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ProtienFiend
New member
I am somewhat lean, but I am insulin resistant... Where does that put me in terms of R-ala's effectiveness?
controversial r-ala post (edit)
- Thread starter OXANDRIN
- Start date
TheMuscleMonster
New member
ProtienFiend said:
how do you know you are insulin resistent?
ProtienFiend
New member
I dont know for sure... but I tend to hold fat on my waste and It is nearly impossible for me to get lean when I eat > 50 carbohydrates per non-lifting day...
TheMuscleMonster said:
Fukkenshredded
New member
R-ALA did not do much for me, and I concluded that it was because I effectively utilize carbs as it is. It is a product for those who can use it, and many have testified that it does work.
If it doesn't work for you, don't buy it. But don't throw silly accusations or make sublime inuendos about the AF store. Those guys research and do their best to bring good stuff to market. I think they do a good job, and no, I don't work for them.
I have not seen any ridiculous claims on any of AFs products, ever. Moreover, Ulter is a fair guy. He does good business. That alone is enough reason to deal with him.
Thermorexin is pretty effective at 6/day. More so than ephedra, and certainly more bearable.
WAY more healthy.
ANd Tyler's Liver Detox, where would we be without that? Normally, doctors charge a pretty good slug for that stuff.
You think you found something about R- ALA, and you did.
You found that it doesn't work for everybody.
If it doesn't work for you, don't buy it. But don't throw silly accusations or make sublime inuendos about the AF store. Those guys research and do their best to bring good stuff to market. I think they do a good job, and no, I don't work for them.
I have not seen any ridiculous claims on any of AFs products, ever. Moreover, Ulter is a fair guy. He does good business. That alone is enough reason to deal with him.
Thermorexin is pretty effective at 6/day. More so than ephedra, and certainly more bearable.
WAY more healthy.
ANd Tyler's Liver Detox, where would we be without that? Normally, doctors charge a pretty good slug for that stuff.
You think you found something about R- ALA, and you did.
You found that it doesn't work for everybody.
variation
New member
Fukkenshredded said:
well said, I don't think I've ever seen a product on their site that looked sketchy, and most everthing there is backed by plenty of research.
unlike just about 99.999999999999999% of other supplement stores on the internet, whom sell products that are more than questionable.
MrMakaveli
New member
Singleton said:
I can attest to this. I've also never gotten as lean as I did when I added R-ALA. It was the only thing that changed (ie cardio and diet didnt) and the difference for me was unbelievable.
We arent rats afterall
Basically it breaks down like this.
If you look like fukkenshredded, and if you say you do I'd have to see it, and you're that lean, then Glucorell R may not be of as much use to you for glucose uptake enhancement as it would be to the average guy. Here's how it works.
To function properly, cells need a steady fuel supply. Blood sugar is the key fuel for most cells in the body, and the body produces the hormone insulin precisely in order to help get energy to the cells that need it. Insulin is like a "key" that turns on the glucose transport "ignition" (insulin receptor) which is located on the surface of the cell.
How the cell takes in blood sugar.
When the "key" (insulin) activates the "ignition" (the insulin receptor), it turns on the engines of the "tanker trucks" (GLUcose Transporters, or GLUTs) that do the work of hauling glucose (blood sugar) out of your bloodstream and into your cells. So to get your cells the energy they need - and to keep blood sugar from building up to dangerously high levels - insulin has to tell your cells to take up blood sugar … and the cell also has to listen to the signal, and mobilize the GLUT transporters.
The system is efficient and remarkably adaptable, but it has its limits. The fact is that there's only so much blood sugar that your cells can take in at a time. And as soaring rates of diabetes show, North Americans have been overtaxing those limits for generations. Our fast-paced lifestyles and processed-food diets cause most of us to take in more Calories - and, especially, more carbohydrate - than our bodies can handle. After years of being asked, by insulin, to take in more glucose than they can use, eventually your cells stop responding properly to insulin's signal. (insulin resistance)
Think of an old car starter whose pins have been so worn down by years of friction against the key's teeth that you have to juggle and twist at the key to get the car to start. When the same thing happens to your body's glucose transport system, your body becomes resistant to the action of insulin. Insulin is still being produced, but the cells no longer respond properly, and fail to mobilize GLUTs in response. As a result, cells don't take in glucose, and blood sugar levels climb.
Thus begins a vicious circle. Because high blood sugar is bad for you, the body responds to insulin resistance by producing more insulin. In the short term, this does the trick, forcing your cells to take in more glucose. But if insulin levels are persistently too high, your cells eventually become even less interested in hearing insulin's cries to take in excessive glucose, and respond by producing even less GLUTs … which makes your cells even more insulin resistant.
