Anyone think CLA is worth taking? I use to take it a while back and was thinking about buying some more.
I believe last time I saw that was only in the obese. But to your point, is it worth the price. In my opinion, no.Studies show it works. Just another case of if the effect is worth the price. It doesn't do any harm, so if you can afford it you might as well
What's the price and dose? If memory serves me correctly, 3.4g was the ideal dose, spaced out with meals... I'd take 4gs a day breakfast, lunch, dinner and night shakeSNS CLA extreme would do you right OP. Cost effective and properly dosed.
The most credible studies that actually show results used dosing of 3g p/day, taken at 1g doses before each meal. One study I read used cohorts of 3, 4, 5 and 6g per day with no significant differences between the groups. So it appears CLA has a point of saturationya I take it just to take it .. I also take garcinia cambogia to aid in the fat burning process. For those who take it how many grams/day ??
Any that don't have researchers on board who profit from CLA?Studies show it works.
What? CLA?It causes fatty liver. Not worth the risk over a long period.
I've been looking into Ammo and DCP.. looks promisingThere are much better things to use your money for. If you want help cutting, use something that's actually proven like: caffeine, ephedrine, yohimbe/alpha-y, forskolin, literally anything from EvoMuse ...
Wise advise here!Most research is done on obese individuals. for the majority of us on here that does not correlate to us. Most of these people have BMI's over 25-30
Most of the doses are also at least 6g. And even in obese patients not much was seen or changed from a fatloss standpoint.
https://www.ncbi.nlm.nih.gov/pubmed/16522907
"A 3.4-g daily CLA supplementation for 1 y does not prevent weight or fat mass regain in a healthy obese population."
https://www.ncbi.nlm.nih.gov/pubmed/21697535
CLA does not decreases body weight as compared with safflower oil in overweight and obese male subjects. (4.5g Dose of CLA)
https://www.ncbi.nlm.nih.gov/pubmed/17490954
CONCLUSION:
Given at a dose of 3.2 g/d, CLA produces a modest loss in body fat in humans.
whereas results in humans have been inconsistent.
https://www.ncbi.nlm.nih.gov/pubmed/21990002
The efficacy of long-term conjugated linoleic acid (CLA) supplementation on body composition in overweight and obese individuals: a systematic review and meta-analysis of randomized clinical trials.
CONCLUSION:
The evidence from RCTs does not convincingly show that CLA intake generates any clinically relevant effects on body composition on the long term.
you are much better spending your money on Yohimbine HCL or Forskolin 95 if you want some bulks. CLA is not really worth the merit or time.
Nope. its great to help elevate cAMP levels and get fatloss rolling.The Solution... Is it true that forskolin is really only good for people with sub %10 BF? Also, what's the optimal dose (mg) and dosing protocol (times per day) for forskolin? Can it be ran with Yohimbine?
Forskolin-95 is a pure 95% forskolin agent intended to deliver the plethora of potent effects associated with this compound. In particular, Forskolin-95 delivers:
- Powerful lipolytic and thermogenic effects
- Regulation of insulin signaling
- Potent cyclic AMP activation devoid of hormonal down-regulation
- Enhanced synthesis of steroid hormones such as testosterone
- Significant anabolic and anti-catabolic effects
So, what exactly is the key active in Forskolin-95, and how does it induce its effects?
A diterpene, forskolin is the key active principle of the Ayurvedic herb, Coleus forskohlii, and has been demonstrated to have a variety of powerful effects. [1] Forskolin’s focal mechanism of action is the stimulation of adenylate cyclase, the enzyme responsible for the downstream activation of the second messenger, cyclic AMP (3,5 cyclic adenosine monophosphate (cAMP)) in cells. [2,6,8] A central cell-regulating compound, cyclic AMP activates a range of other enzymes and membrane proteins involved in diverse cellular actions, such as stimulating anabolic and anti-catabolic effects, promoting the oxidation of fatty acids, inducing an increase in the body’s basal metabolic rates, boosting the levels of serum free testosterone, and promoting an increase in lean mass. [9,10]
Cyclic-AMP Activation
Although hormones, neurotransmitters and adrenergic receptor agonists are capable of activating cyclic AMP, the pathways they employ for this cyclic AMP stimulation might lead to a negative feedback effect, in which receptor or hormonal down-regulation occurs during prolonged or chronic expression of these hormones or stimulation of these agonists. Herein lies the advantage of forskolin: It can not only work in concert with these hormones and agonists, but can also activate adenylate cyclase (and consequently stimulate cAMP) completely independently of these hormones and receptors, averting the risk of hormonal or receptor down-regulation.
