Forskolin

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    Forskolin


    Effect on cAMP


    Pharmacology and Inotropic Potential of Forskolin in the Human Heart


    Abstract. We evaluated the effects of the dis terpene compound forskolin in human myocardial adenylate cyclase preparations, isolated trabeculae and papillary muscles derived from failing human hearts, and acutely instrumented dogs. Forskolin was a potent, powerful activator of human myocardial adenylate cyclase and produced maximal effects that were 4.82 (normally functioning left ventricle) and 6.13 (failing left ventricle) fold greater than isoproterenol. In contrast to isoproterenol, forskolin retained full activity in membrane preparations derived from failing hearts. In cyclase preparations, forskolin demonstrated unique substrate and Mg2+ kinetic properties that could be distinguished from hormone receptor-coupled agonists or fluoride ion. The adenylate cyclase stimulatory effect of forskolin was synergistic with isoproterenol, apparently due to the location of forskolin activation being beyond the level of hormone receptor-agonist in the receptor-cyclase complex. Forskolin was a potent positive inotrope in failing human myocardium, producing a stimulation ofcontraction that was similar to isoproterenol. Finally, in open chest dogs forskolin was a positive inotropic agent that reduced preload and afterload. We conclude that forskolin belongs to a class of agents that may have therapeutic potential in the treatment of congestive heart failure.

    FT- http://www.ncbi.nlm.nih.gov/pmc/arti...00134-0220.pdf


    The mechanism for increasing cAMP


    Skeletal muscle NAMPT is induced by exercise in humans.


    In mammals, nicotinamide phosphoribosyltransferase (NAMPT) is responsible for the first and rate-limiting step in the conversion of nicotinamide to nicotinamide adenine dinucleotide (NAD+). NAD+ is an obligate cosubstrate for mammalian sirtuin-1 (SIRT1), a deacetylase that activates peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), which in turn can activate mitochondrial biogenesis. Given that mitochondrial biogenesis is activated by exercise, we hypothesized that exercise would increase NAMPT expression, as a potential mechanism leading to increased mitochondrial content in muscle. A cross-sectional analysis of human subjects showed that athletes had about a twofold higher skeletal muscle NAMPT protein expression compared with sedentary obese, nonobese, and type 2 diabetic subjects (P < 0.05). NAMPT protein correlated with mitochondrial content as estimated by complex III protein content (R(2) = 0.28, P < 0.01), MRS-measured maximal ATP synthesis (R(2) = 0.37, P = 0.002), and Vo(2max) (R(2) = 0.63, P < 0.0001). In an exercise intervention study, NAMPT protein increased by 127% in sedentary nonobese subjects after 3 wk of exercise training (P < 0.01). Treatment of primary human myotubes with forskolin, a cAMP signaling pathway activator, resulted in an approximately 2.5-fold increase in NAMPT protein expression, whereas treatment with ionomycin had no effect. Activation of AMPK via AICAR resulted in an approximately 3.4-fold increase in NAMPT mRNA (P < 0.05) as well as modest increases in NAMPT protein (P < 0.05) and mitochondrial content (P < 0.05). These results demonstrate that exercise increases skeletal muscle NAMPT expression and that NAMPT correlates with mitochondrial content. Further studies are necessary to elucidate the pathways regulating NAMPT as well as its downstream effects.

    Demonstrating that forskolin can raise cAMP levels in fat cells


    Forskolin as an activator of cyclic AMP accumulation and lipolysis in rat adipocytes.