Something has to give. If the insulin-producing cells of the pancreas just can't produce enough insulin to keep blood sugar levels under control in the face of increasing insulin resistance, then the cycle ends in adult-onset diabetes. On the other hand, if the brute-force strategy of keeping blood sugar levels at manageable levels by cranking insulin levels higher and higher succeeds, a metabolic disorder known as insulin resistance syndrome, or "Syndrome X" ensues. And while full-blown, clinical "Syndrome X" is not diagnosed in most people, almost everyone develops some degree of insulin resistance as part of the "normal" aging. This also occurs with the use of Anabolic Steroids.
Even though the blood sugar of most people with insulin resistance may be within the normal range, their health is still in jeopardy, because insulin resistance itself is a potential killer. The key reason: one of insulin's functions is to control the release of free fatty acids from your tissues into your bloodstream … with the result that, when your body doesn't respond properly to insulin, your plasma levels of free fatty acids rise higher High free fatty acids keep your blood vessels squeezed up tight by interfering with the action of nitric oxide, the molecule that helps your blood vessels to relax as a result, their high free fatty acids cause insulin resistant people to have high blood pressure.
Controlled trials prove that even racemic (R,S)-lipoic acid helps people become more sensitive to insulin - that is, less insulin resistant. But research shows that only the R(+)-Lipoic Acid half of conventional "lipoic acid" supplements makes the body's cells more responsive to insulin. In fact, in some ways the S(-)-form actually makes it harder for your body to healthily process blood sugar!
Even when no insulin is available, cells can still open their doors to a small amount of glucose. This ability is called the cell's basal glucose uptake, and it can be tested by isolating a cell from the influence of insulin and other bodily signals in a test tube. Under these artificial conditions, R(+)-Lipoic Acid effectively increases cells' basal uptake of glucose , whereas the S(-)-form has been found to be either totally ineffective, or just half as effective as R(+)-lipoic acid, depending on what kind of cell you look at.
But the ability to increase cells' glucose uptake when there's no insulin around is more of a laboratory curiosity than a medical breakthrough. In a living, breathing organism, insulin is present - and restoring the cell's ability to respond to insulin's signal is the key factor in controlling both blood sugar and the witches' brew of risk factors that come with "Syndrome X." So the key question is not what effects the two enantiomers have on basal glucose uptake, but how they affect the interplay between insulin, sugar, and the cell.
To get answers to this question, scientists compared the response to insulin in the muscle cells of insulin-resistant lab animals injected with either straight S(-)-enantiomer, or pure R(+)-lipoic acid It immediately became obvious that R(+)-Lipoic Acid was superior. Using a special, "traceable" form of glucose to monitor the two enantiomers' effects, the very first treatment with R(+)-Lipoic Acid caused the animals' muscle cells to take up 31% more glucose in response to insulin, which was 64% more glucose than under basal (non-insulin-stimulated) conditions. By contrast, S(-)-lipoic acid caused no significant increase in muscle cell glucose transport.
Next, the scientist looked at the longer-term effects of the two enantiomers. One group of animals was fed a regular diet, while two other groups' chow was supplemented with one of the two enantiomers. The results were essentially the same. Compared to animals which ate an unsupplemented diet, the muscle cells of animals which were given pure R(+)-Lipoic Acid were able to take up 34% more blood sugar in response to insulin, or 65% more than they did under basal conditions. By contrast, feeding animals the same amount of "lipoic acid" in the artificial S(-)-form had no effect on the animals' ability to clear blood sugar.
In fact, even giving the animals two-thirds more S(-)-enantiomer than had been effective when using R(+)-lipoic acid, still led to no clear-cut improvement: while there did appear to be an increase in the animals' muscle cells' glucose uptake under the influence of insulin, the scientists found that the apparent increase was not strong enough, as compared to their basal intake, to rule out a statistical fluke. 21 And the numbers were about the same (145 vs. 150 pmol/mg muscle mass) when they further upped the dose of the S(-)-form to one that was three times more than what was needed to get clear-cut results with R(+)-lipoic acid!
At the same time, insulin levels in animals that were supplemented with R(+)-Lipoic Acid were pushed down by 17%, proving that the vicious circle of insulin resistance was being put into reverse. By contrast, S(-) lipoic acid actually caused insulin levels to soar 15% higher. Another clear sign that the animals were made less insulin resistant was the fact that animals given R(+)-Lipoic Acid experienced reductions of free fatty acids of greater than a third - an extremely important result, granted the role of increased free fatty acids in causing the high blood pressure and killer cholesterol profile seen in "Syndrome X," and their place as a risk factor for cardiovascular disease and sudden death. It was a different story in the other group: free fatty acids in animals fed S(-)-lipoic acid showed no significant change.