Protein Kinase A and Hormone Sensitive Lipase Activation
As is well known, the rate-limiting step in lipolysis is mediated by a cyclic-AMP mechanism. In particular, in this initial step, adenylate cyclase is hormonally activated, leading to an elevated synthesis of cyclic AMP and cyclic-AMP-dependent protein kinase (PKA), as well as the downstream phosphorylation and activation of enzyme hormone sensitive lipase (HSL). [3] Forskolin has been demonstrated to activate adenylate cyclase action (forskolin directly activates the catalytic subunit of adenylate cyclase), devoid of any upstream hormonal intervention, and increase cyclic AMP accumulation, leading to the release of fatty acids from adipose stores, and ultimately to thermogenesis and lipolysis in fat cells. [4,5,7,8]
Non-Stimulant Thermogenesis and Thyroid-Gland Stimulation
So, by activating cyclic AMP in adipose cells, completely independently of hormonal intervention, Forskolin-95 ultimately activates HSL, inducing potent lipolytic action by liberating free fatty acids in adipocytes to be used as substrates for energy regulation. Forskolin-95 induces this effect without the incorporation of any stimulant. Beyond this, Forskolin-96 enhances human and animal thyroid activity (comparable in strength to thyrotropin or thyroid-stimulating hormone (TSH)) by potently activating adenylate cyclase in the thyroid gland. [11,12] In particular, Forskolin-95 achieves this effect not only by stimulating the production of the thyroid hormones, T4 and T3, but also by stimulating the conversion of T4 into the metabolically more active T3. This thyroid stimulation supports increased basal metabolic rate and promotes thermogenesis.
Insulin Signaling
In another line of exploration relevant to body composition and fat loss, forskolin has been reported, in a rodent trial, to be involved in the beneficial modulation of insulin signaling, influencing macronutrient metabolism for preferential body compositional effects. [13]
Anabolic Effects
Furthermore, studies have demonstrated that forskolin not only induced a statistically significant reduction of adipose mass, but also stimulated increased bone mass and serum free testosterone levels, supporting forskolin’s anti-catabolic and anabolic effects. [9,10]
Synthesis of Steroid Hormones
Protein kinases (activated by cyclic AMP) play a crucial role in steroidogenesis or the synthesis of steroid hormones. [14] Trophic hormones, such as luteinizing hormone (LH) or adrenal corticotrophic hormone activate cyclic AMP, leading to the activation of protein kinase A (PKA) and the downstream phosphorylation of transcription factors that regulate the steroidogenic acute regulatory (StAR) protein transcription. StAR, a Leydig-cell cholesterol-transfer protein, is a critical protein in the biosynthesis of steroid hormones. In particular, StAR facilitates the transfer of cholesterol, the key substrate for all steroid hormones, to the inner mitochondrial membrane where cholesterol is converted to pregnenolone by the P450 side chain cleavage enzyme (P450scc), initiating the crucial formation of steroids. [15,16,17,18,19] This cascade is important, because the activation of the steroidogenic enzymes involved in the synthesis of testosterone from cholesterol cannot occur without the prior activation of the StAR protein by cyclic AMP. By activating cyclic AMP independently of trophic hormones, forskolin activates PKA and stimulates increased expression of the StAR protein, ultimately leading to steroidogenesis. [14] The steroids, including testosterone, produced in this process typically bind to intra-cellular androgen receptors, specifically activating so-called transcription genes. These steroidal molecules instruct the genes to induce specific effects, for instance, delivering anabolic effects such as increasing nitrogen retention and protein synthesis, reducing cortisol, and increasing IGF.
Further Anabolic Effects
Relatedly, as hypothalamic-pituitary-testicular axis (HPTA) shutdown is partly due to low levels of cyclic AMP, forskolin-induced elevation of cyclic AMP expression can stimulate the pituitary gland to increase the secretion of luteinizing hormone (LH), which in turn signals the Leydig cells of the gonads to boost the production of steroid hormones such as testosterone by stimulating the activity of the StAR protein, a Leydig cell cholesterol-transfer protein that plays a foundational role in the synthesis of testosterone. So, by potently elevating cyclic AMP levels, Forskolin-95 exerts a powerful anabolic effect via cyclic AMP-induced steroid biosynthesis.
