TTA-500
- Thread starter rinnelle
- Start date
Synapsin
Well-known member
TTA has the benefits of acting as a hypolipidemic agent, mitochondrial proliferation, increased catabolism of fatty acids, antioxidant properties, antinflam action etc. TTA most definitely works, and you will be safe taking it at 1g for 1-2 months (but cycle off please, don't take it non stop). The good thing about the SNS version is it includes electrolytes which help with cramping people experience from TTA.
If you buy it, try a cycle of 1-2 months at 2 caps a day. Just don't forget to cycle off. Cheers.
If you buy it, try a cycle of 1-2 months at 2 caps a day. Just don't forget to cycle off. Cheers.
3clipseGT
On my grind
Good info right here
MAxximal
Well-known member
Department of Clinical Biology, University of Bergen, Norway
Administration of tetradecylthioacetic acid (a 3-thia fatty acid) increases mitochondrial and peroxisomal beta-oxidative capacity and carnitine palmitoyltransferase activity, but reduces free fatty acid and triacylglycerol levels in plasma compared to palmitic acid-treated rats and controls. The decrease in plasma triacylglycerol was accompanied by a reduction (56%) in VLDL-triacylglycerol. Prolonged supplementation of tetradecylthioacetic acid caused a significant increase in lipogenic enzyme activities (ATP-citrate lyase and acetyl-CoA carboxylase) and diacylglycerol acyltansferase, but did not affect phosphatidate phosphohydrolase. Plasma cholesterol, LDL- and HDL-cholesterol levels were reduced. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase activity was, however, stimulated in 3-thia fatty acid-treated rats compared to controls. In addition. the mRNAs of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and LDL-receptor were increased. Tetradecylthioacetic acid administration affected the fatty acid composition in plasma and liver by increasing the amount of monoenes, especially 18:1(n-9), mostly at the expense of omega-3 fatty acids. Compared to liver a large amount of tetradecylthioacetic acid accumulated in the heart, and this accumulation was accompanied by an increase in omega-3 fatty acids, particularly 22:6(n-3) and a decrease in omega-6 fatty acids, mainly 20:4(n-6). The results show that the hypolipidemic effect of tetradecylthioacetic acid is sustained after prolonged administration and may, at least in part, be due to increased fatty acid oxidation and upregulated LDL-receptor gene expression. The increase in lipogenic enzyme activities as well as increased 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity, may be compensatory mechanisms to maintain cellular integrity. Decreased level of 20:4(n-6) combined with increased omega-3/omega-6 ratio in cardiac tissue after tetradecylthioacetic acid treatment may have influence on membrane dynamics and function.
Tetradecylthioacetic acid a 3-thia fatty acid, is a novel bioactive compound. Besides being an antioxidant, it changes the plasma profile from atherogenic to cardioprotective
Ziad A. Muna, Lise Madsen, and Rolf K. Berge
Department of Clinical Biology, Division of Biochemistry, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway
Tetradecylthioacetic acid (TTA) which can not be ß-oxidized, lowers plasma VLDL-triacylglycerol (TG) and LDL-cholesterol (Chol). Increased mitochondrial ß-oxidation with a concomitant decrease in TG synthesis and secretion, seems to be the primary mechanism underlying the hypotriglyceridemic effect not only of TTA but also of w-3 fatty acids as well as fibrates in rats, rabbits, dogs and possibly also in humans. TTA is an inhibitor of HMG-CoA reductase. We have generated results both in vivo and in vitro that present evidence that TTA besides being a lipid lowering agent, also possesses antioxidant properties. First, TTA inhibits the oxidative modification of LDL which is considered as the key step in the formation of foam cells and in initiation and progression of atherosclerotic plaque. Also TTA changes the antioxidant defense system in a beneficial way i.e. glutathion (GSH) is increased, the total antioxidant status is elevated and TBARS are decreased. Second, TTA has an ³olive oil² effect since the plasma was enriched with oleic acid (18:1 n-9) and a 9-desaturated metabolite of TTA. This was due to upregulation of the hepatic enzyme 9-desaturase gene expression. Third, TTA lowers the plasma homocysteine level and inhibits restenosis. Fourth, TTA reduces the proliferation of smooth muscle cells. In conclusion, TTA is a hypolipidemic drug but also a new antioxidant. This novel bioactive compound is promising as a new therapeutic drug against atherosclerosis as it changes the plasma profile from atherogenic to cardioprotective.