Looking down at these animals' cells, scientists could see what had happened. The amount of GLUT-4, the muscles' main glucose transporter, was actually reduced by 19% by S(-) lipoic acid supplementation! Granted R(+)-lipoic acid's ability to increase the cell's responsiveness to insulin, you might expect that it would increase GLUT-4 levels. In fact, levels of GLUT-4 were not affected one way or the other by the R(+)-form. Instead, other studies have shown, R(+)-Lipoic Acid helps the cell to mobilize its glucose transporters, without affecting GLUT levels. These studies found that S(-)-lipoic acid either has no effect on, or actually interferes with, the cell's ability to mobilize GLUTs.
Other aspects of the response to insulin were also improved by R(+)-, but not S(-)-, lipoic acid, including a 33% restoration in the ability to burn glucose for fuel and a 26% increase in the formation of glycogen, the long-chain molecules used to store carbohydrates for quick use by the liver and muscles.
In short, when you take a racemic mixture of R(+)- and S(-)-enantiomers found in conventional "lipoic acid" supplements, R(+)-Lipoic Acid improves insulin resistance, while the S(-)-form actually makes it worse. The results that are seen in clinical trials using the racemate, then, are the net effects of combining the powerful benefits of R(+)-lipoic acid, with the sometimes weaker, and sometimes even harmful, effects of the S(-)-form.
R(+)-lipoic acid, in other words, is not just fighting against insulin resistance: it's fighting against the "evil twin" present in most commercial supplements. Getting rid of the "fifth column" in your supplement frees up the full potential of R(+)-lipoic acid, allowing its full strength to be unleashed in the battle to restore healthy sugar metabolism.
References:
Estrada DE, Ewart HS, Tsakiridis T, Volchuk A, Ramlal T, Tritschler H, Klip A. Stimulation of glucose uptake by the natural coenzyme alpha-lipoic acid/thioctic acid: participation of elements of the insulin signaling pathway. Diabetes. 1996 Dec;45(12):1798-804
Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A. Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes. Diabetologia. 2000 Mar;43(3):294-303.
Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol. 1997 Jul;273(1 Pt 1):E185-91.
Konrad T, Vicini P, Kusterer K, Hoflich A, Assadkhani A, Bohles HJ, Sewell A, Tritschler HJ, Cobelli C, Usadel KH. alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes. Diabetes Care. 1999 Feb;22(2):280-7.
Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, Rett K. Oral administration of rac-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial. Free Radic Biol Med. 1999 Aug;27(3-4):309-14
Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, Dietze GJ. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoicacid. Arzneimittelforschung. 1995 Aug;45(8):872-4.
Konrad D, Somwar R, Sweeney G, Yaworsky K, Hayashi M, Ramlal T, Klip A. The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation. Diabetes. 2001 Jun;50(6):1464-71
Loeblein K, Rett K, Maerker E, Tritschler HJ, Wessel K, Wicklmayr M, Haring HU. Thioctic acid stimulates translocation of glucose transports in hearts of insulin-resistant Zucker rats. Diabetologia. 1995 Aug; 38(1):A132(Abs512).
If you look like fukkenshredded, and if you say you do I'd have to see it, and you're that lean, then Glucorell R may not be of as much use to you for glucose uptake enhancement as it would be to the average guy. Here's how it works.
To function properly, cells need a steady fuel supply. Blood sugar is the key fuel for most cells in the body, and the body produces the hormone insulin precisely in order to help get energy to the cells that need it. Insulin is like a "key" that turns on the glucose transport "ignition" (insulin receptor) which is located on the surface of the cell.
When the "key" (insulin) activates the "ignition" (the insulin receptor), it turns on the engines of the "tanker trucks" (GLUcose Transporters, or GLUTs) that do the work of hauling glucose (blood sugar) out of your bloodstream and into your cells. So to get your cells the energy they need - and to keep blood sugar from building up to dangerously high levels - insulin has to tell your cells to take up blood sugar … and the cell also has to listen to the signal, and mobilize the GLUT transporters.
