown finals right now.

    However, I will say work is currently being done to specifically target the B3 receptor to induce lipolysis. I will read through this in a couple days after my finals. Good find though.. I am sure it is a very interesting article. What journal or magazine was this?
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    So can it be concluded from this thread that the EC stack is much less effective than the ECY stack?
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    Quote Originally Posted by pitching101 View Post
    So can it be concluded from this thread that the EC stack is much less effective than the ECY stack?
    Im not sure, what I got from it was that E&C is effective, but when Y is added, it can be more effective, only both E&Y cannot be high doses, I may be wrong though
  

  
 

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