The metabolic syndrome and the hepatic fatty acid drainage hypothesis.
Berge RK, Tronstad KJ, Berge K, Rost TH, Wergedahl H, Gudbrandsen OA, Skorve J.
Institute of Medicine, The Lipid Research Group, Haukeland University Hospital, University of Bergen, 5021 Bergen, Norway. [email protected]
Abstract
Much data indicates that lowering of plasma triglyceride levels by hypolipidemic agents is caused by a shift in the liver metabolism towards activation of peroxisome proliferator activated receptor (PPAR)alpha-regulated fatty acid catabolism in mitochondria. Feeding rats with lipid lowering agents leads to hypolipidemia, possibly by increased channeling of fatty acids to mitochondrial fatty acid oxidation at the expense of triglyceride synthesis. Our hypothesis is that increased hepatic fatty acid oxidation and ketogenesis drain fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects on fat mass accumulation and improved peripheral insulin sensitivity. To investigate this theory we employ modified fatty acids that change the plasma profile from atherogenic to cardioprotective. One of these novel agents, tetradecylthioacetic acid (TTA), is of particular interest due to its beneficial effects on lipid transport and utilization. These hypolipidemic effects are associated with increased fatty acid oxidation and altered energy state parameters of the liver. Experiments in PPAR alpha-null mice have demonstrated that the effects hypolipidemic of TTA cannot be explained by altered PPAR alpha regulation alone. TTA also activates the other PPARs (e.g., PPAR delta) and this might compensate for deficiency of PPAR alpha. Altogether, TTA-mediated clearance of blood triglycerides may result from a lowered level of apo C-III, with a subsequently induction of hepatic lipoprotein lipase activity and (re)uptake of fatty acids from very low density lipoprotein (VLDL). This is associated with an increased hepatic capacity for fatty acid oxidation, causing drainage of fatty acids from the blood stream. This can ultimately be linked to hypolipidemia, anti-adiposity, and improved insulin sensitivity.
PMID: 15733731 [PubMed - indexed for MEDLINE]
Transient up-regulation of liver mitochondrial thymidine kinase activity in proliferating mitochondria.
Elholm M, Hollås H, Issalene C, Barroso JF, Berge RK, Flatmark T.
Department of Biochemistry and Molecular Biology, University of Bergen, Norway. [email protected]
Abstract
Administration of the fatty acid analogue tetradecylthioacetic acid (TTA) to rodents up-regulates peroxisomal and mitochondrial lipid-metabolizing enzymes and induces a proliferation of these organelles in hepatocytes. We show here that male NMRI mice fed a diet containing 0.3% (w/w) TTA revealed a transient two-fold increase in the incorporation of [3H]thymidine into the liver mtDNA followed by a 1.6-fold increase in the content of mtDNA. In addition, a transient three-fold increase in the mitochondrial thymidine kinase (TK2) activity and a slight increase in the DNA polymerase gamma activity was observed, indicating that the TTA induced mitochondrial proliferation is linked to an up-regulation of the mitochondrial thymidine kinase activity.
PMID: 11463171 [PubMed - indexed for MEDLINE]
Proliferation of mitochondria and gene expression of carnitine palmitoyltransferase and fatty acyl-CoA oxidase in rat skeletal muscle, heart and liver by hypolipidemic fatty acids.
Totland GK, Madsen L, Klementsen B, Vaagenes H, Kryvi H, Frøyland L, Hexeberg S, Berge RK.
