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

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    Acetyl L-Carnitine (Alcar)....Post info/exp. in here!


    Post what ever you can find or your expierence with it in here!

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    Haven't tried Acetyl-L-Carnitine, but L-Carnitine did nothing for me at 3 grams a day as far as fat loss is concerned
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    Some Quick Info I Found.

    Acetyl L-Carnitine

    ALC improves both Short-Term Memory and Long-Term Memory.

    ALC improves Mood [ALC improves Mood in 53% of healthy subjects].

    Acetyl L-Carnitine retards some aspects of the Aging Process in the Skin:

    ALC improves the reaction times of people afflicted with Cerebral Insufficiency.

    ALC (2-4 grams per day) improves walking distance without Pain in people afflicted with Intermittent Claudication.

    ALC prevents the age-related impairment of Eyesight (by protecting the Neurons of the Optic Nerve and the Occipital Cortex of the Brain.

    ALC enhances the ability of Macrophages to function as Phagocytes.

    ALC improves Athletic Performance [ALC given prior to Exercise increased the maximum running speed of animals].

    ALC enhances the function of Cytochrome Oxidase (an essential enzyme of the Electron Transport System (ETS).

    ALC improves the Energy metabolism of Neurons (by enhancing the transport of Medium-Chain Saturated Fatty Acids and Short-Chain Saturated Fatty Acids across the Cell Membranes of Neurons into the Mitochondria).

    ALC inhibits the damage caused by Hypoxia.
    ALC transports Lipids into the Mitochondria of Cells.

    ALC improves mood and memory in people with Age Associated Memory Impairment.

    ALC improves Mental Function where Alcohol induced cognitive Impairment exists.

    ALC increases Alertness.

    Acetyl-L-Carnitine inhibits the deterioration in Mental Function associated with Alzheimer’s Disease and slows the progression of Alzheimer’s Disease [people afflicted with Alzheimer’s Disease exhibited significantly less deterioration in Mental Function following the administration of supplemental ALC for 12 months. This finding was verified by using nuclear magnetic resonance on the subjects].

    ALC increases Alertness in people afflicted with Alzheimer's Disease - 2,500-3,000 mg per day for 3 months].
    ALC inhibits the toxicity of Amyloid-Beta Protein (ABP) to Neurons.

    ALC improves Attention Span in people afflicted with Alzheimer's Disease.

    ALC improves Short Term Memory in people afflicted with Alzheimer's Disease.

    High concentrations of ALC are naturally present in various regions of the Brain.
    ALC reverses the age-related decline that occurs in Cholinergic Receptors (i.e. the Receptors that receive Acetylcholine).

    ALC improves (eye to hand) Coordination [supplemental ALC @ 1.5 grams per day for 30 days improved eye to hand coordination in healthy, sedentary subjects by a factor of 300-400%].

    ALC improves the Interhemispheric Flow of Information across the Corpus Callosum of the Brain.

    ALC retards the decline in the number of Dopamine Receptors that occurs in tandem with the Aging Process and (more rapidly) with the onset of Parkinson's Disease.

    ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.

    ALC can prevent the destruction of Dopamine Receptors by MPTP (a neurotoxin capable of causing Parkinson's Disease via Dopaminergic Receptor death.

    ALC improves Attention Span and Memory in people afflicted with Down’s Syndrome.

    ALC retards the inevitable decline in the number of Glucocorticoid Receptors that occurs in tandem with the Aging Process.

    ALC enhances the recovery of people afflicted with Hemiplegia (Paralysis of one side of the body) and improves their Mood and Attention Span.

    ALC retards the age-related deterioration of the Hippocampus [research - rats].

    Acetyl-L-Carnitine (ALC) improves Learning ability [women aged 22 - 27 were supplemented with ALC for 30 days. Complex video game tests before and after supplementation concluded that supplemental ALC caused large increases in speed of Learning, speed of reaction and reduction in errors].

    ALC inhibits (and possibly reverses) the degeneration of Myelin Sheaths that occurs in tandem with the progression of the Aging Process [scientific research - hyperglycemic mice treated with ALC for 16 weeks exhibited improved nerve conduction velocity and exhibited thicker Myelin Sheaths and larger myelinated Nerve Fibers].

    ALC retards the inevitable decline in the number of Nerve Growth Factor (NGF) Receptors that occurs in tandem with the Aging Process.