The system is efficient and remarkably adaptable, but it has its limits. The fact is that there's only so much blood sugar that your cells can take in at a time. And as soaring rates of diabetes show, North Americans have been overtaxing those limits for generations. Our fast-paced lifestyles and processed-food diets cause most of us to take in more Calories - and, especially, more carbohydrate - than our bodies can handle. After years of being asked, by insulin, to take in more glucose than they can use, eventually your cells stop responding properly to insulin's signal. (insulin resistance)
Think of an old car starter whose pins have been so worn down by years of friction against the key's teeth that you have to juggle and twist at the key to get the car to start. When the same thing happens to your body's glucose transport system, your body becomes resistant to the action of insulin. Insulin is still being produced, but the cells no longer respond properly, and fail to mobilize GLUTs in response. As a result, cells don't take in glucose, and blood sugar levels climb.
Thus begins a vicious circle. Because high blood sugar is bad for you, the body responds to insulin resistance by producing more insulin. In the short term, this does the trick, forcing your cells to take in more glucose. But if insulin levels are persistently too high, your cells eventually become even less interested in hearing insulin's cries to take in excessive glucose, and respond by producing even less GLUTs … which makes your cells even more insulin resistant.
Something has to give. If the insulin-producing cells of the pancreas just can't produce enough insulin to keep blood sugar levels under control in the face of increasing insulin resistance, then the cycle ends in adult-onset diabetes. On the other hand, if the brute-force strategy of keeping blood sugar levels at manageable levels by cranking insulin levels higher and higher succeeds, a metabolic disorder known as insulin resistance syndrome, or "Syndrome X" ensues. And while full-blown, clinical "Syndrome X" is not diagnosed in most people, almost everyone develops some degree of insulin resistance as part of the "normal" aging. This also occurs with the use of Anabolic Steroids.
Even though the blood sugar of most people with insulin resistance may be within the normal range, their health is still in jeopardy, because insulin resistance itself is a potential killer. The key reason: one of insulin's functions is to control the release of free fatty acids from your tissues into your bloodstream … with the result that, when your body doesn't respond properly to insulin, your plasma levels of free fatty acids rise higher High free fatty acids keep your blood vessels squeezed up tight by interfering with the action of nitric oxide, the molecule that helps your blood vessels to relax as a result, their high free fatty acids cause insulin resistant people to have high blood pressure.
Controlled trials prove that even racemic (R,S)-lipoic acid helps people become more sensitive to insulin - that is, less insulin resistant. But research shows that only the R(+)-Lipoic Acid half of conventional "lipoic acid" supplements makes the body's cells more responsive to insulin. In fact, in some ways the S(-)-form actually makes it harder for your body to healthily process blood sugar!
Even when no insulin is available, cells can still open their doors to a small amount of glucose. This ability is called the cell's basal glucose uptake, and it can be tested by isolating a cell from the influence of insulin and other bodily signals in a test tube. Under these artificial conditions, R(+)-Lipoic Acid effectively increases cells' basal uptake of glucose , whereas the S(-)-form has been found to be either totally ineffective, or just half as effective as R(+)-lipoic acid, depending on what kind of cell you look at.
But the ability to increase cells' glucose uptake when there's no insulin around is more of a laboratory curiosity than a medical breakthrough. In a living, breathing organism, insulin is present - and restoring the cell's ability to respond to insulin's signal is the key factor in controlling both blood sugar and the witches' brew of risk factors that come with "Syndrome X." So the key question is not what effects the two enantiomers have on basal glucose uptake, but how they affect the interplay between insulin, sugar, and the cell.
To get answers to this question, scientists compared the response to insulin in the muscle cells of insulin-resistant lab animals injected with either straight S(-)-enantiomer, or pure R(+)-lipoic acid It immediately became obvious that R(+)-Lipoic Acid was superior. Using a special, "traceable" form of glucose to monitor the two enantiomers' effects, the very first treatment with R(+)-Lipoic Acid caused the animals' muscle cells to take up 31% more glucose in response to insulin, which was 64% more glucose than under basal (non-insulin-stimulated) conditions. By contrast, S(-)-lipoic acid caused no significant increase in muscle cell glucose transport.
Next, the scientist looked at the longer-term effects of the two enantiomers. One group of animals was fed a regular diet, while two other groups' chow was supplemented with one of the two enantiomers. The results were essentially the same. Compared to animals which ate an unsupplemented diet, the muscle cells of animals which were given pure R(+)-Lipoic Acid were able to take up 34% more blood sugar in response to insulin, or 65% more than they did under basal conditions. By contrast, feeding animals the same amount of "lipoic acid" in the artificial S(-)-form had no effect on the animals' ability to clear blood sugar.
In fact, even giving the animals two-thirds more S(-)-enantiomer than had been effective when using R(+)-lipoic acid, still led to no clear-cut improvement: while there did appear to be an increase in the animals' muscle cells' glucose uptake under the influence of insulin, the scientists found that the apparent increase was not strong enough, as compared to their basal intake, to rule out a statistical fluke. 21 And the numbers were about the same (145 vs. 150 pmol/mg muscle mass) when they further upped the dose of the S(-)-form to one that was three times more than what was needed to get clear-cut results with R(+)-lipoic acid!