    Abstract


    Forskolin increased cyclic AMP accumulation in isolated adipocytes and markedly potentiated the elevation of cyclic AMP due to isoproterenol. In adipocyte membranes, forskolin stimulated adenylate cyclase activity at concentrations of 0.1 microM or greater. Forskolin did not affect the EC50 for activation of adenylate cyclase but did increase the maximal effect of isoproterenol. Neither the soluble nor particulate low-Km cyclic AMP phosphodiesterase activity was affected by forskolin. Low concentrations of forskolin (0.1-1.0 microM), which significantly elevated cyclic AMP levels, did not increase lipolysis, whereas similar increases in cyclic AMP levels due to isoproterenol elevated lipolysis. Forskolin did not inhibit the activation of triacylglycerol lipase by cyclic AMP-dependent protein kinase or the subsequent hydrolysis of triacylglycerol. Higher concentrations of forskolin (10-100 microM) did increase lipolysis. Both the increased cyclic AMP production and lipolysis due to forskolin were inhibited by the antilipolytic agents insulin and N6-(phenylisopropyl)adenosine. Hypothyroidism reduced the ability of forskolin to stimulate cyclic AMP production and lipolysis. These results indicate that forskolin increases cyclic AMP production in adipocytes through an activation of adenylate cyclase. Lipolysis is activated by forskolin but at higher concentrations of total cyclic AMP than for catecholamines.
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    Forskolin-induced lean body mass gains


    Diterpene Forskolin (Coleus forskohlii, Benth.): A possible new compound for reduction of body weight by increasing lean body mass


    Maintaining or increasing lean body mass should be one of the important considerations of any weight loss strategy for the following reasons


    1. increase in lean body mass is proportionate to an increase in the body’s thermogenic response to food and the basic metabolic rate (BMR);


    2. food induced thermogenesis controls body weight by an increase in catabolism of body fat (thermogenesis is preferentially fueled by fatty acids derived from body fat and/or from food); and


    3. enhanced thermogenesis contributes to a buildup of lean body mass.


    An extract of Coleus forskohlii root, Benth. (Fam. Labiatae) standardized for diterpene forskolin was tested in an open-field study for weight loss and lean body mass increase. The study’s hypothesis was based on the recognized role of diterpene forskolin as the plant derived compound which stimulates enzyme adenylate cyclase and subsequently cyclic AMP (3’5’adenosine monophosphate) (1,2). Cyclic AMP may release fatty acids from the adipose tissue depots which may result in enhanced thermogenesis (3), loss of body fat, and theoretically increased lean body mass.


    Six overweight, but otherwise healthy, women were selected for the trial. Each participant was informed about the purpose of the study and was asked to sign an informed consent before entering the study. Each participant was examined by a physician at the inception and after 4 and 8 weeks of the study. The body composition was determined by bioelectrical impedance analysis. The forskolin formula was prepared in the form of two piece hard shell capsules. Each capsule contained 250 mg of the extract standardized for 10% forskolin, and each bottle contained 60 capsules. Participants were instructed to take one capsule in the morning and one in the evening, half an hour before a meal. Each participant was asked to maintain their previous daily physical exercise habits and eating habits. In addition, physical activity was monitored based on a questionnaire before and during the trial. The study was performed in an outpatient bariatric clinic at Hilton Head, S.C. and supervised by a physician specializing in bariatric medicine for over 30 years.


    During the eight week trial the mean values for body weight, and fat content were significantly decreased, whereas lean body mass was significantly increased as compared to the baseline (Wilcoxon matched pairs test). Weight loss was statistically significant (p<0.05) after 4 and 8 weeks, and the mean amounted to 4.3 and 9.17 lbs respectively. The body fat values expressed as % body fat were: 0 weeks 33.63 3.02, 4 weeks 30.10 4.34 (statistically not significant or n.s.), and
    8 weeks 25.88 4.77 (p<0.05). The lean body mass values expressed as % lean body mass were: 0 weeks 67.07 3.02, 4 weeks 69.90 4.34 (n.s.), and
    8 weeks 74.13 4.77 (p<0.05).