    ALC stimulates and maintains the growth of new Neurons within the Brain (both independently of Nerve Growth Factor (NGF) and as a result of preserving NGF) and helps to prevent the death of existing Neurons [ALC inhibits Neuron death in the Striatal Cortex, Prefrontal Cortex and the Occipital Cortex of the Brain].

    ALC inhibits the degeneration of Neurons that is implicit in Neuropathy.

    ALC rejuvenates and increases the number of N-Methyl-D-Aspartate Receptors (NMDA Receptors) in the Brain [even a single dose of ALC increases the number of functional NMDA Receptors]:

    ALC protects the NMDA Receptors in the Brain from the natural decline that occurs in tandem with the Aging Process [research - animals].

    ALC is presently being researched as a treatment for Parkinson's Disease.

    ALC inhibits the loss of Vision, degeneration of Neurons and damage to the Retina associated with Retinopathy (including Diabetic Retinopathy).

    ALC improves the quality of Sleep and reduces the quantity of Sleep required.

    ALC improves Spatial Memory (an aspect of Short Term Memory that involves remembering one’s position in space).

    ALC inhibits the excessive release of Cortisol in response to Stress and inhibits the depletion of Luteinising Hormone Releasing Hormone (LHRH) and Testosterone that occurs as a result of excessive Stress.

    ALC improves Verbal Fluency.

    ALC enhances the function of Cytochrome Oxidase (also called Complex IV) - an essential enzyme of the Electron Transport System.

    ALC normalizes Beta-Endorphin levels.
    ALC reduces Stress-induced Cortisol release [research - animals].

    ALC prevents the depletion of Luteinising Hormone Releasing Hormone (LHRH) caused by exposure to excessive Stress.

    ALC retards the decline in the production of Nerve Growth Factor (NGF) that occurs in tandem with the Aging Process.

    ALC increases plasma Testosterone levels (via its influence on Acetylcholine neurotransmission in the Striatal Cortex of the Brain) and prevents the depletion of Testosterone caused by exposure to excessive Stress [research - rats].

    ALC increases the body's levels of circulating Thyrotrophin.

    ALC facilitates the production of Adenosine Triphosphate (ATP) [research - animals].

    ALC "shuttles" Long Chain Fatty Acids between the Cytosol and the Mitochondria of Cells.

    ALC facilitates both the release and synthesis of Acetylcholine.

    ALC's ability to increase the synthesis of Acetylcholine occurs as a result of it donating its Acetyl group towards the production of Acetylcholine.

    ALC increases the Brain's levels of Choline Acetylase (which in turn facilities the production of Acetylcholine).

    ALC enhances the release of Dopamine from Dopaminergic Neurons and improves the binding of Dopamine to Dopamine Receptors.

    References

    De Falco, F. A., et al. Effect of the chronic treatment with L-acetylcarnitine in Down’s syndrome. Clin Ther. 144:123-127, 1994.

    Bowman, B. Acetyl-carnitine and Alzheimer’s disease. Nutr Rev. 50:142-144, 1992.

    Bruno, G., et al. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord (USA). 9(3):128-131, 1995.

    Calvani, M., et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer’s disease. Annals of the New York Academy of Sciences (USA). 663:483-486, 1993.

    Carta, A., et al. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer’s Disease? Annals of the New York Academy of Sciences (USA. 640:228-232, 1991.

    Guarnaschelli, C., et al. Pathological brain ageing: evaluation of the efficacy of a pharmacological aid. Drugs under Experimental and Clinical Research. 14(11):715-718, 1988.

    Passeri, M., et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. International Journal of Clinical Pharmacology Research. 10(1-2):75-79, 1990.

    Pettegrew, J. W., et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer’s disease. Neurobiol Aging. 16:1-4, 1995.

    Rai, G., et al. Double-blind, placebo controlled study of acetyl-L-carnitine in patients with Alzheimer’s dementia. Current Medical Research and Opinion. 11(10):638-647, 1989.

    Sano, M., et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer’s disease. Arch Neurol. 49:1137-1141, 1992.

    Sinforiani, E., et al. Neuropsychological changes in demented patients treated with acetyl-L-carnitine. International Journal of Clinical Pharmacology Research. 10(1-2):69-74, 1990.