Department of Zoology, University of Bergen, Norway. [email protected]
Abstract
Morphological and biochemical effects were induced at the subcellular level in the skeletal muscle, heart and liver of male rats as a result of feeding with EPA, DHA, and 3-thia fatty acids. The 3-thia fatty acid, tetradecylthioacetic acid (TTA) and EPA induced mitochondrial growth in type I muscle fibers in both the diaphragm and soleus muscle, and the size distribution of mitochondrial areas followed a similar pattern. Only the 3-thia fatty acid induced mitochondrial growth in type II muscle fibers. The mean area occupied by the mitochondria and the size distribution of mitochondrial areas in both fiber types were highly similar in DHA-treated and control animals. Only the 3-thia fatty acid increased the gene-expression of carnitine palmitoyltransferase (CPT)-II in the diaphragm. In the heart, however, the gene expression decreased. In hepatocytes an increase in the mean size of mitochondria was observed after EPA treatment, concomitant with an increase in mitochondrial CPT-II gene expression. Administration of 2-methyl-substituted EPA (methyl-EPA) induced a higher rate of growth of mitochondria than EPA. At the peroxisomal level in the hepatocytes a 3-thia fatty acid, EPA, and DHA increased the areal fraction concomitant with the induction of gene expression of peroxisomal fatty acyl-CoA oxidase (FAO). In the diaphragm, mRNA levels of FAO were not affected by EPA or DHA treatment, whereas gene expression was significantly increased after 3-thia fatty acid treatment. In the heart, both 3-thia fatty acid, EPA and DHA tended to decrease the levels of FAO mRNA. The areal fraction of fat droplets in all three tissue types was significantly lower in the groups treated with 3-thia fatty acid. In the group treated with EPA a lower areal fraction of fat droplets was observed, while the DHA group was similar to the control. This indicates that EPA and DHA have different effects on mitochondrial biogenesis.
PMID: 11071041 [PubMed - indexed for MEDLINE]
The metabolic effects of thia fatty acids in rat liver depend on the position of the sulfur atom.
Gudbrandsen OA, Dyroy E, Bohov P, Skorve J, Berge RK.
The Lipid Research Group, Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway. [email protected]
The effects on oxidation and composition of fatty acids in rat liver were compared after administration of fatty acids with sulfur substituted in different positions. It has been hypothesized that drugs with hydrophobic backbone have lipid-lowering effects because they are not easily catabolized by mitochondrial beta-oxidation. Thia fatty acids cannot be beta-oxidized when sulfur is in 3-position, but beta-oxidation is possible when sulfur is positioned further from the carboxyl group. To investigate whether catabolism of thia fatty acids would affect their ability to influence lipid metabolism, a series of thia fatty acids were synthesized and administered by oral gavage to male Wistar rats (300 mg/kg bodyweight/day for 7 days). Depending on the position of the sulfur atom and the chain length, the thia fatty acids were beta-oxidized, desaturated and/or elongated, and the accumulated amounts were lower as the sulfur atom were positioned further from the carboxyl group. All thia fatty acids led to high peroxisomal beta-oxidation of endogenous fatty acids, whereas the mitochondrial beta-oxidation was high when sulfur was in 3-position, low when sulfur was in 4-position and similar to controls when sulfur was in 5- or 7-position. The changes in hepatic fatty acid composition were more pronounced when sulfur was positioned close to the carboxyl group. In conclusion, both the position of the sulfur atom and the chain length appear to determine the catabolic fate of thia fatty acids, and the non-beta-oxidizable thia fatty acids were most potent in regulating oxidation and composition of endogenous fatty acids in rat liver.
Administration of tetradecylthioacetic acid (a 3-thia fatty acid) increases mitochondrial and peroxisomal beta-oxidative capacity and carnitine palmitoyltransferase activity, but reduces free fatty acid and triacylglycerol levels in plasma compared to palmitic acid-treated rats and controls. The decrease in plasma triacylglycerol was accompanied by a reduction (56%) in VLDL-triacylglycerol. Prolonged supplementation of tetradecylthioacetic acid caused a significant increase in lipogenic enzyme activities (ATP-citrate lyase and acetyl-CoA carboxylase) and diacylglycerol acyltansferase, but did not affect phosphatidate phosphohydrolase. Plasma cholesterol, LDL- and HDL-cholesterol levels were reduced. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase activity was, however, stimulated in 3-thia fatty acid-treated rats compared to controls. In addition. the mRNAs of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and LDL-receptor were increased. Tetradecylthioacetic acid administration affected the fatty acid composition in plasma and liver by increasing the amount of monoenes, especially 18:1(n-9), mostly at the expense of omega-3 fatty acids. Compared to liver a large amount of tetradecylthioacetic acid accumulated in the heart, and this accumulation was accompanied by an increase in omega-3 fatty acids, particularly 22:6(n-3) and a decrease in omega-6 fatty acids, mainly 20:4(n-6). The results show that the hypolipidemic effect of tetradecylthioacetic acid is sustained after prolonged administration and may, at least in part, be due to increased fatty acid oxidation and upregulated LDL-receptor gene expression. The increase in lipogenic enzyme activities as well as increased 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity, may be compensatory mechanisms to maintain cellular integrity. Decreased level of 20:4(n-6) combined with increased omega-3/omega-6 ratio in cardiac tissue after tetradecylthioacetic acid treatment may have influence on membrane dynamics and function.