At the same time, insulin levels in animals that were supplemented with R(+)-Lipoic Acid were pushed down by 17%, proving that the vicious circle of insulin resistance was being put into reverse. By contrast, S(-) lipoic acid actually caused insulin levels to soar 15% higher. Another clear sign that the animals were made less insulin resistant was the fact that animals given R(+)-Lipoic Acid experienced reductions of free fatty acids of greater than a third - an extremely important result, granted the role of increased free fatty acids in causing the high blood pressure and killer cholesterol profile seen in "Syndrome X," and their place as a risk factor for cardiovascular disease and sudden death. It was a different story in the other group: free fatty acids in animals fed S(-)-lipoic acid showed no significant change.
Looking down at these animals' cells, scientists could see what had happened. The amount of GLUT-4, the muscles' main glucose transporter, was actually reduced by 19% by S(-) lipoic acid supplementation! Granted R(+)-lipoic acid's ability to increase the cell's responsiveness to insulin, you might expect that it would increase GLUT-4 levels. In fact, levels of GLUT-4 were not affected one way or the other by the R(+)-form. Instead, other studies have shown, R(+)-Lipoic Acid helps the cell to mobilize its glucose transporters, without affecting GLUT levels. These studies found that S(-)-lipoic acid either has no effect on, or actually interferes with, the cell's ability to mobilize GLUTs.
Other aspects of the response to insulin were also improved by R(+)-, but not S(-)-, lipoic acid, including a 33% restoration in the ability to burn glucose for fuel and a 26% increase in the formation of glycogen, the long-chain molecules used to store carbohydrates for quick use by the liver and muscles.
In short, when you take a racemic mixture of R(+)- and S(-)-enantiomers found in conventional "lipoic acid" supplements, R(+)-Lipoic Acid improves insulin resistance, while the S(-)-form actually makes it worse. The results that are seen in clinical trials using the racemate, then, are the net effects of combining the powerful benefits of R(+)-lipoic acid, with the sometimes weaker, and sometimes even harmful, effects of the S(-)-form.
R(+)-lipoic acid, in other words, is not just fighting against insulin resistance: it's fighting against the "evil twin" present in most commercial supplements. Getting rid of the "fifth column" in your supplement frees up the full potential of R(+)-lipoic acid, allowing its full strength to be unleashed in the battle to restore healthy sugar metabolism.
References:
Estrada DE, Ewart HS, Tsakiridis T, Volchuk A, Ramlal T, Tritschler H, Klip A. Stimulation of glucose uptake by the natural coenzyme alpha-lipoic acid/thioctic acid: participation of elements of the insulin signaling pathway. Diabetes. 1996 Dec;45(12):1798-804
Yaworsky K, Somwar R, Ramlal T, Tritschler HJ, Klip A. Engagement of the insulin-sensitive pathway in the stimulation of glucose transport by alpha-lipoic acid in 3T3-L1 adipocytes. Diabetologia. 2000 Mar;43(3):294-303.
Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol. 1997 Jul;273(1 Pt 1):E185-91.
Konrad T, Vicini P, Kusterer K, Hoflich A, Assadkhani A, Bohles HJ, Sewell A, Tritschler HJ, Cobelli C, Usadel KH. alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes. Diabetes Care. 1999 Feb;22(2):280-7.
Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, Rett K. Oral administration of rac-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial. Free Radic Biol Med. 1999 Aug;27(3-4):309-14
Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, Dietze GJ. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoicacid. Arzneimittelforschung. 1995 Aug;45(8):872-4.
Konrad D, Somwar R, Sweeney G, Yaworsky K, Hayashi M, Ramlal T, Klip A. The antihyperglycemic drug alpha-lipoic acid stimulates glucose uptake via both GLUT4 translocation and GLUT4 activation: potential role of p38 mitogen-activated protein kinase in GLUT4 activation. Diabetes. 2001 Jun;50(6):1464-71
Loeblein K, Rett K, Maerker E, Tritschler HJ, Wessel K, Wicklmayr M, Haring HU. Thioctic acid stimulates translocation of glucose transports in hearts of insulin-resistant Zucker rats. Diabetologia. 1995 Aug; 38(1):A132(Abs512).
OMEGA said:
Thanks, but apparently I am not allowed to even put I am an admin at my site...I have to put xxx's in it or something....steroid-ology but without the '-'. Whatever.