    Spagnoli, A. U., et al. Long-term acetyl-l-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732, 1991.
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    Originally posted by Iron Warrior
    Haven't tried Acetyl-L-Carnitine, but L-Carnitine did nothing for me at 3 grams a day as far as fat loss is concerned
    From what I understand they are completly different in effect.
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    I know bro, just heard that a while back, wish I knew then what I know now. The L-Carnitine probably has a very low oral absorption rate
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    This is from Animals site:

    Mechanisms via how you can manipulate nutrient partitioning....i.e. Insulin levels/Blood Glucose levels.

    a)Non-insulin mediated glucose partitioning(Or if you prefer disposal). These types of supplements(For example R-ALA and Acetyl-L-Carnitine) work INDEPENDENT of insulin. They have little effect on its release or degradation in the bloodstream. What they do, is increase translocation of intra-cellular Glut-4’s(Glucose Transporters) to the outside of the cellular membrane albeit in the adipocytes(fat cells) and miocytes(muscle cells). The net result, is that more glucose is diverted to the miocytes, and less to the adipocytes. In hypocaloric diets, this means, more fat-loss, and better muscle preservation. In hypercaloric diets, this means more muscle gain, and less fat gain.
    b) Insulin mediated glucose partitioning(or disposal). These types of supplements actually influence AA transport b/c they work through insulin signalling pathways. CLA is a good example. CLA works by increasing AA and glucose transport into the muscle cells via insulin stimulated pathways, and therefore in hypocaloric diets acts as an anti-catabolic. CLA
    also keeps blood glucose levels more stable. In essence preventing preventing high blood glucose or hypoglycaemia after a carb meal.
    c)Non-stimulating thermogenics. GLA. In order to explain a bit how GLA works, I will briefly explain what prostaglandins are.

    Series 1 Prostaglandins = Good(PgF2A)( Anabolic) They are incredibly thermogenic and help build muscle.
    Series 2 Prostaglandins = Bad(PgE2)(Catabolic) They break down protein.
    Series 1 and 2 produced by your cells always at a 1:1 ratio.
    Series 3 Prostaglandins block the production of series 2.
    Series 1 and 2 Prostaglandins are made from the essential fatty acid Linoleic Acid.
    Linoleic Acid = Omega-6 Fatty Acid .
    Linolenic Acid(Alpha-linolenic acid) is an Omega-3 fatty Acid Series 3 Prostaglandins are derived from this acid.
    GLA = Omega-6 Fatty Acid (Gamma-Linolenic Acid) This BLOCKS series 2 Prostaglandins.
    By Blocking series 2 prostaglandins, GLA shifts the normal 1:1 Prostaglandin ratio to the PgF2A(Anabolic) side. In essence, promoting thermogenesis. As can be shown in my study of GLA. Its anabolic effects were not measured(As this is also a direct consequence of a positive PgF2A environment) .

    These explanations for the different workings of each substance can be seen to be true when one compares each to the Placebo measurements.
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    *acetyl L-Carnitine (ALC) is the acetyl ester of carnitine, which transports fats into the mitochondria. In the mitochondria these fats are converted to an energy source. ALC is found in the brain but its levels are dramatically reduced as we age. Recent research has vaulted ALC as one of the premiere anti-aging compounds, especially in relation to brain and nervous system deterioration. ALC not only increases the release and synthesis of acetylcholine it now appears that it has neuroprotective and neuroenhancing properties as well. ALC can prevent dopaminergic neuron death by the neurotoxin MPTP which causes symptoms similar to Parkinson's disease. It has also been established that the density of NMDA receptors declines with age along with a decreased amount of NGF (Nerve Growth Factor). Treatment with ALC restores the NMDA receptor numbers and enhances the effects of NGF.

    ENHANCING ENERGY & ENDURANCE FOR GREATER ATHLETIC PERFORMANCE
    You're blasting your biceps. Pushing hard to get in one last repetition. But muscle failure sets in and you just can't do it. No more energy. No more ATP. No chance of finishing your set. You turn to your left and the guy next to you is still going to town, doing the same exercise with the same weight. How come he can do more than you? Isn't there anything you can do to improve your energy and endurance to help power you through your workout? Yes, there is! You can use a revolutionary dietary supplement called Acetyl L-Carnitine. This supplement can provide you with critical nutritional support to improve long-term energy and endurance in physical performance.