Tetradecylthioacetic acid a 3-thia fatty acid, is a novel bioactive compound. Besides being an antioxidant, it changes the plasma profile from atherogenic to cardioprotective
Ziad A. Muna, Lise Madsen, and Rolf K. Berge
Department of Clinical Biology, Division of Biochemistry, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway
Tetradecylthioacetic acid (TTA) which can not be ß-oxidized, lowers plasma VLDL-triacylglycerol (TG) and LDL-cholesterol (Chol). Increased mitochondrial ß-oxidation with a concomitant decrease in TG synthesis and secretion, seems to be the primary mechanism underlying the hypotriglyceridemic effect not only of TTA but also of w-3 fatty acids as well as fibrates in rats, rabbits, dogs and possibly also in humans. TTA is an inhibitor of HMG-CoA reductase. We have generated results both in vivo and in vitro that present evidence that TTA besides being a lipid lowering agent, also possesses antioxidant properties. First, TTA inhibits the oxidative modification of LDL which is considered as the key step in the formation of foam cells and in initiation and progression of atherosclerotic plaque. Also TTA changes the antioxidant defense system in a beneficial way i.e. glutathion (GSH) is increased, the total antioxidant status is elevated and TBARS are decreased. Second, TTA has an ³olive oil² effect since the plasma was enriched with oleic acid (18:1 n-9) and a 9-desaturated metabolite of TTA. This was due to upregulation of the hepatic enzyme 9-desaturase gene expression. Third, TTA lowers the plasma homocysteine level and inhibits restenosis. Fourth, TTA reduces the proliferation of smooth muscle cells. In conclusion, TTA is a hypolipidemic drug but also a new antioxidant. This novel bioactive compound is promising as a new therapeutic drug against atherosclerosis as it changes the plasma profile from atherogenic to cardioprotective.
The metabolic syndrome and the hepatic fatty acid drainage hypothesis.
Berge RK, Tronstad KJ, Berge K, Rost TH, Wergedahl H, Gudbrandsen OA, Skorve J.
Institute of Medicine, The Lipid Research Group, Haukeland University Hospital, University of Bergen, 5021 Bergen, Norway. [email protected]
Abstract
Much data indicates that lowering of plasma triglyceride levels by hypolipidemic agents is caused by a shift in the liver metabolism towards activation of peroxisome proliferator activated receptor (PPAR)alpha-regulated fatty acid catabolism in mitochondria. Feeding rats with lipid lowering agents leads to hypolipidemia, possibly by increased channeling of fatty acids to mitochondrial fatty acid oxidation at the expense of triglyceride synthesis. Our hypothesis is that increased hepatic fatty acid oxidation and ketogenesis drain fatty acids from blood and extrahepatic tissues and that this contributes significantly to the beneficial effects on fat mass accumulation and improved peripheral insulin sensitivity. To investigate this theory we employ modified fatty acids that change the plasma profile from atherogenic to cardioprotective. One of these novel agents, tetradecylthioacetic acid (TTA), is of particular interest due to its beneficial effects on lipid transport and utilization. These hypolipidemic effects are associated with increased fatty acid oxidation and altered energy state parameters of the liver. Experiments in PPAR alpha-null mice have demonstrated that the effects hypolipidemic of TTA cannot be explained by altered PPAR alpha regulation alone. TTA also activates the other PPARs (e.g., PPAR delta) and this might compensate for deficiency of PPAR alpha. Altogether, TTA-mediated clearance of blood triglycerides may result from a lowered level of apo C-III, with a subsequently induction of hepatic lipoprotein lipase activity and (re)uptake of fatty acids from very low density lipoprotein (VLDL). This is associated with an increased hepatic capacity for fatty acid oxidation, causing drainage of fatty acids from the blood stream. This can ultimately be linked to hypolipidemia, anti-adiposity, and improved insulin sensitivity.
