[windwords7]

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

[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

[windwords7]

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.

[windwords7]

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.

[Iron Warrior]

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

[windwords7]

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.

[wojo]

*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*

[wojo]

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.

[wojo]

http://www.discover.com/oct_02/featradical.html

[windwords7]

Originally posted by wojo
http://www.discover.com/oct_02/featradical.html

That is one brilliant article! I love it!

[wojo]

got that from animals too..this is one informative thread here fellas enjoy

[windwords7]

Bump!

[spike1205]

so--lots of good articles, any personal opinons from anyone who has used it?

[windwords7]

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!