    L-Carnitine and ATP.
    The amino acid l-carnitine is well known for its key role in the burning of fats. Specifically, l-carnitine transports fatty acids to the innermost section of the mitochondria (the cellular powerplants for energy) where they are used to create adenosine triphosphate (ATP), the energy currency of the body. Studies have shown that carnitine deficiency lowers ATP levels in various tissues. Carnitine deficiency also increases the susceptibility to fatigue from, and decreased the rate of recovery following, strenuous physical activity

    Acetyl L-Carnitine (ACL).

    Is the acetyl ester of the amino acid l-carnitine, which transports fats into the mitochondria. In the mitochondria these fats are converted to an energy source. It is a nutrient and naturally occurring metabolite that is involved in lipid, carbohydrate and protein, metabolism. ALC is naturally present in the human and animal body. The heart, brain, the muscles, and the testicles contain considerable concentrations of ALC but its levels are dramatically reduced as we age.

    The esterified form is particularly well absorbed. As a matter of fact, when radioactively labeled ALC is administered, it is readily taken up in the cells. The distribution inside the cells was found to be 60% free l-carnitine, which was to be expected, and 40% ALC, which underscores the importance of this unique substance in the body.

    ALC and coenzyme A.
    Though closely related to l-carnitine, ALC surpasses the metabolic potency of carnitine. ALC is a source of precious acetyl groups that facilitate energetic pathways and which carnitine cannot supply. Acetyls from ALC can be combined with coenzyme A (the metabolized form of the vitamin pantothenic acid) to create Acetyl-Coenzyme A (A-CoA). It is the A-CoA acting within the Krebs cycle that helps to generate ATP. The acetyl groups of ALC, once incorporated into A-CoA, can be used interchangeably in a variety of metabolic pathways. When energy charge is low, A-CoA stores are being depleted, and ALC can be drawn upon to replenish A-CoA. When the cell's energy charge is high, carnitine can be converted back to ALC, thereby conserving the acetyl until it is needed for energy generation or for the other metabolic purposes

    ALC and endurance.
    The bottom line is that ALC can improve energy and endurance in physical performance. ALC represents a substance which is a high energy storage compound. Research has shown that ALC can increase the amount of ATP produced in the body for energy. Furthermore, a Russian study in 1993 demonstrated that ALC administration for 10 days statistically and significantly increased maximum running speed and endurance.

    Other ALC contributions.
    In addition, ALC has other valuable contributions to make to human health and fitness. Research has demonstrated that ALC is capable of reducing cortisol levels after administration. This is important since cortisol is a catabolic hormone that can increase the breakdown of muscle tissue, which is certainly an important consideration for bodybuilders and other athletes. Other research has shown that besides reducing cortisol levels, ALC can reduce prolonged intracellular lactic acidosis, secondary tissuedegeneration, and neuronal cell death.

    ALC and aging.
    Recent research has vaulted ALC as one of the premiere anti-aging compounds, especially in relation to brain and nervous system deterioration. ALC not only increases the release and synthesis of acetylcholine it now appears that it has neuroprotective and neuroenhancing properties as well. ALC can prevent dopaminergic neuron death by the neurotoxin MPTP which causes symptoms similar to Parkinsons disease. It has also been established that the density of NMDA receptors declines with age along with a decreased amount of NGF (Nerve Growth Factor). Treatment with ALC restores the NMDA receptor numbers and enhances the effects of NGF. Thus, both animal and human research has demonstrated that ALC has improved age-related memory impairment in elderly subjects.

    from nubrain*
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    more from animals site--------------------------------------------------------------------------------

    http://www.pnas.org/cgi/content/abstract/99/4/2356

    Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 2356-2361, February 19,
    2002

    Memory loss in old rats is associated with brain mitochondrial
    decay and RNA/DNA oxidation: Partial reversal by feeding
    acetyl-L-carnitine and/or R--lipoic acid

    [names and research institutes cut for brevity, see URL above]