    The eight week therapy with 50 mg of forskolin per day did not adversely affect the systolic/diastolic blood pressure nor the pulse rate. A trend has been observed to lower the systolic/diastolic pressure in the course of treatment. Systolic pressure (mm Hg) was
    0 weeks 113.67 14.50,
    4 weeks 110.00 18.93(n.s.), and
    8 weeks 104.50 17.54(n.s.). Diastolic pressure (mmHg) was 0 weeks
    71.00 12.76, 4 weeks 69.33 9.93 (n.s.), and 8 weeks 66.00 8.49(n.s.). Pulse rate (beats/min) was 0 weeks 66.33 8.02, 4 weeks 69.00 7.97(n.s.), and 8 weeks 74.67 11.55(n.s.).


    This preliminary data obtained with 250 mg bid of a 10% extract of Coleus forskohlii indicate that this botanical bears promise as a safe and effective weight loss regimen. The effect of Coleus forskohlii is particularly valid in the absence of change in frequency and intensity of physical exercise and without diet restrictions during the course of the trial. This study warrants a double-blind clinical trial evaluating effects of forskolin on body composition and its possible thermogenic mechanism.




    REFERENCES


    1) LEAMON, KB; PADGETT, W; DALY, JW. “Forskolin: Unique diterpene activator of adenylate cyclase in membrane and intact cells” Proc. Natl. Acad. Sci. USA 1981,78, 3363-67


    2) DE SOUZA, NJ; DOHADWALLA, AN; REDEN, J; Forskolin, A. “Labdane Diterpenoid with Antihypertensive, Positive Inotropic, Platelet Aggregation Inhibitory, and Adenylate Cyclase Activating Properties” Medicinal Research Reviews 1983, 3(2), 201-219


    3) GIRARDIER, L. “Brown Fat: An Energy Dissipating Tissue”; In: Mammalian Thermogenesis; Girardier, L.; Sock M.J. Eds.; Chapman and Hall Ltd.:London New York, 1983, pp.50-98




    And there is also this one


    Body composition and hormonal adaptations associated with forskolin consumption in overweight and obese men.


    Abstract
    OBJECTIVE: This study examined the effect of forskolin on body composition, testosterone, metabolic rate, and blood pressure in overweight and obese (BMI > or = 26 kg/m(2)) men.


    RESEARCH METHODS AND PROCEDURE: Thirty subjects (forskolin, n = 15; placebo, n = 15) were studied in a randomized, double-blind, placebo-controlled study for 12 weeks.


    RESULTS: Forskolin was shown to elicit favorable changes in body composition by significantly decreasing body fat percentage (BF%) and fat mass (FM) as determined by DXA compared with the placebo group (p < or = 0.05). Additionally, forskolin administration resulted in a change in bone mass for the 12-week trial compared with the placebo group (p < or = 0.05). There was a trend toward a significant increase for lean body mass in the forskolin group compared with the placebo group (p = 0.097). Serum free testosterone levels were significantly increased in the forskolin group compared with the placebo group (p < or = 0.05). The actual change in serum total testosterone concentration was not significantly different among groups, but it increased 16.77 +/- 33.77% in the forskolin group compared with a decrease of 1.08 +/- 18.35% in the placebo group.


    DISCUSSION: Oral ingestion of forskolin (250 mg of 10% forskolin extract twice a day) for a 12-week period was shown to favorably alter body composition while concurrently increasing bone mass and serum free testosterone levels in overweight and obese men. The results indicate that forskolin is a possible therapeutic agent for the management and treatment of obesity.
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    Effects on muscle protein synthesis by...


    increasing the activity of adenylate cyclase in skeletal muscle


    Activation of hormone-sensitive adenylate cyclase by forskolin


    An overview of the organization of adenylte cyclase systems and various sites for regulation is presented. These components are discussed with respect to the activation of adenylate cyclase by forskolin. Evidence for direct activation of adenylate cyclase as well as potentiation of hormone-activated adenylate cyclase by forskolin is reviewed, as these data relate to the possible site(s) of action of forskolin. Studies of the action of forskolin in different systems and interaction studies with different regulators of adenylate cyclase have yielded valuable information about the regulation of adenylate cyclase and the relationship of its various components. A better understanding of these relationships may reveal new therapeutic potential for forskolin.

    and by increasing cAMP forskolin can increase muscle protein synthesis by activating PI3K and Akt (independent of the insulin receptor)


    Mechanism of protein kinase B activation by cyclic AMP-dependent protein kinase.


