DCP and sesamin
- 09-03-2007, 06:32 PM
DCP and sesamin
The search function wasn't working all that well for researching this, and links to the DCP writeup are not working either, so I apologize if this topic has been beaten to death.
I know I've read to cut sesamin dosage in half if you're using DCP...however I take higher doses than usual of Sesathin.
Is it even worth it to use these products together? Or should U just take a break from sesathin and use DCP?
If i AM going to use DCP and sesathin together, how exactly should I dose them? DCP as directed and 1/8TSP of sesamin 3X a day?
Also I know people like TTA preworkout, should DCP be taken then?
- 09-03-2007, 06:35 PM
DCP would be a good idea pre-WO because of the PLCAR and RK. Stick with 6 caps of DCP/day and try normal dosing on SesaThin. See how that works for you and then adjust if needed.M.Ed. Ex Phys
- 09-03-2007, 07:05 PM
Damage Control Protocol™
By Recomp Performance Nutrition™
This is a short, highly simplified write-up introducing our fat prevention/burning product. For those of you who enjoy a deeper read, an extensive write-up detailing each system involved and dietary suggestions will follow with more citations.
DCP is an effective combination of TetradecylThioacetic Acid (250mg), Salvia Miltiorrhiza Extract (standardized for 40% Mixed Tanshinones) (250mg), Propionyl-L-Carnitine (300mg), Potassium Pyruvate (300mg), and Raspberry Ketones (100mg). You may have seen some of these ingredients in
other products, but lets look at why we chose them specifically to work in concert to help you become the lean, mean, muscle building machine you want to be.
The center ingredient in which our product is based off of is of TetradecylThioacetic Acid (TTA). TTA is a 3-thia fatty acid which increases mitochondrial activity, which in itself provides numerous benefits. Insulin resistance is strongly linked to the reduction of glucose oxidation in mitochondria and a subsequent build up of glycolysis byproducts. Adipocytes also contribute hormones when fat is stored in them, so, the more fat you are carrying, the more inhibition of mitochondrial function you have (1). Mitochondria proteins function mainly to produce ATP, enhancing their function will, in short, burn more fuel. TTA enhances mitochondrial oxidative capacity and reduces free fatty acid and triglyceride levels as described below.
The peroxisome proliferator-activated receptors (PPARs) are transcription factors regulated by fatty acid derivatives, among others. These receptors are intimately involved in glucose regulation, cellular proliferation and differentiation, inflammation, and most important to us, fat metabolism. There are at present three types of PPARs: alpha, gamma, and delta. The liver is the main site where fatty acids are stored or burned for energy, depending on calorie intake. When fasting, fuel sources switch from carbohydrates and fats to mainly fats, and fatty acids are released from adipocytes. In the liver, they are either reesterified to triglycerides and form very low-density lipoproteins (VLDL), which then go on to restore in adipocytes or go to cardiac and skeletal muscle for energy. They can also be broken down through beta-oxidation to form ketones. PPAR-alpha mediates the genes controlling fatty acid uptake, beta-oxidation, and gamma-oxidation, which are upregulated when in a fasted state. TTA is a PPARalpha agonist, meaning it activates these receptors. Thus, you experience the same benefits even if you are in a fed state (9,15-18). PPAR-alpha also down-regulates apolipoprotein C-III which inhibits triglyceride hydrolysis, further enhancing lipid oxidation (2).
However, long term supplementation with TTA will force the body to compensate by upregulating fat storing enzymes. This discovery was the inspiration for DCP, and an explanation why TTA supplemented by itself for extended periods of time may lose its efficacy. Diacylglycerol acyltransferase (DGAT) stores fat, and is increased when TTA is consumed regularly (3). Enter Salvia Miltiorrhiza. Salvia Miltiorrhiza is a traditional Chinese herbal medicine commonly used to treat liver diseases for centuries, and contains constituents called tanshinones, which inhibit DGAT, preventing fat storage (4). Even though this could be the end of Salvia's role in DCP, lets take a brief look at some of its other underrated benefits. In rat studies, it may be neuroprotective (5), a free radical scavenger (6), antitumor (7), and anti-inflammatory (8), to name a few.