    Accumulation of oxidative damage to mitochondria, protein, and
    nucleic acid in the brain may lead to neuronal and cognitive
    dysfunction. The effects on cognitive function, brain
    mitochondrial structure, and biomarkers of oxidative damage were
    studied after feeding old rats two mitochondrial metabolites,
    acetyl-L-carnitine (ALCAR) [0.5% or 0.2% (wt/vol) in drinking
    water], and/or R--lipoic acid (LA) [0.2% or 0.1% (wt/wt) in diet].
    Spatial memory was assessed by using the Morris water maze;
    temporal memory was tested by using the peak procedure (a time-
    discrimination procedure). Dietary supplementation with ALCAR
    and/or LA improved memory, the combination being the most
    effective for two different tests of spatial memory (P < 0.05;
    P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical
    analysis showed that oxidative damage to nucleic acids (8-
    hydroxyguanosine and 8-hydroxy-2'-deoxyguanosine) increased with
    age in the hippocampus, a region important for memory. Oxidative
    damage to nucleic acids occurred predominantly in RNA. Dietary
    administration of ALCAR and/or LA significantly reduced the
    extent of oxidized RNA, the combination being the most effective.
    Electron microscopic studies in the hippocampus showed that ALCAR
    and/or LA reversed age-associated mitochondrial structural decay.
    These results suggest that feeding ALCAR and LA to old rats
    improves performance on memory tasks by lowering oxidative damage
    and improving mitochondrial function.

    ****************************** ****************************** ****

    http://www.pnas.org/cgi/content/abstract/99/4/1876

    Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 1876-1881, February 19,
    2002

    Age-associated mitochondrial oxidative decay: Improvement of
    carnitine acetyltransferase substrate-binding affinity and
    activity in brain by feeding old rats acetyl-L-carnitine
    and/or R--lipoic acid

    [names and research institutes cut for brevity, see URL]

    We test whether the dysfunction with age of carnitine
    acetyltransferase (CAT), a key mitochondrial enzyme for fuel
    utilization, is due to decreased binding affinity for substrate
    and whether this substrate, fed to old rats, restores CAT
    activity. The kinetics of CAT were analyzed by using the brains
    of young and old rats and of old rats supplemented for 7 weeks
    with the CAT substrate acetyl-L-carnitine (ALCAR) and/or the
    mitochondrial antioxidant precursor R--lipoic acid (LA). Old
    rats, compared with young rats, showed a decrease in CAT activity
    and in CAT-binding affinity for both substrates, ALCAR and CoA.
    Feeding ALCAR or ALCAR plus LA to old rats significantly restored
    CAT-binding affinity for ALCAR and CoA, and CAT activity. To
    explore the underlying mechanism, lipid peroxidation and total
    iron and copper levels were assayed; all increased in old rats.
    Feeding old rats LA or LA plus ALCAR inhibited lipid peroxidation
    but did not decrease iron and copper levels. Ex vivo oxidation of
    young-rat brain with Fe(II) caused loss of CAT activity and
    binding affinity. In vitro oxidation of purified CAT with Fe(II)
    inactivated the enzyme but did not alter binding affinity. However,
    in vitro treatment of CAT with the lipid peroxidation
    products malondialdehyde or 4-hydroxy-nonenal caused a decrease
    in CAT-binding affinity and activity, thus mimicking age-related
    change. Preincubation of CAT with ALCAR or CoA prevented
    malondialdehyde-induced dysfunction. Thus, feeding old rats high
    levels of key mitochondrial metabolites can ameliorate oxidative
    damage, enzyme activity, substrate-binding affinity, and
    mitochondrial dysfunction.

    ****************************** ****************************** ****

    http://www.pnas.org/cgi/content/abstract/99/4/1870

    Proc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 1870-1875, February 19,
    2002

    Feeding acetyl-L-carnitine and lipoic acid to old rats significantly
    improves metabolic function while decreasing oxidative stress

    [names and research institutes cut for brevity, see URL above]