PMID: 15733731 [PubMed - indexed for MEDLINE]
Transient up-regulation of liver mitochondrial thymidine kinase activity in proliferating mitochondria.
Elholm M, Hollås H, Issalene C, Barroso JF, Berge RK, Flatmark T.
Department of Biochemistry and Molecular Biology, University of Bergen, Norway. [email protected]
Abstract
Administration of the fatty acid analogue tetradecylthioacetic acid (TTA) to rodents up-regulates peroxisomal and mitochondrial lipid-metabolizing enzymes and induces a proliferation of these organelles in hepatocytes. We show here that male NMRI mice fed a diet containing 0.3% (w/w) TTA revealed a transient two-fold increase in the incorporation of [3H]thymidine into the liver mtDNA followed by a 1.6-fold increase in the content of mtDNA. In addition, a transient three-fold increase in the mitochondrial thymidine kinase (TK2) activity and a slight increase in the DNA polymerase gamma activity was observed, indicating that the TTA induced mitochondrial proliferation is linked to an up-regulation of the mitochondrial thymidine kinase activity.
PMID: 11463171 [PubMed - indexed for MEDLINE]
Proliferation of mitochondria and gene expression of carnitine palmitoyltransferase and fatty acyl-CoA oxidase in rat skeletal muscle, heart and liver by hypolipidemic fatty acids.
Totland GK, Madsen L, Klementsen B, Vaagenes H, Kryvi H, Frøyland L, Hexeberg S, Berge RK.
Department of Zoology, University of Bergen, Norway. [email protected]
Abstract
Morphological and biochemical effects were induced at the subcellular level in the skeletal muscle, heart and liver of male rats as a result of feeding with EPA, DHA, and 3-thia fatty acids. The 3-thia fatty acid, tetradecylthioacetic acid (TTA) and EPA induced mitochondrial growth in type I muscle fibers in both the diaphragm and soleus muscle, and the size distribution of mitochondrial areas followed a similar pattern. Only the 3-thia fatty acid induced mitochondrial growth in type II muscle fibers. The mean area occupied by the mitochondria and the size distribution of mitochondrial areas in both fiber types were highly similar in DHA-treated and control animals. Only the 3-thia fatty acid increased the gene-expression of carnitine palmitoyltransferase (CPT)-II in the diaphragm. In the heart, however, the gene expression decreased. In hepatocytes an increase in the mean size of mitochondria was observed after EPA treatment, concomitant with an increase in mitochondrial CPT-II gene expression. Administration of 2-methyl-substituted EPA (methyl-EPA) induced a higher rate of growth of mitochondria than EPA. At the peroxisomal level in the hepatocytes a 3-thia fatty acid, EPA, and DHA increased the areal fraction concomitant with the induction of gene expression of peroxisomal fatty acyl-CoA oxidase (FAO). In the diaphragm, mRNA levels of FAO were not affected by EPA or DHA treatment, whereas gene expression was significantly increased after 3-thia fatty acid treatment. In the heart, both 3-thia fatty acid, EPA and DHA tended to decrease the levels of FAO mRNA. The areal fraction of fat droplets in all three tissue types was significantly lower in the groups treated with 3-thia fatty acid. In the group treated with EPA a lower areal fraction of fat droplets was observed, while the DHA group was similar to the control. This indicates that EPA and DHA have different effects on mitochondrial biogenesis.
PMID: 11071041 [PubMed - indexed for MEDLINE]
The metabolic effects of thia fatty acids in rat liver depend on the position of the sulfur atom.
Gudbrandsen OA, Dyroy E, Bohov P, Skorve J, Berge RK.