    Activation of protein kinase B (PKB) by growth factors and hormones has been demonstrated to proceed via phosphatidylinositol 3-kinase (PI3-kinase). In this report, we show that PKB can also be activated by PKA (cyclic AMP [cAMP]-dependent protein kinase) through a PI3-kinase-independent pathway. Although this activation required phosphorylation of PKB, PKB is not likely to be a physiological substrate of PKA since a mutation in the sole PKA consensus phosphorylation site of PKB did not abolish PKA-induced activation of PKB. In addition, mechanistically, this activation was different from that of growth factors since it did not require phosphorylation of the S473 residue, which is essential for full PKB activation induced by insulin. These data were supported by the fact that mutation of residue S473 of PKB to alanine did not prevent it from being activated by forskolin. Moreover, phosphopeptide maps of overexpressed PKB from COS cells showed differences between insulin- and forskolin-stimulated cells that pointed to distinct activation mechanisms of PKB depending on whether insulin or cAMP was used. We looked at events downstream of PKB and found that PKA activation of PKB led to the phosphorylation and inhibition of glycogen synthase kinase-3 (GSK-3) activity, a known in vivo substrate of PKB. Overexpression of a dominant negative PKB led to the loss of inhibition of GSK-3 in both insulin- and forskolin-treated cells, demonstrating that PKB was responsible for this inhibition in both cases. Finally, we show by confocal microscopy that forskolin, similar to insulin, was able to induce translocation of PKB to the plasma membrane. This process was inhibited by high concentrations of wortmannin (300 nM), suggesting that forskolin-induced PKB movement may require phospholipids, which are probably not generated by class I or class III PI3-kinase. However, high concentrations of wortmannin did not abolish PKB activation, which demonstrates that translocation per se is not important for PKA-induced PKB activation.
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    Yeah, the dual action on Akt and cAMP make forskolin a great compound for body recomposition. If you have the time, would you be able to pull up forskolin's biological halflife? I'm curious as to whether the effects are mediated by forskolin, or if they persist beyond the forskolin dose/HL (i.e. you take 50mg forskolin in the morning, would adenylyl cyclase activity still be elevated at night?).
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    This has gotta be one of the most interesting herbal extracts to read about. Just in trying to understand its MOA and all it can do you learn a lot. Examine has a great compilation of work on this.

    I don't remember, but is the absorption of this low? I recall it not being water or fat soluble(alcohol soluble though). Either it is one of my favorite ingredients.

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    Im glad i saw this. Interesting read for sure. forskolin looks like a great supp. Thanks for the post!
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    Quote Originally Posted by mr.cooper69 View Post
    Yeah, the dual action on Akt and cAMP make forskolin a great compound for body recomposition. If you have the time, would you be able to pull up forskolin's biological halflife? I'm curious as to whether the effects are mediated by forskolin, or if they persist beyond the forskolin dose/HL (i.e. you take 50mg forskolin in the morning, would adenylyl cyclase activity still be elevated at night?).
    Bump for this. Was under the assumption that forskolin had a short half-life (hence me always splitting dosing throughout the day), but would love to see more on the possibility of the second bolded sentence.

    Did some searching myself but don't have as great of access to research as I used to.
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    IIRC, forskolin is absorbed in fats no? If so than the half life is really irrelevant
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    After a quick search on pubmed this is all I found

    The pharmacodynamics of 6-(3-dimethylaminopropionyl)forskol in and a possible metabolite in beagles.