    Mitochondrial-supported bioenergetics decline and oxidative stress
    increases during aging. To address whether the dietary addition of
    acetyl-L-carnitine [ALCAR, 1.5% (wt/vol) in the drinking water]
    and/or (R)--lipoic acid [LA, 0.5% (wt/wt) in the chow] improved
    these endpoints, young (2-4 mo) and old (24-28 mo) F344 rats were
    supplemented for up to 1 mo before death and hepatocyte isolation.
    ALCAR+LA partially reversed the age-related decline in average
    mitochondrial membrane potential and significantly increased (P =
    0.02) hepatocellular O2 consumption, indicating that mitochondrial-
    supported cellular metabolism was markedly improved by this
    feeding regimen. ALCAR+LA also increased ambulatory activity in
    both young and old rats; moreover, the improvement was
    significantly greater (P = 0.03) in old versus young animals and
    also greater when compared with old rats fed ALCAR or LA alone.
    To determine whether ALCAR+LA also affected indices of oxidative
    stress, ascorbic acid and markers of lipid peroxidation
    (malondialdehyde) were monitored. The hepatocellular ascorbate
    level markedly declined with age (P = 0.003) but was restored to
    the level seen in young rats when ALCAR+LA was given. The level of
    malondialdehyde, which was significantly higher (P = 0.0001) in
    old versus young rats, also declined after ALCAR+LA supplementation
    and was not significantly different from that of young unsupplemented
    rats. Feeding ALCAR in combination with LA increased metabolism and
    lowered oxidative stress more than either compound alone.
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    That is one brilliant article! I love it!
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    got that from animals too..this is one informative thread here fellas enjoy
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    Bump!
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    so--lots of good articles, any personal opinons from anyone who has used it?
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    Originally posted by spike1205
    so--lots of good articles, any personal opinons from anyone who has used it?
    LMAO- http://www.animalkits.be/phpBB/viewt...54&forum=1&224

    Another Admin here swears by it in combonation with ALA and CLA which is now called the "anarchy stack". Yeah the stack works and works well. 28 pounds in 2 months with little to no muscle loss is outsanding!
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    But from a manufacturers standpoint you will have to pay out the ass to put it in a product...the man holding the patent is charging unbelievable amounts of money to put it in a product.

    But for homebrewers...

    Chemo
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    Originally posted by Chemo
    But from a manufacturers standpoint you will have to pay out the ass to put it in a product...the man holding the patent is charging unbelievable amounts of money to put it in a product.

    But for homebrewers...

    Chemo
    That sucks bro! It would be cool to see the anarchy stack improved upon then packaged together! Thanks for the info. But as you said it is great for the do it yourselfer....
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    Originally posted by windwords7


    LMAO- http://www.animalkits.be/phpBB/viewt...orum=1&amp;224

    Another Admin here swears by it in combonation with ALA and CLA which is now called the &quot;anarchy stack&quot;. Yeah the stack works and works well. 28 pounds in 2 months with little to no muscle loss is outsanding!
    Hey bro, do you know how many grams of each he was using ? This sounds interesting to me because ALC is supposed to transport fat for better fat metabolism
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    What I have to offer:

    1. Anecdotal: I have been taking up to 2 grams/day of ALCAR away from meals for around a month. I believe it results in increased energy and focus. This effect seems to be in line with the findings of cognitive studies cited above. On the boards (particularly Animal's) I have read numerous anecdotal postings on ALCAR's benefits.

    2. I have read that taking ALCAR during the day may increase testosterone production. Of course, a study could easily determine whether this claim is valid. Also, ALCAR reputably aids in fat loss, though I haven't found a study to support this claim. This would be a harder/more expensive study to conduct.

    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-...=ornithine&OS="acetyl+l+carnitine"+AND+ornit hine&RS="acetyl+l+carnitine"+A ND+ornithine

    4. I think more study is needed but there are already studies out there and ample anecdotal evidence to support ALCAR supplementation for cognitive improvement, fat loss, and GH release. I will continue to take ALCAR supplements and look forward to more studies.
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    As I mentioned in another post...I love ALCAR. I use about 2 grams a day and it is quickly becoming a favorite supplement. I just read another experiment where one individual shows ALCAR and theanine to reduce sleep requirements. Not sure if its true, but I have been taking ALCAR and a green tea extract (part of the anarchy stuff) that is equal to 4 cups of green tea (decaf)...so I am getting a decent amount of theanine there. And I have been waking up feeling very alert in the mornings.
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    i personally believe that green tea extract of more importantly egcg's should have been added to the ucp-1 because of there thermogenic activity but more importantly because of there anti-ox properties
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    well i was usinfg the anarchy stack myself ,for some reason without the alcar,but using just cla (18 grams)and green tea(15 caps of vitamin shoppes a day(30% egcgs)) alone with 1800mgs of ala and loved it
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    Originally posted by wojo
    i personally believe that green tea extract of more importantly egcg's should have been added to the ucp-1 because of there thermogenic activity but more importantly because of there anti-ox properties
    That's cool, your entitled to your opinion but let's have that conversation in the other thread. This is about ALCAR and the Anarachy stack.
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    which is why my next post was about the anarchy stack ..sorry ww7
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    Originally posted by wojo
    which is why my next post was about the anarchy stack ..sorry ww7
    No probs!
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    Bump!
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    Diagram...
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    My Results


    My results with the anarchy stack are nothing short of amazing for being otc supps...and I was not even using the CLA.