The Lipid Research Group, Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021 Bergen, Norway. [email protected]
The effects on oxidation and composition of fatty acids in rat liver were compared after administration of fatty acids with sulfur substituted in different positions. It has been hypothesized that drugs with hydrophobic backbone have lipid-lowering effects because they are not easily catabolized by mitochondrial beta-oxidation. Thia fatty acids cannot be beta-oxidized when sulfur is in 3-position, but beta-oxidation is possible when sulfur is positioned further from the carboxyl group. To investigate whether catabolism of thia fatty acids would affect their ability to influence lipid metabolism, a series of thia fatty acids were synthesized and administered by oral gavage to male Wistar rats (300 mg/kg bodyweight/day for 7 days). Depending on the position of the sulfur atom and the chain length, the thia fatty acids were beta-oxidized, desaturated and/or elongated, and the accumulated amounts were lower as the sulfur atom were positioned further from the carboxyl group. All thia fatty acids led to high peroxisomal beta-oxidation of endogenous fatty acids, whereas the mitochondrial beta-oxidation was high when sulfur was in 3-position, low when sulfur was in 4-position and similar to controls when sulfur was in 5- or 7-position. The changes in hepatic fatty acid composition were more pronounced when sulfur was positioned close to the carboxyl group. In conclusion, both the position of the sulfur atom and the chain length appear to determine the catabolic fate of thia fatty acids, and the non-beta-oxidizable thia fatty acids were most potent in regulating oxidation and composition of endogenous fatty acids in rat liver.
MAxximal
Well-known member
antihero
Well-known member
I couldn't have said it any better myself.
MAxximal
Well-known member
Great!!!
ax1
Legend
TTA will be coming back
Sounds good....I may get it and stack it with bulk Dan Shen.
ax1
Legend
Well....I didnt get it yet, but I will be ordering from a Chinese medicine shop online. I have the option of going to China Town in NYC too if I felt like it.
It would be difficult to match up to what you would get in DCP.
I already like TTA.....wouldnt hurt to see the addition of Dan Shen. Im considering dosing the Dan Shen a little higher but not too much higher.
ax1
Legend
TTA is back
Cool!
Oh....and thanks for the info Max....Ill look into it.
I have a pretty cheap source for Salvia in 10gr bulk powder packets, at about 35 cents a packet that I may try from a TCM shop.
Dunno when I will for sure though.
Outstanding
Well-known member
Synapsin
Well-known member
Why does it need to be cycled? Thanks
As with anything of it's nature, it can be potentially dangerous to run it long term (and I mean > 6 months), not to mention not as effective with the concept of homeostasis in mind. Better safe than sorry.
Outstanding
Well-known member
Invalid Link Removed
What happens at month 6, to make it dangerous, that doesn't happen at month 1-5?
Also, has the concept of homeostasis ever been proven legitimate with clinical findings based on blood profiles where DAA is concerned, or any other natural supplement taken for an extended duration?
sns8778
Board Sponsor
Why does it need to be cycled? Thanks
I am not sure why you are intent on wanting to start drama as this was carried over from you getting angry in the DAA thread. I really think you took my and Synapsin's reply over there the wrong way.
To give you an answer though - as with most fat loss products/ingredients, the thought is that tolerance can develop over time, and most people feel that it is best to cycle these types of products.
You can also find further information on TTA and cycling from years back from some very intelligent people such as Dsade, Matt Cahill, some of the DS reps when they made their Melting Point, etc.
You seemed to take offense in the other thread by the fact that in the absence of evidence saying that something can be taken safely for indefinate periods of time that we would recomend cycling of things, but that is the stance of most supplement companies.
As I did in the DAA thread, I have attempted to answer your question. If you have any further questions, feel free to ask me in the thread, or by pm.
We are here to to provide top quality products at cost effective prices, and try to help customers to the best of our ability, not argue.
Outstanding
Well-known member
I wasn't angry, you injected a lot of your perception into my one sentence question with a smiley face at the end, but thanks for your response.
I simply bowed out of the thread because it was obvious where it was going. There is no such this as certainty in supplementation science, that's all I was saying. Dr. D and other members have been using DAA for a very long time and experienced no ill effect.
Anyway, I like both DAA and TTA, I've used and am using one or the other right now and plan to keep doing so for a long time to come. Please, don't be swayed to believe anything less than the truth simply because I have a competing company's acronym attached below my posts.
sns8778
Board Sponsor
I tried my best to answer your questions the best I could. You made the implication that we used a blanket approach to providing directions and that isnt the case. We suggest using each individual supplement the way we feel it is best suited for use. If other companies take a different approach, that is their right.