Calpains, Calpastatin Gene Transcription and Anti-Catabolic Effects
Forskolin-95 also exerts an anti-catabolic effect, an effect that is also cyclic-AMP-dependent. Catabolism, in the sense of skeletal muscle mass, is the breakdown of muscle tissue, and reflects the hydrolytic degradation of muscle proteins, partially into peptides or completely into amino acids. This process, also called proteolysis, unlike other posttranslational modifications or changes (such as protein methylation, protein phosphorylation, and so on), is completely irreversible. Under normal circumstances, muscle mass is regulated by a balance between protein synthesis and protein degradation, and muscle breakdown can result when this equilibrium is impaired. [23]
The breakdown of muscle tissue is predominantly governed by calcium-dependent enzymes, known as calpains. Calpains are calcium-activated proteases that are involved in myofribrillar disassembly and channel the resulting myofibrillar structures into the ubiquitin-proteosome pathway (UPP), the primary proteolytic system in skeletal muscle, for degradation. [21] Apart from injury and calcium leak, calpains can be activated by physiological mechanisms in intact cells. [22] Calpain activity can be regulated by the endogenous inhibitor, calpastatin. Calcium, beyond being an important activator of calpains, also regulates the binding of calpastatins to caplains, leading to inhibition of calpain activity. [22] As it turns out, the activation of calpastatin is cyclic-AMP-dependent. As such, by activating cyclic AMP, Forskolin-95 exerts considerable anti-catabolic action by stimulating calpastatin gene transcription, thus inhibiting caplain activity, and ultimately promoting the preservation of lean muscle mass. [24]
Summary
So, Forskolin-95, predominantly via cyclic AMP activation, recruits a variety of pathways to elicit considerable thermogenic and lipolytic activity (and stimulate noticeable fat loss), exert powerful anabolic and anti-catabolic effects, induce thyroid-gland stimulation, boost steroid-hormone biosynthesis, and modulate beneficial insulin signaling.
A truly powerful and versatile compound, Forskolin-95 is a safe, reliable and effective agent that delivers a spectrum of results consistent with the different goals of bodybuilders, as well as fitness and sports enthusiasts.
References
1) Agarwal KC, Parks RE (1983).Forskolin: a potential antimetastic agent. Int J Cancer 32, 801-804.
2) Leamon KB, Padgett W & Daly, JW (1981). Forskolin: Unique diterpene activator of adenylate cyclase in membrane and intact cells. Proc. Natl. Acad. Sci 78, 3363-3367.
3) Belfrage P, Fredrikson G, Olsson H & Strilfors P (1982). Hormonal regulation of adipose tissue lipolysis by reversible phosphorylation of hormone-sensitive lipase. Prog. Clin. Biol. Res 102, 213-223.
4) Mooney RA, Swicegood CL & Marx RB (1986). Coupling of adenylate cyclase to lipolysis in permeabil- ized adipocytes: direct evidence that an antilipolytic effect of insulin is independent of adenylate cyclase. Endocrinology 119, 2240-2248.
5) Daly, JW (1984). Forskolin, adenylate cyclase and cell physiology: an overview. Adv. Cyclic Nucleotide Protein Phospholylution Res 17, 81-89.
6) De Souza NJ, Dohadwalla AN & Reden J (1983). Forskolin, A Labdane Diterpenoid with Antihypertensive, Positive Inotropic, Platelet Aggregation Inhibitory, and Adenylate Cyclase Activating Properties. Medicinal Research Reviews 3, 201-219.
7) Girardier L (1983). “Brown Fat: An Energy Dissipating Tissue”; In: Mammalian Thermogenesis; Girardier L, Sock M.J. Eds, Chapman and Hall Ltd, 50-98.
8) Burns TW, Langley PE, Terry BE, Bylund DB, Forte LR Jr (1987). Comparative effects of forskolin and isoproterenol on the cyclic AMP content of human adipocytes. Life Sci 40,145-154.
9) Godard MP, Johnson BA, Richmond SR (2005). Body Composition and Hormonal Adaptations Associated with Forskolin Consumption in Overweight and Obese Men. Obesity Research 13, 1335-1343.
10) Srivasta SK, Khatoon CS, Mehrotra SR (2002). Pharmacognostic evaluation of coleus forskohlii. Pharmaceutical Biology 40, 129-134.
11) Haye, B. et al. (1985) Chronic and acute effects of forskolin on isolated thyroid cell metabolism. Molecular and Cellular Endocrinology 43, 41-50.
12) Lauerberg P (1984). Forskolin stimulation of thyroid secretion of T4 and T3. FEBS Lett. 21, 273-276.
13) Yajima H. et al (1999). cAMP enhances insulin secretion by an action on the ATP-sensitive K+ channel-independent pathway of glucose signaling in rat pancreatic islets. Diabetes 48, 1006-12
14) Jones PM, Sayed SB, Persaud SJ, Burns CJ, Gyles S & Whitehouse BJ (2000). Cyclic AMP-induced expression of steroidogenic acute regulatory protein is dependent upon phosphoprotein phosphatase activities. Journal of Molecular Endocrinology 24, 233–239.
15) Clark BJ, Wells J, King SR, Stocco DM (1994). The purification, cloning, and expression of a novel luteinizing hormone-induced mitochondrial protein in MA-10 mouse Leydig tumor cells. Characterization of the steroidogenic acute regulatory protein (StAR). J. Biol. Chem. 269, 28314–28322.