    ALCAR: min 2000mg/day up to 3000mg/day.
    ALA: 300-600mg 5 minutes before each meal (amount of ala taken is dependent on estimated carbs in meal plan to consume)

    The ALCAR has given me endurance while training never before had by me, I feel as I can train for hours, and have, I have energy threw the roof.

    The ALCAR seems to keep my mind in "overdrive" I seem to always have dozens of different thoughts circulating in my mind all the time, I cant sit still, I can, but If I do, I go off into some thought process that makes me think of something to do...lol...

    And of couse I am getting noticably leaner, while eating basically the same, and strength is goin UP while getting leaner.

    I also took, glutamine, biotin and a multivit 2 x day with the ala & alcar.
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    newbie question. where do i get alcar.

    JWest
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    https://www2.acadia.net/cgi-bin/BAC/...=8350830_20688

    scroll down a bit they have powder or caps
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    Re: My Results


    Originally posted by Stroyer
    My results with the anarchy stack are nothing short of amazing for being otc supps...and I was not even using the CLA.

    ALCAR: min 2000mg/day up to 3000mg/day.
    ALA: 300-600mg 5 minutes before each meal (amount of ala taken is dependent on estimated carbs in meal plan to consume)

    The ALCAR has given me endurance while training never before had by me, I feel as I can train for hours, and have, I have energy threw the roof.

    The ALCAR seems to keep my mind in &quot;overdrive&quot; I seem to always have dozens of different thoughts circulating in my mind all the time, I cant sit still, I can, but If I do, I go off into some thought process that makes me think of something to do...lol...

    And of couse I am getting noticably leaner, while eating basically the same, and strength is goin UP while getting leaner.

    I also took, glutamine, biotin and a multivit 2 x day with the ala &amp; alcar.
    i always thought the cla was the cheif component of the stack,guess i was wrong..how much biotin were u taking?
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    Biotin


    I only started at 1mg 3 x day, but since biotin is ass cheap even at wal-mart, i have upped it to 3mg 3 x day.

    Some of the tell tale signs of biotin deficiency are dryin of the skin and achy joints and man, did my joints ache after using the ALA for a few weeks, once I started the biotin, and even more so since I increased the amount/day, the soreness seems to have decreased a bit, though I would not mind still having the dry skin...lol...dry out some of these pimples..lol..

    Using that amount of CLA, for me at the time I started was a bit expensive to spend on otc supps, at 4gr of cla 4-5 x day, (and keep in mid alot of the cla is on 750mg of acutally cla per cap, not the full 1gr, so thats even more one has to take to reach a true 4gr dose) gets a bit pricey fast.

    I would LOVE to run the alcar at at higher dose as well, such as 5gr/day but that do, would get expensive kinda fast...man, I could not imagine how I would feel on 5gr/alcar day..

    One other note on alcar, in one of the posts above, that listed alot of very good info on alcar, is stated something to the extent that alcar helps sleep, it may help to improve the quality of your sleep while sleeping, but If I took the alcar anywhere later in the day/night, I could not fall asleep for ****, cause of the stimulating effects of the alcar.
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    yeah i have heard that myself which is why i have tryptophan on hand but man that too is expensive..gonna try alcart with piracetam myself and now it looks like biotin
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    tryptophan


    Does the tryptophan work well for you?
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    Anarchy Stack


    The genearal guidline for the anarchy stack is along the lines of:

    AlCAR: 1.5-5 grams a day
    ALA: 1200-2400mg day
    CLA: 12-20 grams day (4 gram dosing)

    That had both the low end and the high end of the doses, most people will ahve to "play" with it to see what dose work best for them and what can be afforded.
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    Re: tryptophan


    Originally posted by Stroyer
    Does the tryptophan work well for you?
    seems to be i sleep pretty well and at only 6 hours of sleep i feel very well rested prob is after awhile u experience what is called wakefulness so i alternate periods of tryptophan and then switch back to melatonin if needed.
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    Well I am starting my Anarachy stack on Friday! Looking VERY forward to this. I wil be running CLA, ALA and Alcar for now. I will be drinking my Green Tea as well. I will add in other things as I go but want to start with this as the foundation first. I will let you all know how I do.
  

  
 

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