TTA also increases the activity of enzymes of the carnitine palmitoyltransferase (CPT) sytem (9), which shuttles the newly freed up fatty acids into mitochondria to be burned for fuel (10). This system is highly underestimated in a fat loss quest, and it's activity is depressed with increased fat. Propionyl-LCarnitine (PLCAR) was added to further stimulate the CPT system (11), and is converted into propionylcoenzyme A and free carnitine (12). PLCAR has also been suspected to scavenge free radicals, as well as protect DNA from UV damage (12). PLCAR also has some interesting performance enhancements, specifically on endurance, from anecdotal feedback and possible mechanisms will be elucidated in the extended write-up.
Pyruvate is involved in another complex system called the Pyruvate Dehydrogenase Complex (PDC), which interacts with the CPT system (13). Pyruvate is a Krebs Cycle intermediate, which is rate controlled by the amount of acetyl-CoA that enters the cycle, one of the conversions from pyruvate (13). For simplicity's sake, the result is an ATP/energy enhancement from the mitochondria and an increase in fuel consumption. The electrolyte potassium form was added to attenuate cramping issues observed from previous TTA products.
Raspberry Ketones (RK) add the finishing touch to DCP. RK is similar in structure to capsaicin and synephrine, and also has been shown to modulate fat metabolism. RK stimulates the release of norepinephrine (NE), a catecholamine with many functions. Most importantly to us is its role in the sympathetic nervous system. NE, having a great affinity on beta and alpha-1 adrenoreceptors in the body, activates lipolysis that normally only occurs during exercise or other intensive activity. This results in an increase of free fatty acids which will be burned via methods described above (14).
As you can see, DCP attacks fat from many angles. It can be especially effective when bulking to prevent fat storage and also has appetite suppressive properties in some users, or used in a cut to potentiate the body's fasting enzymatic response.
Take control of your body with Damage Control Protocol!
1. Petersen KF. Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes. The New England journal of medicine 2004;350(7):664-.
2. Lee CH, Olson P, Evans RM. Minireview: lipid metabolism, metabolic diseases, and peroxisome proliferator-activated receptors. Endocrinology 2003;144(6):2201-7.
3. Asiedu DK, Frøyland L, Vaagenes H, Lie O, Demoz A, Berge RK. Long-term effect of
tetradecylthioacetic acid: a study on plasma lipid profile and fatty acid composition and oxidation in different rat organs. Biochimica et biophysica acta 1996;1300(2):86-96.
4. Ko JS, Ryu SY, Kim YS, Chung MY, Kang JS, Rho MC, Lee HS, Kim YK. Inhibitory activity of diacylglycerol acyltransferase by tanshinones from the root of Salvia miltiorrhiza. Archives of pharmacal research 2002;25(4):446-8.
5. Lam BY, Lo AC, Sun X, Luo HW, Chung SK, Sucher NJ. Neuroprotective effects of tanshinones in transient focal cerebral ischemia in mice. Phytomedicine 2003;10(4):286-91.
6. Zhao BL, Jiang W, Zhao Y, Hou JW, Xin WJ. Scavenging effects of salvia miltiorrhiza on free radicals and its protection for myocardial mitochondrial membranes from ischemia-reperfusion injury. Biochemistry and molecular biology international 1996;38(6):1171-82.
7. Liu J, Shen HM, Ong CN. Salvia miltiorrhiza inhibits cell growth and induces apoptosis in human ="" size="1">8. Kim SY, Moon TC, Chang HW, Son KH, Kang SS, Kim HP. Effects of tanshinone I isolated from Salvia miltiorrhiza bunge on arachidonic acid metabolism and in vivo inflammatory responses. Phytotherapy research 2002;16(7):616-20.