    A specific gas chromatography/mass spectroscopy method with a detection limit of 0.1 ng/mL was developed for the measurement of 6-(3-dimethylaminopropionyl)forskol in (1) in beagle plasma. Using this method, plasma concentrations of 1 in beagles given pharmacologically effective intravenous doses of 1.HCl were determined. The observed maximal plasma concentrations rapidly decreased with time, and half-lives of the alpha-phases were &lt; 9 min. Pharmacological effects of 1 on the cardiovascular parameters were simultaneously evaluated in one of the studies. Decreases of the pharmacological effects were slower than decreases in plasma concentration of 1. In addition, 6-(3-methylaminopropionyl)forskolin (N-monodemethyl 1), an expected initial metabolite of 1, was prepared and found to be as pharmacologically active as 1 in beagles. These results and others strongly suggest that a metabolite(s) of 1 contributes to the pharmacological effects of 1 in beagles.



    PMID: 8901072
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    Quote Originally Posted by mr.cooper69 View Post
    Yeah, the dual action on Akt and cAMP make forskolin a great compound for body recomposition. If you have the time, would you be able to pull up forskolin's biological halflife? I'm curious as to whether the effects are mediated by forskolin, or if they persist beyond the forskolin dose/HL (i.e. you take 50mg forskolin in the morning, would adenylyl cyclase activity still be elevated at night?).
    Based on the in vivo effects it suggests it persists well beyond the short half life.
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    Awesome thread!
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    Never mind, looks like it doesn't need fat

    Quote Originally Posted by strategicmove View Post
    As far as I know, Forskolin is best taken before food, as it is better absorbed on an empty stomach. The suggestion that it should be taken with food or fats was probably influenced by the fact that, other than the active diterpene, forskolin, coleus forskohlii also contains other diterpenes as well as volatile oils. However, these volatile oils are not only available in trace amounts in coleus, but practically all the pharmacological properties of coleus are traceable to forskolin. So the volatile oils do not play a role here. The simultaneous intake of fats is not a requirement for forskolin efficacy, either. As a matter of fact, forskolin even stimulates digestive enzymes such as amylase and pepsin, and also regulates saliva production. So, taken on an empty stomach, forskolin will also help prepare our digestive system to function better when we eat later. Just an additional benefit!
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    Word of the wise, never take forskolin your first time on an empty stomach unless you're near a bathroom.
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    Quote Originally Posted by Royd The Noyd View Post
    Word of the wise, never take forskolin your first time on an empty stomach unless you're near a bathroom.
    For me, this only happens with the low quality stuff. The higher the extract, the less I see this.
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    Quote Originally Posted by DAdams91982 View Post
    For me, this only happens with the low quality stuff. The higher the extract, the less I see this.
    Like what %? Forslean is typically 20% and considered quality.
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    Quote Originally Posted by Royd The Noyd View Post
    Like what %? Forslean is typically 20% and considered quality.
    So far I have only tried two of the 95% ones.

    I didn't get it from USPs Bolic, or Forsk-95

    The 20%s I do get that effect.
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    Quote Originally Posted by DAdams91982

    So far I have only tried two of the 95% ones.

    I didn't get it from USPs Bolic, or Forsk-95

    The 20%s I do get that effect.
    I can second this from multiple forskolin runs.

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    What high quality brands would you guys recommend? Also, What are you opinions on stacking forskolin product(any brand) with 1dhea and
    4dhea products over a six week period as opposed to using it after a six week cycle-consider it for use in pct?
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    I have always been wary of forskolin unless it was Sabinsa licensed. Right now the best option IMO is Forskolin-95 due to the licensing from Sabinsa and the fact it is 95% extract alleviates chances of stomach issues at lower percentages that some people run into.

    Edit: Idk about the DHEA stuff though.
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    Thanks for the info. Any specific brands?
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    Quote Originally Posted by JosNYC View Post
    Thanks for the info. Any specific brands?
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    Quote Originally Posted by JosNYC View Post
    Thanks for the info. Any specific brands?
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    Quote Originally Posted by JudoJosh View Post
    After a quick search on pubmed this is all I found
    great thread and good job finding a good chunk of evidence.

