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The Lipoic Acid Project
Posted by Fcontact on Steriod Support
The Lipoic Acid Project
A Case Study by Layne Norton and Eric Satterwhite
Lipoic acid (aka alpha lipoic acid and thiotic acid) is a naturally occurring co-factor in several dehydrogenase enzymes in the metabolic pathway (i.e. pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, etc). In order for the body to produce energy lipoic acid must be present. Fortunately the liver produces enough lipoic acid to cover basic metabolic requirements. The structure of lipoic acid is as follows…
The actual chemistry of the compound occurs at the dithiol (referring to the two sulfur atoms). During the step in the krebs cycle where pyruvate is converted to acetyl CoA, lipoic acid performs oxidation/reduction chemistry by acting first as a hydrogen acceptor to form dihyrolipoic acid (its reduced metabolite) and then later as a hydrogen donor (whereby it re-forms lipoic acid).
Lipoic acid has been implemented in the treatment of Alzheimer’s disease, cancer, and liver disease. However, lipoic acid’s most interesting property may be its ability to counter diabetic symptoms and combat hyperglycemia (high blood sugar). There have literally been hundreds of studies concluding that lipoic acid significantly improves insulin stimulated glucose uptake in patients with type II diabetes. Lipoic acid increases glucose uptake into cells by increasing the expression of GLUT-4 receptors (also called transporters) at the genomic level and increasing translocation of GLUT-4 receptors via its involvement in the insulin-signaling pathway in type II diabetics1, [4,6,8,10].
In normal individuals, insulin promotes glucose uptake in peripheral tissues by stimulating GLUT-4 translocation to the plasma membrane from intracellular compartments via insulin signaling. GLUT-4 is a unique glucose receptor because its concentration at the cell surface is relatively small in the absence of insulin (more than 95% is sequestered intracellularly). Binding of insulin to the insulin receptor on the cell surface results in the autophosphorylation of seven specific tyrosine residues on the cytoplasmic side of the insulin receptor. The autophosphorylation of these tyrosine residues causes IRS-1 (Insulin receptor substrate -1) to bind to them on the catalytic portion of the insulin receptor via a PTB (Protein Tyrosine Binding domain). After binding, IRS-1 undergoes a conformational change that causes specific tyrosine residues on the IRS-1 to become phosphorylated. PI3K (phosphatidyl Inisitol 3 kinase) then binds to the phosphorylated tyrosine residues on the IRS-1 via a specific SH2 (Src Homology-2) domain which recognizes these residues. This binding activates PI3K, which then translocates to the membrane and phosphorylates PIP2 (Phosphatidylinositol-4,5-biphoshpate) to generate PIP3. PDK1 (PIP3-dependent kinase) and PKB (protein kinase B, also called Akt). Both then interact with PIP3.
This complex causes the activation of PKB, which serves two major functions. First, PKB causes the translocation of GLUT-4 transporters from an intracellular pool to the plasma membrane. The insertion of these transporters into the plasma membrane increases glucose transport into the cell and stabilizes blood glucose. Once circulating insulin levels decline, GLUT-4 transporters are removed from the plasma membrane via endocytosis and are recycled back to their storage compartments. PKB also facilitates glycogen synthesis by phosphorylating and inactivating Glycogen Synthase Kinase 3, the protein responsible for inhibiting glycogen synthesis.
Lipoic acid supplementation in micromolar concentrations increases insulin stimulated glucose transport by increasing the activity of the insulin signaling pathway and the expression of GLUT-4 transporters at the genomic level. It is lipoic acid’s direct involvement in the insulin signaling pathway that makes it unique among current anti-hyperglycemic treatments. As is often times the case, many athletes and weight trainers have become quite curious about compounds such as lipoic acid. Increasing glucose transport into muscle cells would produce a host of positive results including increased nutrient partitioning, increased glycogen storage, and increased cell volume. However, most studies examining lipoic acid’s effect on blood glucose in non-insulin resistant patients have found little difference from that of a placebo group [22, 23]. But, none of these studies examined lipoic acid’s effect on athletes or weight trainers. The purpose of this experiment was to examine lipoic acid’s effect on blood glucose in a healthy, weight training subject and to propose a possible mechanism(s) that might explain the results.
All testing was done on a single, apparently healthy 21-year-old male free of metabolic disorders.
ALA was administered prior to (20 min) and immediately following the resistance training protocol. During the 300mg/day protocol, ALA was consumed only after the exercise training. During the 600mg/day protocol, 300mg were consumed both prior to and after exercise. During the 900mg/day training protocol, 300mg were consumed prior and 600mg of ALA were consumed after resistance training. During the 1200mg/day protocol 600mg were consumed both prior to and after exercise training. All dosage increases were separated by a 4-day washout period where no ALA was consumed. The ALA was supplied in 300mg capsules by 1Fast400.com.