16) Lin D, Sugawara T, Strauss JF III, Clark BJ, Stocco DM, Saenger P, Rogol A, Miller WL (1995). Role of steroidogenic acute regulatory protein in adrenal and gonadal steroidogenesis. Science 267, 1828–1831.
17) Stocco DM (1997). The steroidogenic acute regulatory (StAR) protein two years later. Endocrine 6, 99–109.
18) Wang X, Liu Z, Eimerl S, Timberg R, Weiss AM, Orly J, Stocco DM (1998). Effect of truncated forms of the steroidogenic acute regulatory protein on intramitochondrial cholesterol transfer. Endocrinology 139, 3903–3912.
19) Reinhart AJ, Williams SC, Stocco DM (1999). Transcriptional regulation of the StAR gene. Mol. Cell. Endocrinol 151, 161–169.
20) Averna M, De Tullio R, Capini P, Salamino F, Pontremoli S, Melloni E (2003). Changes in calpastatin localization and expression during calpain activation: a new mechanism for the regulation of intracellular Ca2+-dependent proteolysis. Cellular and Molecular Life Sciences 60, 2669-2678.
21) Hasselgreen PO, Wray C, Mammen J (2002). Molecular regulation of cachexia: it may be more than the proteasome. Biochem Biophys Res Common 290, 1-10.
22) Goll DE, Thompson VE, Li H, Wei W, Cong J (2003). The calpain system. Physiol Rev 83, 731–801.
23) Lang CH, Frost RA, Vary CV (2007). Regulation of muscle protein synthesis during sepsis and inflammation. Am J Physiol Endocrinol Metab 293, E453–E459.
24) Cong M, Goll DE, Antin PB (1998). cAMP responsiveness of the bovine calpastatin gene promoter. Biochem Biophys Acta. 1443, 186-92.
It causes fatty liver. Not worth the risk over a long period.
From this CLA thread: http://anabolicminds.com/forum/supplements/158943-cla-fat-loss.htmlNever rely on a secondary source; ever moreso when it's written on a meta-study.
the whole ihealth thing is based off two conflicting papers - one in mice and another in rats. Neither included work in a human model or trial. Both species of rodent responded differently - the rats saw improved insulin sensitivity and lower liver fat while the mice responded oppositely.
There is evidence from Belury 2003 that CLA improves insulin sensitivity in humans, which in turn relates to body mass. This would imply that the rat model is more inline with human data.
The point? Not all species necessarily react identically to a given substance, and there is good support for the correlation of moderate CLA to insulin sensitivity and body mass.
i took 6 grams a day for 4 months. When i had blood work, my liver enzymes were well above normal range. i even noticed increase inflammation(gum irritation and joint pain). CLA is one of the biggest lies in the supplement industry.. Better off with spending more on high grade fish oil.It causes fatty liver. Not worth the risk over a long period.
You want to make sure you have nothing in your stomach when taking the Yohimbine in the AM for fasted anything.TheSolution I workout in the am and have been taking PA (Tr1umph) pwo... if I add Yohimbine would it be wasteful? I mean will the fat and kcals in the PA prevent the Yohimbine from releasing fat stores since I won't be taking it fasted?
What are your thoughts on fasted HIIT? Would that be too catabolic?You want to make sure you have nothing in your stomach when taking the Yohimbine in the AM for fasted anything.
Personally if I were you I would do fasted AM Cardio with Yohimbine and train later. I would never train on a 100% fasted stomach (just me)
being how training is very catabolic.
But yes ingesting kcals from the Fat sources in that product would negate the effects of Y. you are almost intaking 100 kcals from that product alone.
Very bad idea. Hiit is far more catabolic then LISS (which taps fat reserves), HIIT utilizes glucose in the body due to the high demand and intensity. Especially if you are doing it right and 100% full throttle.What are your thoughts on fasted HIIT? Would that be too catabolic?
So you recommend just going for a walk (LISS) fasted or would jogging be ok?Very bad idea. Hiit is far more catabolic then LISS (which taps fat reserves), HIIT utilizes glucose in the body due to the high demand and intensity. Especially if you are doing it right and 100% full throttle.
HIIT can be more catabolic then training depending on intensity and length. Steer clear of doing that in a fasted state.
LISS + Yohimbine + Caffeine for AM (Caffeine enhances the properties of Yohimbine)So you recommend just going for a walk (LISS) fasted or would jogging be ok?
What if you're already on all that (and all Evomuse)?There are much better things to use your money for. If you want help cutting, use something that's actually proven like: caffeine, ephedrine, yohimbe/alpha-y, forskolin, literally anything from EvoMuse ...
I 2nd SNS Cla if your looking to try CLA. Cant beat the valueSNS CLA extreme would do you right OP. Cost effective and properly dosed.
Except it doesn't do much and isn't good for you IMHO.I 2nd SNS Cla if your looking to try CLA. Cant beat the value