9. Raspé E, Madsen L, Lefebvre AM, Leitersdorf I, Gelman L, Peinado-Onsurbe J, Dallongeville J, Fruchart JC, Berge R, Staels B. Modulation of rat liver apolipoprotein gene expression and serum lipid levels by tetradecylthioacetic acid (TTA) via PPARalpha activation. Journal of lipid research 1999;40(11):2099-110.
10. McGarry JD. The mitochondrial carnitine palmitoyltransferase system. From concept to molecular analysis. The FEBS journal 1997;244(1):1-.
11. Karlic H, Lohninger S, Koeck T, Lohninger A. Dietary l-carnitine stimulates carnitine
acyltransferases in the liver of aged rats. The journal of histochemistry and cytochemistry 2002;50(2):205-12.
12. Vanella A, Russo A, Acquaviva R, Campisi A, Di Giacomo C, Sorrenti V, Barcellona ML. L -propionylcarnitine as superoxide scavenger, antioxidant, and DNA cleavage protector. Cell biology and toxicology 2000;16(2):99-104.
13. Sugden MC, Holness MJ. Interactive regulation of the pyruvate dehydrogenase complex and the carnitine palmitoyltransferase system. The FASEB journal 1994;8(1):54-61.
14. Morimoto C, Satoh Y, Hara M, Inoue S, Tsujita T, Okuda H. Anti-obese action of raspberry ketone. Life sciences 2005;77(2):194-204.
15. Berge K, Tronstad KJ, Flindt EN, Rasmussen TH, Madsen L, Kristiansen K, Berge RK.
Tetradecylthioacetic acid inhibits growth of rat glioma cells ex vivo and in vivo via PPAR-dependent and PPAR-independent pathways. Carcinogenesis 2001;22(11):1747-55.
16. Bocos C, Göttlicher M, Gearing K, Banner C, Enmark E, Teboul M, Crickmore A, Gustafsson JA. Fatty acid activation of peroxisome proliferator-activated receptor (PPAR). The Journal of steroid biochemistry and molecular biology 1995;53(1-6):467-73.
17. Madsen L, Guerre-Millo M, Flindt EN, Berge K, Tronstad KJ, Bergene E, Sebokova E, Rustan AC, Jensen J, Mandrup S, Kristiansen K, Klimes I, Staels B, Berge RK. Tetradecylthioacetic acid prevents high fat diet induced adiposity and insulin resistance. Journal of lipid research 2002;43(5):742-50.
18. Berge RK, Skorve J, Tronstad KJ, Berge K, Gudbrandsen OA, Grav H. Metabolic effects of thia fatty acids. Current opinion in lipidology 2002;13(3):295-304.
09-03-2007, 07:09 PM
I think 2 caps 30min pre-workout would be a good time, otherwise, DCP should be taken 30min before a meal.
Sesamin.. as you have taken before, after a meal, but preferably not around (pre/post) workout. You may not need so much, but go by how you feel on your normal sesathin dose and adjust accordingly. When you read about the half dosage issue, was this with DCP or MP?
There is definitely some potential for synergy between sesathin and DCP, both are PPARalpha agonists.
Please keep us updated on how it goes for you.
09-03-2007, 08:20 PM
I'll try it 6 caps/day with normal doses of sesathin, and just cut back my dose of sesathin until cramps fade or become manageable.
Another question, I take 5-7g Fish oil per day as well, is this too much PPAR inhibition, in other words would it be more cost efficient to just cut sesathin out during my DCP usage?
I only ask because money is tight (I've been out of work for 8 weeks and cannot be cleared to return to work for another 2 months as I had a pretty nasty break in my fibula) and it might behoove me to not use all three at once.
09-05-2007, 07:23 PM
You can certainly do DCP + fish oil.. I logged this a few months back using just those two and some antioxidants with good results.
09-05-2007, 07:37 PM
I take DCP and sesathin together with no cramping or problems, I also take it with 3 fish oil caps a day.
09-05-2007, 10:25 PM
Okay im going to try it out soon.
Unfortunately is one of those leaky bottles so it looks like a total mess in there lol.
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