Dietary intake was kept constant for the duration of the study. Prior to (20 min) exercise training a liquid meal was consumed. During all supplementation protocols that were >300mg/day this meal was consumed simultaneously with the ALA dosage that was taken prior to weight training. Immediately after the training period, a similar meal was consumed along with appropriate doses of ALA. Thereafter, numerous small meals were consumed within 3 hours of cessation of the training session. Each of these meals was held constant in composition, size and time of consumption throughout the study. The meals were as follows.
Prior to exercise training a liquid meal was consumed; it consisted of 25g of hydrolyzed whey protein isolate and 34g of dextrose. This meal was consumed at 5:40am.
Immediately prior to exercise a liquid meal was consumed; it consisted of 50g of hydrolyzed whey isolate and 34g of dextrose. This meal was consumed at 6:55 am.
At 7:25am 1 serving of rice krispies (27g carbohydrate, 3g protein) and 25g of hydrolyzed whey isolate was consumed.
At 7:50am a meal consisting of a casein-based meal replacement (40g protein, 22g carbohydrate, 1.5g fat), ½ a banana (17.5g carbohydrate), and 10g of honey (8.5g carbohydrate) was consumed.
At 9:30am a meal identical to that served at 7:25 was consumed.
Blood Glucose Testing:
Blood glucose was measured using a One Step Ultra Blood Glucose Monitor (LifeScan). Finger prick readings were taken < 1 minute prior to the consequent meal (I.E. 6:54am, 7:24am, etc). To ensure the most accurate reading, the lancet was changed with every reading, as was the blood-testing strip. Hands were also washed and cleansed with a sanitizing hand wipe (lever2000). Once the hand that was to have the blood drawn was clean, it was not allowed to come in contact with any object other than the testing strip. The majority of the readings were taken from the left index and middle finger.
Exercise Training: Exercise training consisted of high intensity resistance training that followed the Max-OT principles (ast-ss.com). All sessions lasted less than one hour. Bodyparts trained on a given day were held constant for the duration of the study.
Monday: Biceps & Triceps
Wednesday: Back & Traps
Friday : Chest & Calves
Sessions started at 6:00am and ended before 6:55 am everyday.
Mean glucose levels demonstrated a significant reduction in peak values (151.75±45.4 to 88.25mg±5.5 ***9679;dl-1) as incremental dosages of Alpha lipoic acid (ALA) increased (0 to 1,200 mg***9679;day-1). Weekly values of mean glucose levels became more consistent with increases in dosages of ALA. Values ranged from 151.75 to 129.5 mg***9679;day-1 (Monday and Friday respectively) with 0 mg***9679;day-1 and ended with a range of 85.75 ±5.5 to 92.5±17.4 mg***9679;dl-1 with 1,200mg***9679;day-1. There were also significant same-day reductions of peak blood glucose levels with administration of ALA across time (7:25am through 9:30 am). Same day Means±SDEV peak values of blood glucose demonstrated a similar trend across time in the respect of becoming more consistent from Monday to Friday as doses of ALA increased (151.75 ± 45.44, 88.25mg***9679;dl-1 ± 11.32mg***9679;dl-1 at 0mg***9679;day-1, 1200mg***9679;day-1 and 129.6 ±46.06mg***9679;dl-1, 90.25mg***9679;dl-1 at 0mg***9679;day-1, 1200mg***9679;day-1
These results indicate that Alpha Lipoic Acid has the ability to lower blood glucose concentrations in both short term and long term durations. It also indicates that ALA appears to have an ability to constrict blood glucose concentrations to a smaller physiologic range. ALA may also be able to prevent hyper as well as hypoglycemia. The current study demonstrates that ALA has the ability to control blood glucose concentrations in an apparently health male.
The results of this study clearly indicate that lipoic acid decreased blood glucose levels in the subject tested. This decrease in blood glucose would likely be concurrent with an increase in glucose uptake into cells. However, using the testing equipment available to us, it is not possible to discern which cells the glucose is preferentially being disposed to: muscle cells or adipocytes. Another question is why our experiment showed increased glucose uptake in a non-diabetic, non-obese subject when all other studies showed no difference. Fortunately diligent research has allowed us to compose what we believe is a very solid theory that is consistent with our results.
It has been firmly established that patients suffering from type II diabetes have elevated levels of oxidative stress. Reactive oxygen species (ROS) include superoxide, hydroxyl radicals, hypochlorous acid, peroxynitrite, singlet oxygen, and peroxide. ROS are produced by several different mechanisms including glycation reactions, decompartmentalization of transition metals, byproducts of oxidative metabolism, and a shift in the reduced-oxygen status of the cell1. For a period of time, it was believed that increased levels of ROS were due to hyperglycemia. However, it now appears that increased levels of ROS, in particular peroxide, may actually contribute to hyperglycemia itself [2-9].
Although several studies have determined that insulin stimulated glucose uptake is severely hampered in cells exposed to increased oxidative stress (particularly peroxide), it is only recently that the mechanism behind this action has begun to be understood. It appears that ROS decreases insulin stimulated glucose uptake by directly interfering in the expression of the GLUT-4 receptor9 and by disrupting the insulin signaling pathway [2,3,4,5,6,7,8].
A recent study examined the effect of oxidative stress upon GLUT-4 expression in 3T3-L1 adipocytes. Cell cultures were treated with micromolar concentrations of peroxide and the researchers measured the amount of GLUT-4 mRNA transcripts before and after peroxide administration. The results of this study showed that GLUT-4 mRNA was decreased after exposure to peroxide without any changes in the stability of the mRNA transcripts, indicating that peroxide was affecting the DNA transcription rather than de-stabilizing the mRNA produced from DNA transcription. The researchers concluded that peroxide decreased the expression of the GLUT-4 receptor by impairing DNA binding of nuclear proteins to the insulin responsive element in the GLUT-4 promoter . A promoter in a DNA sequence is essentially a “trigger.” In this case, to pull the trigger and start DNA transcription, a certain protein must bind to it. Peroxide prevents this action, therefore inhibiting insulin’s stimulatory effect on GLUT-4 synthesis. It is logical to conclude that insulin stimulated glucose uptake may at least be partially reduced due to the reduction in GLUT 4 production (i.e. less GLUT-4 produced, less GLUT-4 translocated to the plasma membrane, and less glucose transported into the cell). This study also noted that supplementation with a reducing agent partially reversed these effects.
ROS also decreases glucose uptake by reducing the insulin-induced activity of several kinases in the insulin signaling pathway including PKB, IRS-1, PI 3-Kinase, and even reduces the autophosphorylation (thus decreasing the activity) of the insulin receptor itself. (For an explanation of how the insulin signaling pathway works, please see the introduction) Peroxide and ROS reduce the insulin-induced phosphorylation of key tyrosine residues on all of the aforementioned kinases. The activity of these kinases becomes markedly decreased when these residues are unphosphorylated. It is quite evident that decreasing the activity of these kinases would lead to a decrease in the plasma membrane concentration of GLUT-4 transporters by reducing their translocation to the membrane. It is interesting to note however, that peroxide actually slightly increases basal rates of glucose uptake in the absence of insulin by increasing the phosphorylation of several kinases in the insulin signaling pathway [2,3,6,7] and by increasing the membrane content of GLUT-12. However, in the presence of insulin, peroxide administration caused massive impairment of the insulin signaling pathway [2,3,4,5,6,7] This impairment in insulin signaling caused a decrease in the insulin stimulated GLUT-4 translocation to the membrane, and promoted insulin resistance in the tested subjects.
How significant are the effects of ROS on GLUT-4 action and insulin stimulated glucose transport? The answer is very significant. A study performed by Rudich, et. al, found that although insulin induced a 2.5 fold increase in plasma membrane GLUT-4 content, micromolar concentrations of peroxide completely prevented these insulin-induced responses. They also found that insulin-induced IRS-1 associated with PI 3-kinase activity was completely prevented by micromolar concentrations of peroxide2. These findings were also supported by the results in a study performed by Maddux, et. al, who found that micromolar (40-50 um) concentrations of peroxide nearly abolished insulin stimulated glucose transport in the treated cells. They further found that micromolar concentrations of lipoic acid only slightly increased basal (absence of insulin) glucose uptake but completely restored insulin-induced glucose uptake. Another point of interest is that the researchers found lipoic acid did not increase insulin-induced glucose disposal in cells that had not been oxidatively stressed6. This indicates that the effects of lipoic acid on insulin-induced glucose disposal are closely tied to its anti-oxidant properties. Conclusions from several other researchers support this statement [4,8,10].
The reason we believe that this case study was successful is that the subject under scrutiny engaged in high intensity exercise while taking lipoic acid. Intense training increases the production of ROS beyond normal physiological levels, [11,12,13,14]. Since the previous studies using lipoic acid with non-type II diabetics involved untrained subjects, there is no reason why lipoic acid would have improved glucose uptake, since those people would not have been prone to higher than normal levels of oxidative stress. The study done by Maddux et. Al. supports this since they found that lipoic acid did not increase insulin stimulated glucose uptake in cells not exposed to oxidative stress. Even though people who exercise experience increase in GLUT4 concentration and glucose transport into muscle tissue , this still may not be the optimal level of glucose disposal due to ROS impairment of glucose transport. Therefore, we postulate that lipoic acid may help optimize the already increased glucose transport that an athlete experiences by acting as an ROS scavenger. In addition, we also believe the lipoic acid may act as a nutrient partitioning agent, directing glucose preferentially to muscle tissue and away from fat tissue in people who exercise since its improvement of ROS impaired glucose transport will primarily take place in muscle cells producing ROS.
A few more points that are interesting to note include…
Maddux et. al, found that both isomers of lipoic acid were equally effective in preventing oxidative stress induced impairment of glucose transport6. Rudich et. al., found that S-LA was more effective than R-LA in protecting against oxidant induced insulin action impairment in 3T3-L1 adipocytes .
Lipoic acid prevents the ROS induced decrease in the body’s natural anti-oxidant, glutathione [4,6,10,15], and also regenerates the body’s stores of vitamin E and vitamin C [1,6].
Several other anti-oxidants increase insulin stimulated glucose uptake into cells via a similar ROS scavenging mechanism including vitamin E, NAC, glutathione, ALCAR, Coenzyme Q10, EGCG, and others [6,16,17,18]. However, before you start taking massive doses of vitamin E, realize that lipoic acid is a much stronger anti-oxidant than most of the compounds listed, as it has a redox potential of -290mV compared with vitamin E which has a redox potential of 370mV [10,19].
In addition to preventing oxidative stress induced insulin resistance, researchers also found that lipoic acid protects against other oxidative stress induced ailments such as hypertension and Alzheimer’s disease [8,10,20,21].
Well that is a lot of technical information. But, what does it all mean for you? How can you use this information to get the most out of your supplementation. Just from looking at the way we broke down the data, there are some very obvious trends. As the amount of ALA that was consumed per day increased, the average blood glucose levels decreased. We can also see that ALA appears to keep blood glucose levels more consistent over time as dosages increase. As the amount of ALA goes up, not only does the average blood glucose go down, but the Standard Deviation decreases as well. Standard Deviation is a number that represents the amount of variation between a grouping of values. In this case, less is more! The standard deviation dropped from 31 to 5! I interpret this as ALA having the ability to improve glucose uptake by muscle tissue in the entire body, not just the worked muscle. Common sense would tell you that your biceps and triceps are not going to take up as much glucose as quickly as your legs. But this is the trend we started to see.
Another interesting turn of events was the difference in degree of effect from an increased dosage. We saw rather dramatic changes in blood glucose dynamics when the dosages were increased from 0 to 300mg/day. Likewise when they were increased from 300 to 600/mg a day. However, increasing from 600 to 900, or 900 to 1200mg a day, the degree of difference was not very noticeable. It was like throwing a match into a bonfire. On the other hand the degree of improvement when going from 600 to 1200 mg /day was rather significant and something to note. Based on these observations, I see no reason to consume more than 600mg of ALA within any six-hour period.
Ok, so 600mg. But when? Well we now have a better understanding of ALA’s mode of action through our enhanced understanding of its anti-oxidant activity. We also know that exercise increases the oxidative load and creates a high amount of free radicals. So it would make sense to take your first dose of ALA before you set foot in the gym. You do not want to subject yourself to a trauma that might allow for any drop in insulin sensitivity due to oxidative stress. I would suggest approximately 300mg 20-30 minutes before you being your workout. The next dose should be taken immediately after you are done with your last set. This will deliver what we have found to be the optimal dosage exactly when you need it most.
So we have taken two 300mg doses at key times to keep oxidative stress to a minimum and maintain a high level of insulin sensitivity right when we need it. But we can take it a step further. If you don't feel that 600mg a day is enough, you still have another 600mg to work with. Remember, 900mg doesn't seem to provide much more benefit over 600mg, so if you want to take the next step, I recommend that you go for the full 1200mg. This dose is not so much to reduce blood sugar levels to prevent hyperglycemia, but to control optimal blood glucose levels. There of course will be a reduction in overall glucose levels, however, as this graph shows, the drastic variation of glucose levels seen on 0 mg per day is virtually abolished with 1200 mg per day. Maintaining glucose/insulin levels within that tight physiological range is critical to the production of key anabolic hormones. The most important of these hormones would be IGF-I. For these various reasons, I feel that this next dose of ALA would be of most benefit a few hours before bed. Do note take this dose with your last meal of the night, but with the one before that. So if you eat eight meals per day, this last dose would come with meal number seven. This spacing will also ensure that this latter dose does not cross over into a potential morning dose.
