Ok this compound is sold as fat loss agent, i was beta tester, and i got very painful muscle cramp from it. It had very wiered side effects on my body. But i looked into it and researched little and couldnt explain side i got from it. I think TTA can act as pro-oxidant if taken at large doses. Its chemical structure is very similar to alkylation agent used in chemotherapy treatment, which mean it maybe dangerous. It seem to act as chelating agent, and potent anti-oxidant at same time.TTA is a strong chelating agent, so binds calcium, potasiumn and copper or iron ions in radical scavenging. So that will cause lower NA+ and K+ in the cell, and thus an electrolyte imbalance, and you get the muscle cramps!! im not sure
Here is summary of my research finding on pubmed:
tetradecylthioacetic acid involve both peroxisome proliferator-activated receptor alpha (PARPA)-dependent and -independent pathways
TTA shows a very anti-proliferative effect with cells
TTA changes of fatty acids on lipid accumulation in adipocytes and primary hepatocytes. It reduces total cholesterol, and inhibts LDL oxidation
Im thinking to give this compound another try, but do you guys think it may be harmfull from data and research ......ect. There are limitted data on this compund, and its seems to me it mess up memebrane bound ion channel signaling pathways, which worries me.
well there are some positive studies particularly with respect to the oxidation of ldl leading to a reduction of foam cells, definitely a plus when talking about atherosclerotic plaque.
Tetradecylthioacetic Acid Inhibits the Oxidative Modification of Low Density Lipoprotein and 8-Hydroxydeoxyguanosine Formation In Vitro
Ziad A. Muna; Khaled Doudin; Jon Songstad; Rune J. Ulvik; ; Rolf K. Berge
From the Department of Clinical Biology, Division of Biochemistry, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway (Z.A.M., R.J.U., R.K.B) and the Department of Chemistry, University of Bergen, N-5007 Bergen, Norway (K.D., J.S.).
Correspondence to Ziad A. Muna, Department of Clinical Biology, Division of Biochemistry, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway. E-mail email@example.com
Abstract Oxidative modification of low-density lipoprotein (LDL) is thought to play a key role in the formation of foam cells and in initiation and progression of atherosclerotic plaque. The hypolipidemic 3-thia fatty acids contain a sulfur atom and might therefore possess reducing (antioxidant) properties. Consequently, the effects of 3-thia fatty acids on the susceptibility of LDL particles to undergo oxidative modification in vitro were studied. Tetradecylthioacetic acid (TTA), incorporated into the LDL particle and increased the lag time of copper ion induced LDL oxidation in a dose-dependent manner. 80 �mol/L TTA reduced the generation of lipid peroxides during copper ion induced LDL oxidation (for 2 hours) by 100%, 2,2'-azobis-(2,4-dimethylvaleronitrile) induced LDL oxidation by 64%, and 2,2'-azobis-(2-amidinopropane hydrochloride) induced LDL oxidation (for 6 hours) by 21%. The electrophoretic mobility of the oxidized LDL was reduced by TTA in both copper ion and azo-compounds initiated oxidation. This fatty acid analogue was effectively able to reduce in a dose dependent manner the formation of 8-hydroxydeoxyguanosine from 2-deoxyguanosine with ascorbic acid as the radical producer. TTA bound copper(II) ions and did not reduce copper(II) to copper(I). It failed to scavenge the 1.1-diphenyl-2-picrylhydrazyl radicals. The results suggest that the modification of LDL in the lipid and protein moieties can be significantly reduced by TTA. This acid may exert its antioxidant effect partially through metal ion binding and through free radical scavenging.
there aer also some compelling studies on fat loss.
J Lipid Res. 2002 May;43(5):742-50. Related Articles, Links
Tetradecylthioacetic acid prevents high fat diet induced adiposity and insulin resistance.
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.
Department of Clinical Biochemistry, University of Bergen, Haukeland Hospital, N-5021 Bergen, Norway.
Tetradecylthioacetic acid (TTA) is a non-beta-oxidizable fatty acid analog, which potently regulates lipid homeostasis. Here we evaluate the ability of TTA to prevent diet-induced and genetically determined adiposity and insulin resistance. In Wistar rats fed a high fat diet, TTA administration completely prevented diet-induced insulin resistance and adiposity. In genetically obese Zucker (fa/fa) rats TTA treatment reduced the epididymal adipose tissue mass and improved insulin sensitivity. All three rodent peroxisome proliferator-activated receptor (PPAR) subtypes were activated by TTA in the ranking order PPARalpha > PPARdelta > PPARgamma. Expression of PPARgamma target genes in adipose tissue was unaffected by TTA treatment, whereas the hepatic expression of PPARalpha-responsive genes encoding enzymes involved in fatty acid uptake, transport, and oxidation was induced. This was accompanied by increased hepatic mitochondrial beta-oxidation and a decreased fatty acid/ketone body ratio in plasma. These findings indicate that PPARalpha-dependent mechanisms play a pivotal role, but additionally, the involvement of PPARalpha-independent pathways is conceivable. Taken together, our results suggest that a TTA-induced increase in hepatic fatty acid oxidation and ketogenesis drains fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects of TTA on fat mass accumulation and peripheral insulin sensitivity.