Just because you dont agree with the directions doesnt make them any less true. I would much rather tell someone not to exceed ___ period of use, and it later be proved that they could have taken it indefinately than to say to take someone indefinately and then it turn out they shouldnt have exceeded a certain period of time. In the case of DAA, it makes logical sense to run it the way people do most products that affect hormone levels, which is by cycling them.
In regards to D or other people running it indefinately, I cannot control how long they run things. That is their right to exercise their personal choice. It still doesnt make it the right way to do it. It doesnt mean its wrong, but doesnt make it right either. And in absence of knowing, I prefer to suggest our customers err on the side of caution.
I would have replied the same, I really didnt even pay attention to you representing another company. Some companies may make certain replies based off things like that, but I focus on what SNS is doing, not other companies, and I treat forum posters all as potential customers whether affiliated with another company or not.
chedapalooza
Legend
So tta is non stim correct? I'm gonna be logging 3z for Ann innovations in sept- I USUALLY take a pm fat loss product/sleep but the 3z is purely sleep aid so I want to add something to help with overnight leaving... Thinking tta, any thing else I can add as well (non stim obviously ) thanks guys
kingjameskjf
Well-known member
TTA is the perfect addition then. No stims and I've taken it for months pre-bed with no problem. You can probably add RK-125 or RK-500 too if you'd like. I did that combo too.
mr.cooper69
Legend
I realize this post is old, but this is quite irresponsible, to say the least.
chedapalooza
Legend
Did u notice any bloating?? There's a warning on the label .. I'm worried now
MAxximal
Well-known member
in some people TTA tends to cause a little water retention the first days but this occur when you double the dose (8 caps per day)
and ever stay good hydrated with TTA
chedapalooza
Legend
So one cap at bed shouldn't?
And then one cap morning and one cap bed? I wouldn't go over 2/day cuz I'm not really fat.. More so for maintenance /little recomp
And then one cap morning and one cap bed? I wouldn't go over 2/day cuz I'm not really fat.. More so for maintenance /little recomp
MAxximal
Well-known member
you can go with 3 caps the last before bed
chedapalooza
Legend
Well I really only want to do one before bed, none during the day.. So ur saying I'll be ok w no bloating??
MAxximal
Well-known member
is ok no bloat bud.
chedapalooza
Legend
Lol ur paying for my bottle if I bloat!! I'm taking erase and oep too so ii guess it's worth a shot..
kingjameskjf
Well-known member
I didn't notice any bloating but it's put on there because some people do experience it, although it's pretty nominal in most cases. I usually did 1 am, 1 pre, and 1 pm.
ConcreteConny
Well-known member
I had some bloating at 4 caps but it was minimal. Never needed to go over 4 caps cuz it is potent stuff
The minimal bloat went away as fast as it came though :thumbsup:
The minimal bloat went away as fast as it came though :thumbsup:
Whacked
Well-known member
Edumucate me here 
1) Why there is fluid retention/oedema associated with this stuff. As a PPAR-beta agonist; why is it causing water weight? I think PPARy (gamma) agonists do this (similar to drugs like Avandia)
2) Any lethargy from using this product
3) Why aren't people using OTC diuretics concomitantly?
1) Why there is fluid retention/oedema associated with this stuff. As a PPAR-beta agonist; why is it causing water weight? I think PPARy (gamma) agonists do this (similar to drugs like Avandia)
2) Any lethargy from using this product
3) Why aren't people using OTC diuretics concomitantly?
MAxximal
Well-known member
Edumucate me here
1) Why there is fluid retention/oedema associated with this stuff. As a PPAR-beta agonist; why is it causing water weight? I think PPARy (gamma) agonists do this (similar to drugs like Avandia)
2) Any lethargy from using this product
3) Why aren't people using OTC diuretics concomitantly?
1.Some people report this issue with TTA hold more subQ water same thing with use of Yohimbine but IME is due a high dose but the normal dose no.
and apart some people report “drains strength” (high dosed too).
2. If you consume “complex carbs” lethargy is not a problem so if you on Atkins Diet be ready. and again this is reported on high doses (4-6g)
3. Diuretics is not necessary
If you planning use SNS TTA-500 I recommend you stay hydrated all the way and stack with PLCAR and RK and you will see :firedevil:
ConcreteConny
Well-known member
Maxx got it covered :thumbsup:
