Acetyl L-Carnitine (Alcar) and the Anarchy Stack...post in here!

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    Thank you, that is VERY clearly explained.

    I would also like to know what the job of Biotin is in the stack. I know someone said that ALA depletes biotin, but how and why?

    PubMed, well, I'm trying but I always get like 180 studies or nothing...

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    Originally posted by Scottyo
    The glucose disposal properties are hotly debated. Some people still claim that it does not affect glucose transport to the muscles, as Ex-banana eater showed in one study, while others see that it does. It gets even more confusing when one considers how the glucose is transported, either by insuligenic means or non-insulinigenic. Spook on AL claims it is only possible through insulin induced channels, while Fonz from Elite (the post you mentioned) and others believe otherwise. To tell you the truth, Im not sure if anyone has established a definitive answer, but I do believe regardless that it DOES affect glucose transport. The hypo type symptoms plus the muscle fullness are enough proof for me.

    With that all said, we are ignoring the bigger picture. Regardless of its glucose disposal properties, ALA is included with the ALCAR for 2 main reasons. First, they work synergestically off each other, requiring lower dose/greater results. Secondly, as has been stated, ALA is a very potent antioxidant that is both water and fat soluble especially in the mitochondria of the cell, where pro-ox effects caused by ALCAR can be contained and controlled.
    Thats because everyone has a different insulin sensitiviy based on diet, age, etc...THe Zucker study clearly stated that if your healthy and have normal insulin sensitivity that ALA wouldn't have much benefit. If you think about it, it makes snense. The majority of glucose ingested will be taken care of whether through insulin or non insulin realted means (ALA) so what would be the point of taking ALA for its glucose disposal if your normal insulin functions will do the job? THe only reason is if your insulin resistant (which the majority will be due to aging). Another aspect is the increased glycogen storage some state. Thats all good and fine as it will increase your pump but there in no evidence that increased glycogen storage increases the rate of synthesis. The amount increases but the rate at which resythenesis occurs does not. So if your taking for glucose disposal at a young age, its pointless. For others it can serve well (for me metabilsim and insulin sensivity changed around 25) so anyone 25-30+ it can definetly help. This is a generalized recommendation as insulin resistance seems to be occuring at a younger age due to western carb based diets.
    For answers to board issues, read the Suggestion and News forum at the bottom of the main page.
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    very nice post bobo and scottyo
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    ALA Info !


    Not sure what site I pulled this from, but I had it saved on my pc with my other ala/rala info.

    I hope this formats OK.


    Alpha Lipoic Acid : A lipid and water soluble antioxidant, the pure R(+) enantiomer of which is produced in minute quantities by the body.

    Below we present a summary of the major research results for alpha lipoic acid (aLA) taken from published scientific studies. We give evidence that most of these highly beneficial effects derived from the R(+) enantiomer (RLA). We show why this is particularly true for the benefits of aLA with respect to mitochondria, which benefits are almost certainly the most important for life extensionist purposes. We also present studies of the properties of the S(-) enantiomer (synthesized only by man) and of the racemate (50/50 mixture of R & S - RSLA). Finally, we present evidence of the relative merits of the different forms of aLA which are available (ie pure R(+) and racemate).

    Safety and Interactions

    10 patients with diabetic neuropathy were given 70 days of treatment with a single dose of 600 mg of alpha lipoic acid [RSLA] per dayR.
    "Seventy-four patients with type-2 diabetes were randomized to either placebo (n = 19); or active treatment for 4 weeks in various doses of 600 mg once daily (n = 19), twice daily (1200 mg; n = 18), or thrice daily (1800 mg; n = 18) alpha-lipoic acid [RSLA]"R.
    "the chronic administration of lipoic acid reduces the activities of biotin-dependent pyruvate carboxylase and beta-methylcrotonyl-CoA carboxylase; enzyme activities remain normal if biotin at pharmacological doses is administered together with lipoic acid. Even without supplemental biotin, the decreases in enzyme activities are not dramatic and would presumably not cause pathology in patients"R.
    However, this last conclusion is likely made for moderate doses of aLA and biotin is so importantR that it should probably be supplemented for dosages of aLA above 50 mg daily.
    In a trial of 39 NIDDM patients with cardiac autonomic neuropathy (CAN), treatment with RSLA using a well-tolerated oral dose of 800 mg/day for 4 months slightly improved CAN.R
    Proven Benefits

    " feeding old rats ALCAR and/or [RLA] improved performance on memory tasks, reduced brain mitochondrial structure decay, and reduced oxidative damage in the brain. The combination of ALCAR and [RLA] showed a greater effect than ALCAR or [RLA] alone. These results suggest that feeding a combination of mitochondrial metabolites to old animals may prevent mitochondrial decay in neurons and restore cognitive dysfunction. These results also suggest that consumption of high levels of mitochondrial metabolites may be an efficient intervention in humans for delaying brain aging and age-associated neurodegenerative diseases"R.
    "feeding old rats high levels of key mitochondrial metabolites [RLA and ALCAR] can ameliorate oxidative damage, enzyme activity, substrate-binding affinity, and mitochondrial dysfunction"R.
    "ALCAR+[RLA] partially reversed the age-related decline in average mitochondrial membrane potential and significantly increased hepatocellular O2 consumption, indicating that mitochondrial-supported cellular metabolism was markedly improved by this feeding regimen. ALCAR+[RLA] also increased ambulatory activity in both young and old rats; moreover, the improvement was significantly greater in old versus young animals and also greater when compared with old rats fed ALCAR or [RLA] alone"R.
    In an investigation of "the role of the thiol antioxidant dihydrolipoic acid (DHLA) and intracellular glutathione (GSH) in RLA-stimulated glucose transport" and an exploration of "the hypothesis that RLA could increase glucose uptake into 3T3-L1 adipocytes in an oxidant-mimetic manner"R, the following was found:
    "3T3-L1 adipocytes have a low capacity to reduce R-LA and the oxidized form of lipoic acid is responsible for stimulating glucose uptake,
    R-LA modulates glucose uptake by changing the intracellular redox status, and
    the insulin receptor is a potential cellular target for R-LA action."
    In obese Zucker rats, RLA (30 mg/kg body weight by ip injection once daily) and exercise training "interact in an additive fashion to improve insulin action in insulin-resistant skeletal muscle"R. However, in insulin-sensitive lean Zucker rats, "the beneficial interactive effects of exercise training and RLA on skeletal muscle insulin action --- are not apparent"R. An important observation of the study of lean rats was that chronic supplementation with RLA was associated with a significantly reduced rate of body weight gain of fat mass. In both studies, RLA supplementation reduced the levels of protein carbonyls (an indicator of long-term oxidative damage). Another important finding was that use of RLA without exercise caused a significant increase in serum free fatty acid levels.
    "600 mg [RLA] was given daily to nine patients with AD and related dementias (receiving a standard treatment with acetylcholinesterase inhibitors) in an open study over an observation period of, on average, 337+/-80 days. The treatment led to a stabilization of cognitive functions in the study group ... Despite the fact that this study was small and not randomized, this is the first indication that treatment with [RLA] might be a successful 'neuroprotective' therapy option for AD and related dementias"R.
    In a study in which "some rats were ... supplemented with 0.2% (w/w) [RLA] for 2 wk prior to death"R, the following statements were made and results found:
    RLA "increases or maintains levels of other low molecular weight antioxidants such as ubiquinone, glutathione (GSH), and ascorbic acid."
    "Overall, our results show that the aging rat myocardium exhibits increased oxidant production, significantly lower ascorbic acid levels, and a marked increase in steady-state levels of oxidative DNA damage. [RLA] supplementation significantly reverses the age-related decline in myocardial ascorbic acid content, and lowers the rate of oxidant production and the steady-state levels of oxidative DNA damage. Our results thus indicate that dietary supplementation with lipoic acid may be an effective means to lower increased myocardial oxidative stress with age."
    "Thus, in addition to its antioxidant effect, dihydrolipoic acid [reduced RLA] may protect against lipid peroxidation by chelating free metal ions in vivo."

    "Our present findings suggest that [RLA] supplementation may be a safe and effective means of improving systemic decline in over all metabolic function and also increase protection against both endogenous and external production of ROS."
    "However, long-term feeding studies with [RLA] are needed to determine whether benefits of [RLA] seen in old animals can be sustained over time."

    In an in vivo study of ischaemia-reperfusion (I-R) of rats, a 14 week supplementation of 10,000 IU vitamin E/kg and 1.65 g alpha-LA/kg of diet did not influence cardiac performance or the incidence of dysrhythmias, even though it did decrease lipid peroxidation during I-R in young (4 months) adult ratsR. However, in a concurrent experiment with old (18 months) adult rats, the same supplemental regimen was found to protect the aged rat heart from I-R-induced lipid peroxidation by scavenging numerous reactive oxygen species, and this protection was associated with improved cardiac performance during reperfusionR.

    In a randomized clinical trial, "a total of 31 healthy adults were supplemented for 2 months either with alpha lipoic acid (LA) (600 mg/d, n = 16), or with alpha tocopherol (AT) (400 IU/d, n = 15) alone, and then with the combination of both for 2 additional months. LA significantly increased the lag time of LDL lipid peroxide formation for both copper-catalyzed and AAPH-induced LDL oxidation, decreased urinary F2-isoprostanes levels, and plasma carbonyl levels after AAPH oxidation. AT prolonged LDL lag time of lipid peroxide formation and conjugated dienes after copper-catalyzed LDL oxidation, decreased urinary F2-isoprostanes, but had no effect on plasma carbonyls. The addition of LA to AT did not produce an additional significant improvement in the measures of oxidative stress. In conclusion, LA supplementation functions as an antioxidant, because it decreases plasma- and LDL-oxidation and urinary isoprostanes"R.

    "This placebo-controlled explorative study confirms previous observations of an increase of insulin sensitivity in type-2 diabetes after acute and chronic intravenous administration of ALA. The results suggest that oral administration of alpha-lipoic acid can improve insulin sensitivity in patients with type-2 diabetes"R.

    "We also observed that the insulin-mimetic nutrient alpha-lipoic acid (LA; R-enantiomer) is able to stimulate glucose uptake in cytokine-treated cells that are insulin resistant. This study shows that cytokine-induced glucose uptake in skeletal muscle cells is redox sensitive and that, under conditions of acute infection that is accompanied with insulin resistance, LA may have therapeutic implications in restoring glucose availability in tissues such as the skeletal muscle."R

    "When a diet supplemented with RLA (0.5% w/w), a mitochondrial coenzyme, was fed to old rats to determine its efficacy in reversing the decline in metabolism seen with age for 2 wk, hepatocytes from untreated old rats vs. young controls had significantly lower oxygen consumption and mitochondrial membrane potential, whereas supplementation reversed the age-related decline in O2 consumption and increased mitochondrial membrane potential in old rats. Ambulatory activity, a measure of general metabolic activity, was almost threefold lower in untreated old rats vs. controls, but this decline was reversed in old treated rats. Malondialdehyde (MDA) levels, an indicator of lipid peroxidation, were increased fivefold with age in cells from unsupplemented rats, whereas supplementation reduced MDA levels markedly. Both glutathione and ascorbic acid levels declined in hepatocytes with age, but their loss was completely reversed with RLA acid supplementation. Thus, RLA supplementation improves indices of metabolic activity as well as lowers oxidative stress and damage evident in aging"R.
    "A two-week dietary supplementation of old animals with 0.5% RLA acid prior to cell isolation almost completely reversed the age-associated effects on ascorbic acid concentration, recycling and biosynthesis after oxidative stress"R.

    The chelating power of LA against copper is due solely to its reduced form, DHLA. "in our LDL experiments at physiological pH, DHLA [but not LA] is able to either reductively inactivate Cu2+ when Cu2+ is in excess, or effectively chelate Cu2+ when DHLA is in excess. The Cu2+ HLA complex [which is stable at low pH or in the absence of oxygen] eventually undergoes copper-catalyzed oxidation, copper is released and LDL peroxidation proceeds. DHLA, thus, has both pro- and antioxidant properties depending upon the ratio of Cu2+ HLA and the pH. These results provide an additional mechanism of thiol-mediated formation of radicals and metal chelation."R

    "In the Alpha-Lipoic Acid in Diabetic Neuropathy Study, 328 patients with NIDDM and symptomatic peripheral neuropathy were randomly assigned to treatment with intravenous infusion of alpha-lipoic acid using three doses (ALA 1,200 mg; 600 mg; 100 mg) or placebo (PLAC) over 3 weeks. The total symptom score (TSS) (pain, burning, paresthesia, and numbness) in the feet decreased significantly from baseline to day 19 in ALA 1,200 and ALA 600 vs. PLAC. Each of the four individual symptom scores was significantly lower in ALA 600 than in PLAC after 19 days. The total scale of the Hamburg Pain Adjective List (HPAL) was significantly reduced in ALA 1,200 and ALA 600 compared with PLAC after 19 days. In the Deutsche Kardiale Autonome Neuropathie Studie, patients with NIDDM and cardiac autonomic neuropathy diagnosed by reduced heart rate variability were randomly assigned to treatment with a daily oral dose of 800 mg alpha-lipoic acid (ALA) (n = 39) or placebo (n = 34) for 4 months. Two out of four parameters of heart rate variability at rest were significantly improved in ALA compared with placebo. A trend toward a favorable effect of ALA was noted for the remaining two indexes. In both studies, no significant adverse events were observed. In conclusion, intravenous treatment with alpha-lipoic acid (600 mg/day) over 3 weeks is safe and effective in reducing symptoms of diabetic peripheral neuropathy, and oral treatment with 800 mg/day for 4 months may improve cardiac autonomic dysfunction in NIDDM"R.

    In a group of 14 immunosuppressed NMRI-mice (nu/nu) raised and kept under germ-reduced conditions, RLA "(9 mg/kg body weight) expanded the total life span of its group"R.
    RLA "improved longer-term memory of aged female NMRI mice in the habituation in the open field test at a dose of 100 mg/kg body weight for 15 days"R.
    Potential Benefits

    RLA "supplementation may increase cellular and mitochondrial antioxidant status, thereby effectively attenuating any putative increase in oxidative stress with age"R.

    Negative Results and Limitations

    "we only observed a beneficial effect of [RLA] only in old and not in young animals"R.
    "The decline observed in the plasma concentration was steep (t1/2, 0.5 h)"R. ie RLA or RSLA have short plasma half-lives.
    RLA did not improve "longer-term memory ... in the habituation in the open field test at a dose of 100 mg/kg body weight for 15 days ... for young mice"R.

    Nill Value, Different, or Negative Results for the S enantiomer

    "Maximum plasma concentrations (Cmax) of the R-(+)-enantiomer were about 40-50% higher than those of the S-(-)-enantiomer (50 mg: 135.45 ng/ml R-(+)-TA, 67.83 ng/ml S-(-)-TA; 600 mg: 1812.32 ng/ml R-(+)-TA, 978.20 ng/ml S-(-)-TA; geometric means)"R.

    The individual effects of the pure R-(+) and S-(-) enantiomers of alpha-lipoic acid to enhance insulin-stimulated glucose metabolism in skeletal muscle was studied in obese Zucker rats: an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia. Generally, RLA had major positive effects on all studied parameters. SLA had either no effect on all parameters except: 1) a negative chronic effect on insulin (15% increase versus 17% decrease for RLA), 2) a lesser positive chronic effect on 2-deoxyglucose uptake (65% increase by RLA versus 29% by SLA), 3) glucose transporter (GLUT-4) protein was unchanged after chronic RLA treatment but was reduced to 81 +/- 6% of obese control with SLA treatment. The study conclusion was: "the R-(+) enantiomer being much more effective than the S-(-) enantiomer"R.

    In a group of 14 immunosuppressed NMRI-mice (nu/nu) raised and kept under germ-reduced conditions, SLA, even at 75 mg/kg body weight per day, increased the 50% survival rate, but did not expand "the total life span of its group"R.

    "An intact organ, the isolated perfused rat heart, reduced R-lipoate six to eight times more rapidly than S-lipoate ... On the other hand, erythrocytes, which lack mitochondria, somewhat more actively reduced S- than R-lipoate ... Thus, mechanisms of reduction of alpha-lipoate are highly tissue-specific and effects of exogenously supplied alpha-lipoate are determined by tissue glutathione reductase and dihydrolipoamide dehydrogenase activity"R.

    This study revealed a marked stereospecificity in the prevention of induced cataract, and in the protection of lens antioxidants, in newborn rats by alpha-lipoate, R- and racemic alpha-lipoate Cataract formation was decreased from 100% to 55% by R-alpha-lipoic acid and 40% by rac-alpha-lipoic acid. S-alpha-lipoic acid had no effect on induced cataract formation. The lens antioxidants glutathione, ascorbate, and vitamin E were depleted to 45, 62, and 23% of control levels, respectively, by the cataract inducing treatment, but were maintained at 84-97% of control levels when R-alpha-lipoic acid or rac-alpha-lipoic acid were administered; S-alpha-lipoic acid administration had no protective effect on lens antioxidants. When enantiomers of alpha-lipoic acid were administered to animals, R-alpha-lipoic acid was taken up by lens and reached concentrations 2- to 7-fold greater than those of S-alpha-lipoic acid, with rac-alpha-lipoic acid reaching levels midway between the R-isomer and racemic form. Reduced lipoic acid, dihydrolipoic acid, reached the highest levels in lens of the rac-alpha-lipoic acid-treated animals and the lowest levels in S-alpha-lipoic acid-treated animals. These results indicate that the protective effects of alpha-lipoic acid against induced cataract are probably due to its protective effects on lens antioxidants, and that the stereospecificity exhibited is due to selective uptake and reduction of R-alpha-lipoic acid by lens cellsR.

    "Racemic lipoic acid is therapeutically applied in pathologies in which free radicals are involved. The in vivo reduction of lipoic acid may play an essential role in its antioxidant effect. It was found that mitochondrial lipoamide dehydrogenase reduces the R-enantiomer 28 times faster than the S-enantiomer of lipoic acid. S-lipoic acid inhibits the reduction of the R enantiomer only at relatively high concentrations"R.

    The reduction of exogenous alpha-lipoic acid to dihydrolipoate by mammalian cells and tissues confers additional antioxidant protection to the cell. Both (R+) and (S-) isomers of alpha-lipoic acid were analyzed as substrates with glutathione reductase from several sources and with mammalian lipoamide dehydrogenase. Mammalian glutathione reductase catalyzed faster reduction of (S)-lipoic acid (1.4-2.4-fold greater activity) than of (R)-lipoic acid, whereas lipoamide dehydrogenase had a very marked preference for (R)-lipoic acid (18-fold greater activity) over (S)-lipoic acid"R.

    "The hyperglycemic effects of D-glucose [on erythrocyte membrane fluidity] were corroborated with isolated, reconstituted membrane proteins and erythrocyte glucose carrier, indicating that, in general, the observed divergent biochemical/biophysical changes of the red cell membrane are influenced by the glucose transport protein GluT1. The natural R-form and the S-form of alpha-lipoic acid were compared with racemic R-/S-forms for their efficiencies in alterations of red cell membrane fluidity. Decreased fluidities in presence of 10 mM glucose were found to be influenced in differentiated ways: the S-form was highly active in increasing fluidity at 4 nmol/mg and increasingly less active up to 20 nmol/mg protein. By contrast the R-form of lipoic acid was moderately efficient in increasing fluidity through a larger concentration range between 4 and 80 nmol/mg protein"R.

    Conclusions

    The studies listed above have shown that:
    SLA has effects in the body which are different than RLA.
    Although SLA is an excellent antioxidant (but RLA is better) none of the other effects of SLA have been shown to be beneficial.
    Since SLA does not naturally occur in the body and consequently the body has not developed mechanisms to deal with it, the effects of non-physiological doses of SLE are more likely to be harmful than are non-physiological doses of RLA which does occur naturally in the body and for which it does have mechanisms to deal with it.

    Therefore, SLA should not be considered as mere filler in the racemic mixture of enantiomers which is widely available on the supplement market, but should be considered potentially harmful until proven otherwise. This not to say that non-physiological doses of RLA may not also be harmful, only that they are less likely to be so. In particularly, RLA is likely to be less harmful and more beneficial than the racemate generally used.
    Additional Reading

    Thiol homeostasis and supplements in physical exercise.
    "Thiols are a class of organic sulfur derivatives (mercaptans) characterized by the presence of sulfhydryl residues. In biological systems, thiols have numerous functions, including a central role in coordinating the antioxidant defense network. Physical exercise may induce oxidative stress. In humans, a consistent marker of exercise-induced oxidative stress is blood glutathione oxidation. Physical training programs have specific effects on tissue glutathione metabolism that depend on the work program and the type of tissue. Experimental studies show that glutathione metabolism in several tissues sensitively responds to an exhaustive bout of exercise. Study of glutathione-deficient animals clearly indicates the central importance of having adequate tissue glutathione to protect against exercise-induced oxidative stress. Among the various thiol supplements studied, N-acetyl-L-cysteine and alpha-lipoic acid hold the most promise."R

    Neuroprotection by the metabolic antioxidant alpha-lipoic acid.
    "Very few neuropharmacological intervention strategies are currently available for the treatment of stroke and numerous other brain disorders involving free radical injury. We propose that the various metabolic antioxidant properties of alpha-lipoate relate to its possible therapeutic roles in a variety of brain and neuronal tissue pathologies: thiols are central to antioxidant defense in brain and other tissues. The most important thiol antioxidant, glutathione, cannot be directly administered, whereas alpha-lipoic acid can. In vitro, animal, and preliminary human studies indicate that alpha-lipoate may be effective in numerous neurodegenerative disorders."R
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    looks a little familar..this was taken from elite
    http://www.anabolicminds.com/forum/s...light=ala+info
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    I've been taking alcar, r-ala, and green tea for about a week now, and love it. I feel better and better each day. Mood and energy is heightened. No physical changes to my body yet, but I do have more endurance. Alcar definitely seems to enhance the effects of eca - my normal dose of clenbutrx has me sweating like a pig! As I'm 34, I'm also interested in the GH study posted earlier by GuyinLA - those are dramatic results, aren't they? Would my GH levels have dropped much at 34? Wouldn't alcar keep you awake taken before bed though?

    Here's the snippet from GuyinLA's post:

    3. There has been a patent filed for an ALCAR/Ornithine combo to release GH. (Or course, one can easily buy Ornithine and ALCAR separately and not violate any patent). The patent application references a study to support the claim, as follows:

    Measurements of GH release occurring at 1.5 hours post sleep were performed on serum samples from a healthy 52 year old male volunteer. Controls and serum analysis for GH were measured by standard commercially avialable antibody capture technique. Experiments and measurement of results occurred between June and October 2000. Each single night experimental serum collection was separated from any other experiments by 1 week. All determinations represent averaged value of triple determinations. Acetyl-l-carnitine and l-ornithine values are in milligrams (mg). Measurements were each performed on serum collected 1.5 hours post night time sleep. Choice of 1.5 hours post sleep represents one complete sleep cycle with slow wave sleep during which GH is released. Oral ingestions of stated substances occurred just before night sleep. . The normal range of serum GH at 1.5 hours post sleep is in the 1-10 nanograms per milliliter (ng/ml) range. The variance in measurement precision is given by the second value. All experiments were preceded by a period of 3-4 hours since the last meal.

    1 Measured GH Experimental Conditions (ng/ml) Control (no treatment) 1.5 hour post sleep serum collection 0.55 .+-. 0.2 500 mg Acetyl-l-carnitine at sleep, 1.5 hour post sleep serum 0.55 .+-. 0.1 collection 500 mg l-ornithine at sleep, 1.5 hour post sleep serum 0.55 .+-. 0.2 collection 500 mg acetyl-l-carnitine + 25 mg l-ornithine at sleep, 1.25 .+-. 0.3 1.5 hour post sleep serum collection 500 mg acetyl-l-carnitine + 35 mg l-ornithine at sleep, 7.5 .+-. 1.2 1.5 hour post sleep serum collection 500 mg acetyl-l-carnitine + 45 mg l-ornithine at sleep, 34.5 .+-. 3.7 1.5 hour post sleep serum collection

    This data shows the absence of effect of either acetyl-l-carnitine or l-ornithine alone to augment GH release at 1.5 hours post sleep. Ingestion of both acetyl-l-carnitine and l-ornithine at night sleep displays a synergy that increases GH release with the level of l-ornithine. This data also indicates a non-linear increase in GH release with increasing l-ornithine in the the active mixture of acetyl-l-carnitine and l-ornithine. This data accords with our choice of 20 to 40 milligrams of l-ornithine along with the 500 milligrams of acetyl-l-carnitine as a proper range for maintenance of young adult levels of augmented human GH release.

    Here's the link to the patent application:

    http://appft1.uspto.gov/netacgi/nph...2=ornithine&OS="acetyl+l+carnitine"+AND+ornit hine&RS="acetyl+l+carnitine"+A ND+ornithine
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    the prob with taking this combo before bed is u need to not eat for 3 hours,add in that with 6-8 hrs of sleep and then u have a huge fast going on,no matter how much gh u have in ur system u still need food imo
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    I saw that 1Fast400 is now carrying liquid CLA, Clarinol CLA Plus. It's not quite cost competitive compared to softgels (21.9 cents per gram of actual CLA compared to legalgear.com's 10.0 cents per gram of actual CLA).

    What is so different about CLA that makes the price of softgels cheaper than liquids because that is completely the opposite of EFA pricing?

    ~Todd
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    Hm... It doesn't say that you NEED to have not eaten for 3 hours. That's what they did in the study, but that doesn't make it necessarily an absolute prerequisite.

    I think if your glycemia is low, you can release GH just fine. So if you eat just protein, or take a good bit of ALA with your meal just before bed, your glycemia will be low. Should be OK. Anyways, 120 caps of 500mg Ornithine is below $15. I'mma give it a try. Heck, that's 10x the ornithine that they use in the study!
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    Yeah wojo, you're right - I've gotta have my cottage cheese before I sleep. Luna, you may be onto something with the ALA - my blood sugar seems pretty sensitive to ALA (if I take it w/out food, I crash), I may try some ALA w/cottage cheese, wait 30 minutes, take the Alcar and Ornithine and see how it does. I just hope it doesn't keep me up. Not sure if my GH levels are subpar, but it sure takes longer to get results (lean gains, fat loss, strength) than 10 years ago.
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    intv the decrease in GH levels in relation to age is well-known.

    At 34, your GH levels are somewhere around HALF what they were when you were 19 or so. I'm 35 and I'm seriously considering EVERYTHING I can do to get my GH back up. In the mid-30's, the skin is already less elastic (not hugely so, but it still is) and some small wrinkles are usually found around the eyes and mouth. I have some and most people think I look younger than my real age... Except when I shave my head, then people just run away from me

    Essentially, we can't really turn back the clock. BUT we can slow it down. I'm always wondering what happens when someone eats well, sleeps well, exercices well, all life long, AND ALSO takes supplements like alcar, ALA, and GH releasers, some steroidal precursors or hormones, basically doing EVERYTHING for their health and longevity.

    Heck, someone doing all that - me - might get to 100 and still seem 60? That seems possible, and there is very little to lose by trying.

    My take on it all is to do all I can. Man, what use is it to be in GREAT SHAPE at 35 and begin looking old at 45? I wanna keep what I got, as long as possible... I didn't take androgens in my '20s as many do, in a hurry to look good. I'm more muscular than many guys who shoot roids, but it took me 10 years getting there... Anyways, if there IS a way, I'm going to find it and still be in GREAT SHAPE at 65.

    Er... Anyways I'mma spend the $11.00 on Ornithine - a 4-month supply.
    Last edited by LunaHotel; 07-21-2003 at 12:57 PM.
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    Interestingly, that study has ONE volunteer.

    It's not really a huge statistical base on which to ensure quality measurements. Experience will tell.
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    Scotty,

    Thanks for the reclarification. This thread was HUGE and I was skimming through this as well as the other sites and that's the idea I got. Take R+ with carbs but w/o it isn't necessary...Again, thx for the help
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    Thanks for the info Luna, I hadn't noticed that the study was only one guy! I'm trying it anyway though, got some l-ornithine today. I'll probably try 100mg r-ala, 500mg alcar, and 100mg l-ornithine. I'll take it tonight about an hour after I have my cottage cheese, and right before I go to sleep. I'll report back on how much sleep I get tomorrow!
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    No prob Sawastea...long post, a lot to digest.

    More is NOT always better, as is the case with the l-ornithine. The ratio of the GH booster is supposedly unstable, meaning changing one parameter or the other (or adding food) supposedly disrupts it. That said, I know a few people who gave it a try for a good while and said it did jack for them. Too many variables as to why that 1 guy increased his GH. Fasting itself at night causes a rise in GH so that could be a big part. My advice....dont bank on it. That said....lets keep this post on target.
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    Thanks, Scottyo, good info. FWIW, I tried it last night, had a little trouble sleeping (my mind was going full throttle), but felt very well rested this morning. I'll keep at it a little while and see how it goes.

    Back to alcar - I love the energy (mentally and physically) and endurance this stuff gives me, would 5gm/day be overdoing it? Are there any contraindications; does it compete with or deplete any other nutrients? Thanks,

    Matt
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    Some people are reporting 6g a day, no problems, they feel great.

    I think my strength just increased MARKEDLY from taking this stuff. My Barbell curl just went from a somewhat steady 95 to 110. In like 10 days of taking alcar. I was stuck there for a bit, too.

    I think I'll keep it up
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    Excessive ALCAR does deplete choline stores in your body. Spook over at AL suggested spreading it out (which most people do) as over 2.5 grams at a time floods your system with an overabundance of ALCAR it cant handle. If going above 3 grams, Id suggest a choline supp, such as lecithin granules.
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    Ok so someone wanna recap the cycle and all the "options" again? =D
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    dude it's been posted several times already, look in the last few pages it was summarized again
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    Sorry Rome you got to read alittle.. expand the mind my man!!
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    How long does BOC take to get there stuff out to ya on normal delivery? I placed an order last week not really expecting it but since the dont confirm when it ships Im alittle curious.. Thanks oh and I checked the take your time tab....
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    i got mine in like 2-3 days..it was insanely fast lol
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    well how did your arrive? was it via ups or mail and did u just pay for the regular shipping or upgrade? Thanks for the info...
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    Shipping will be delayed as Chemo is leaving to go serve the country and many changes are being made. Sorry for the incovenience.
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    Originally posted by whosyourdaddy02
    Shipping will be delayed as Chemo is leaving to go serve the country and many changes are being made. Sorry for the incovenience.
    LOL, not related bro. BOC was meant to be BAC(Beyond a Century). This is anarchy bro not BDC products!

    On a side note lets take shipping questions to a different thread please! Thanks!
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    sorry about the mix up and just thought I would throw in the shipping question here as I had just gotten done re-reading through the 15 pages again and had to leave so posted it here in a hurry...sorry....
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    No Biggie breezed....
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    Great thread!
    About a month a go I was looking to take this Stack but some people told me it was insanely expensive. So no go.. But now everyone is taking it, so I might do it. But I do have a question. Other then ww7 I have not heard any measureable changes in BF. I read observations but not anything more. For example when I take ALA for a few days I look dramaticly leaner, but I have not lost a real amount of BF. Do you see what I mean? This would be the main reason for me to take this Stack. Everything else is a bonus. So has anyone else lost any real change in BF?
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    2 weeks on the stack and i have't noticed much
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    hat dosages are you using? Whats your diet like? what are your stats
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    Originally posted by maggmaster
    hat dosages are you using? Whats your diet like? what are your stats
    600mg r-ala
    3-3.5g alcar
    3x 1/4 tsp green tea extract from BAC

    i'm currently bulking, taking in 3k calories, 320g protein 280g carbs 60g fat. i'm 19 yrs old, 5'7 165
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    Good questions mag and most guys took a month notice anything substantial.
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    I cant imagine losing a lot of bf bulking
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    I think some of the guy's on Animals board have reported otherwise. Statements like "I am eating a ton but still getting leaner" is a phrase i heard over there before they closed that board.
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    i have never used bodyfat calipers i just use pictures and the mirror, so i can't tell you if my bodyfat has dropped but i do look a lot leaner.
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    Hey if thats true then this stuff is more amazing than steroids.
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    Shhhhhh, you're gonna make the FDA ban green tea!
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    Originally posted by maggmaster
    I cant imagine losing a lot of bf bulking
    i'm not expecting to lose a lot of bf from this stack, i just haven't noticed anything at all like from what others have said. it's only been 2 weeks so may be too early to say anything.
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    I just started using Alcar myself, and already really like the feeling on the stuff. The enhanced mental focus and "buzzing" feeling behind the eyes is good stuff indeed. I am 4 days into a clen cycle and just added in the alcar, as I was already taking r-ala and biotin with carb meals, and green tea throughout the day. I'm not sure if it's coincidence or just because I'm losing water at the start of a cut, but one day after starting on Alcar I'm down 3 pounds on the scale.
  

  
 

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