This is all assuming that you train early in the morning. If you don't, it is not a big deal. You can easily flip doses to fit your schedule. For example, if you work out later in the evening, the doses you take around your workout would suffice for the before bed dose. Then you would take one serving in the mid morning. If you work out midday, then we can compromise and use a little metabolic carryover to our advantage. I would recommend taking 300mg prior to bed and another 300mg with your first meal of the day. This will keep an even stream of ALA in the body around the clock. Insulin management is critical to creating a hormonal environment that is conductive to muscle growth. It needs to be kept in a very small physiological range, and it would appear that ALA is a nutrient that keeps it there.
So yes, ALA does in fact "work." But lets not take it too far. From this small study we can conclude that ALA is effective for blood glucose management. We can only assume that this is a reflection of insulin management. However, it is also possible that ALA stimulates insulin receptors itself. If that is the case, we would have to question the effectiveness of ALA as a bodybuilding supplement. If ALA only stimulated insulin receptors then this may in fact short-circuit the hormonal cascade that insulin initiates.
One the other hand, other anti-oxidants have been reported to have the ability to lower blood glucose levels as well—Vitamin E and Vanadyl Sulfate in particular. In this situation, our hypothesis only supports previous accounts of anti-oxidants behaving as insulin mimickers and confirms our theory of free radicals disturbing the insulin pathway. The only downside is that the research on the effectiveness of anti-oxidant supplements to eliminate free radicals is conflicting at best. In many cases a single anti-oxidant is used. Why is that a problem? Mainly because any anti-oxidant has the ability to become an oxidant. Don't forget that many nutrients work together to yield a single effect, so don't rely solely on ALA as your ray of light. Be sure to include other anti-oxidants such as vitamins A, C, E, Selenium and others.
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prevention of diabetes complications.” Nutrition. 17(10): 888-95.
2. Rudich, et al., “Prolonged Oxidative Stress Impairs Insulin-Induced GLUT-4 Translocation in 3T3-L1 Adipocytes.” Diabetes. 47: 1562-1569.
3. Hanson et al., “Insulin signaling is inhibited by micromolar concentrations of peroxide. Evidence for a role of peroxide in tumor necrosis factor alpha-mediated insulin resistance.” Journal of Biological Chemistry. 274(35): 25078-84.
4. Rudich et al., “Lipoic acid protects against oxidative stress induced impairment in insulin stimulation of protein kinase B and glucose transport in 3T3-L1 adipocytes.” Diabetologia. 42(8): 949-57.
5. Gardner et al., “Hydrogen peroxide inhibits insulin signaling in vascular smooth muscle cells.” Experimental Biological Medicine. 228(7): 836-42.
6. Maddux et al., “Protection against oxidative stress-induced insulin resistance in rat L6 muscle cells by micromolar concentrations of alpha lipoic acid.” Diabetes. 50(2): 404-17.
7. Tirosh, et al., “Oxidative stress disrupts insulin-induced cellular redistribution of insulin receptor substrate-1 and phosphatidylinositol 3-kinase in 3T3-L1 adipocytes.” Journal of Biological Chemistry. 274(15): 10595-10605.
8. Adil et al., “Lipoic acid prevents hypertension, hyperglycemia, and the increase in heart mitochondrial superoxide production.” American Journal of Hypertension. August 2002.
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20. Zhang et al., “Alpha-lipoic acid protects rat cortical neurons against cell death induced by amyloid and hydrogen peroxide through the Akt signaling pathway.” Neuroscience Letters. 312(3): 125-8.
21. Lovell et al., “Protection against amyloid beta peptide and iron/hydrogen peroxide toxicity by alpha lipoic acid.” Journal of Alzheimers Disease. 5(3): 229-39.
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metabolism in experimental diabetic neuropathy.” Diabetes. 48(10): 2045-51.
23. Dicter N, Madar Z, and Tirosh O, “Alpha-lipoic acid inhibits glycogen synthesis
in rat soleus
muscle via its oxidative activity and the uncoupling of mitochondria.” Journal of
President LG Sciences
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GQ on AS!
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Good post liftsiron.
So if this study was used using Ala then one should assume that the doses for r-Ala should be 1/3-1/2 of the above stated correct?
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