    I noticed that most [if not all] involve obsese populations, are there any involving either a.) trained individuals or at least normal body compositions?

    edit: no i couldnt find any and im sure you would have posted if there was
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    Is this something that should be cycled?. From my limited understanding of this product, its best used long-term.
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    Quote Originally Posted by T-Bone View Post
    Is this something that should be cycled?. From my limited understanding of this product, its best used long-term.
    Use it long-term (8-12 weeks), but cycle it for about a month after
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    Quote Originally Posted by mr.cooper69 View Post
    Use it long-term (8-12 weeks), but cycle it for about a month after

    Would there be any benefit to go above the 1 cap twice a day suggested on the Forskolin 95?.
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    Quote Originally Posted by T-Bone View Post
    Would there be any benefit to go above the 1 cap twice a day suggested on the Forskolin 95?.
    Certainly. You need to remember forskolin dose-dependently increases cAMP production. The higher you go (I like 4 caps daily), the more you notice the fat loss and testosterone elevation
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    Quote Originally Posted by mr.cooper69 View Post
    Certainly. You need to remember forskolin dose-dependently increases cAMP production. The higher you go (I like 4 caps daily), the more you notice the fat loss and testosterone elevation

    Interesting. So would the dosage be based on body-weight?. I read in this thread that it should be taken on an empty stomach. So are you better off taking it several times a day, twice daily, or what?. Since you like 4 caps daily, do you do 2 AM and 2PM, or 1 cap 4 times a day?. My stomach just isn't empty 4 times a day. Two times a day I can handle.
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    Quote Originally Posted by T-Bone View Post
    Interesting. So would the dosage be based on body-weight?. I read in this thread that it should be taken on an empty stomach. So are you better off taking it several times a day, twice daily, or what?. Since you like 4 caps daily, do you do 2 AM and 2PM, or 1 cap 4 times a day?. My stomach just isn't empty 4 times a day. Two times a day I can handle.
    Empty stomach + fed state doesn't matter too much. If you take it on empty, you may "feel" something though, like a natural energy. You can take them together, apart, whatever...all that matters is that you take it consistently for 1-3 months
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    Quote Originally Posted by mr.cooper69 View Post
    Empty stomach + fed state doesn't matter too much. If you take it on empty, you may "feel" something though, like a natural energy. You can take them together, apart, whatever...all that matters is that you take it consistently for 1-3 months

    Excellent. Thanks for the help. Now as for the dosage is there a formula for that or something?. Like so many mg per kg?. Since you say the higher you go the more you notice the fat loss and testosterone elevation, is there a "cut off point"?. Or I guess you call it the point of diminishing returns?.
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    Quote Originally Posted by T-Bone View Post
    Excellent. Thanks for the help. Now as for the dosage is there a formula for that or something?. Like so many mg per kg?. Since you say the higher you go the more you notice the fat loss and testosterone elevation, is there a "cut off point"?. Or I guess you call it the point of diminishing returns?.
    No, the studies didn't really normalize for bodyweight, though I'm sure it does make a mild difference. I simply wouldn't exceed 150mg daily, as that seems to be the built-in cut-off due to GI issues
    http://pescience.com/
    http://selectprotein.com/
    The above is my own opinion and does not reflect the opinion of PES
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    Thanks cooper. I hope Nutraplanet does a good sale soon!.
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    Quote Originally Posted by T-Bone View Post
    Thanks cooper. I hope Nutraplanet does a good sale soon!.
    Hoping next weekend for Memorial Day. ::fingerscrossed::
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    Quote Originally Posted by good2Badawg View Post
    Hoping next weekend for Memorial Day. ::fingerscrossed::

    That'd be nice!.
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