Acetyl L-Carnitine

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SKU: TN-N-0005

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Acetyl-L-Carnitine is an amino acid that is synthesized to create a more bioavailable form of the naturally occurring L-carnitine (L-3-hydroxytrimethylamminobutanoate). Acetyl-L-Carnitine has been associated with various nootropic-like benefits. L-carnitine is an amino acid that is a derivative of two dietary essential amino acids lysine and methionine, and it is produced within the body by the kidneys and the liver. Acetyl-L-Carnitine mimics L-carnitine by acting as an antioxidant and boosts the production of glutathione that is a free radical scavenger within the cells. It also assists in energy generation within the body and as such it is vital for the functioning of brain and heart, muscle movement, and a variety of body processes. It is also referred to as ALCAR, ALC, Acetil-L-Carnitina, Acetyl-L-Carnitine Arginate Dihydrochloride, Acetylcarnitine, Carnitine Acetyl Ester, ST-200, N-Acetyl-L-Carnitine, Levacecarnine, (3-carboxy-2-hydroxy-propyl)trimethylammonium hydroxide inner salt acetate.

Most people suffering from a nutritional deficiency of ALCAR and as such ALCAR supplements are used to boost the levels of ALCAR and result in some very powerful cognitive effects. Within the human body, carnitine is found in two forms, as L-carnitine or as Acetyl-L-Carnitine (ALCAR). ALCAR is the acetylated form of Carnitine. The synthesis of these two molecules occurs endogenously from the two essential amino acids Lysine and L-methionine. During the synthesis, the peptide-bound lysine is converted into e-N-trimethyl lysine by donation of S-adenosylmethionine whereby it is passively lysed from the peptide. The e-N-trimethyllysine undergoes hydroxylation to form β-hydroxy-e-N-trimethyllysine after which it is converted into y-Trimethyl Aminobutyraldehyde by aldolase enzyme. The final process involves the dehydrogenation process and then a hydroxylation to form L-Carnitine, that can be acetylated to create ALCAR. During this process, the hydroxylase enzymes are both dependent on Vitamin C and, therefore, the lack of Vitamin C will impair the biosynthesis of L-carnitine.

Acetyl-L-Carnitine is widely used in a variety of mental conditions including Alzheimer's, late-life depression, age-related memory deficits, and thinking problems linked to alcoholism and Lyme disease. In other instances, it is used for cataracts, Down syndrome, facial paralysis, poor circulation in the brain, and nerve pain caused by diabetes or caused by AIDs treatment drugs.


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Acetyl-L-Carnitine use was initially approved in Europe in the early 1980s where it was mostly employed in the treatment for neurological conditions and heart disease. The supplement became available in the U.S. market in 1994. In various European countries, this nootropic agent is sold as a drug but within America it is only available as a dietary supplement. Acetyl-L-Carnitine has a relatively short history, but several studies have been carried out since it was first synthesized. These studies have positively indicated that Acetyl-L-Carnitine is well tolerated, and it has cognition effects, and memory enhancing properties that are already published.


Various studies performed in both animal and human based studies have been performed to assess the effects of Acetyl-L-Carnitine on age-related conditions. In rat modeled studies, it has been observed that administration of Acetyl-L-Carnitine in aged rats helped correct the age-related decreases in levels of L-carnitine within tissues and it also reversed several age-related alterations in liver mitochondrial function. The researchers noted that when administered in high dosages, ALCAR lead to increases in liver mitochondrial oxidant generation. In other studies, rats were observed to positively affect age-related mitochondrial declines within cardiac and skeletal muscles. When contrasted with or α-lipoic acid (a mitochondrial antioxidant and cofactor), both supplements caused increases in rats mitochondrial energy metabolism, improved energy, and lowered oxidative stress. A combined supplementation with both ALCAR and α-lipoic acid resulted in greater enhancements than supplementation with a single compound. Prolonged (3 months) co-supplementation with both compounds was observed to improve the number of intact mitochondria as well as the total and the ultra mitochondrial structure of neurons in the hippocampus. In most of these studies, ALCAR supplementation was in high doses. There are no clinical trials performed to support similar effects in humans.

To assess the therapeutic effects of ALCAR supplementation on heart failure, a number of clinical trials have been performed. One particular placebo-controlled and a randomized clinical trial was used to evaluate these effects in 70 patients who had heart failure complications. An oral dose of 2gm daily was observed to significantly boost survival in the three years of study when compared to the placebo group. Another single-blind, randomized, and placebo-controlled clinical trial was performed in 30 patients who had heart failure problems. When administered orally with 1.5gm of propionyl-L-carnitine daily for one month, the researchers observed enhancements in measures of exercise tolerance and a small though significant decrease in left ventricular size when contrasted with the placebo.

A larger double-blind, randomized, and placebo-controlled clinical trial, compared the administration of 1.5gm per day of propionyl-L-carnitine for six months in 271 patients with heart failure problems to a placebo group that had 266 patients. The results showed no variations in tolerance among the two groups. Propionyl-L-carnitine was observed to exhibit significantly higher exercise tolerance among patients with higher LVEF values (over 30%) compared to the placebo that indicates that propionyl-L-carnitine may enhance exercise tolerance among higher functioning heart failure patients. Another recently published study that employed 29 patients suffering from mild diastolic heart failure (with LVEF exceeding 45%) established that 1.5gm of oral L-Carnitine per day administered for three months enhanced a number of measures of diastolic function contrasted with the baseline.

A number of clinical trials have been performed to evaluate the effects of Acetyl-L-Carnitine on Alzheimer's disease or dementia. An administration of 2-3gm per day of ALCAR for 6-12 months was observed to slow the rate of cognitive decline in patients who had been diagnosed with Alzheimer's disease. In a larger multicenter, placebo-controlled, and randomized trial of 417 patients who had Alzheimer's disease discovered that an administration of 3gm of ALCAR daily for 12 months had no variations from the placebo treatment concerning cognitive decline. When the results from this study were statistically analyzed, there were indications that patients who had early onset (below 65 years) of Alzheimer's condition had a higher cognitive decline, and this was significantly slowed by ALCAR therapy. In another case, a randomized, placebo-controlled and multi-center clinical trial that employed 167 patients who had early on-set (between 45-65 years of age) of Alzheimer's disease showed that 3gm/day ALCAR treatment within a period of 12 months had no impact on majority of the measures of cognitive decline although it was linked to an insignificant fall in attention-related decline when compared with the placebo.

Studies have also been conducted to assess the therapeutic benefits of ALCAR in lowering the adverse effects of drugs used to treat HIV/AIDs. One cross-sectional study established that nerve concentrations of ALCAR were substantially lower among individuals suffering from HIV, who developed peripheral neuropathy due to treatment with nucleoside analogs compared to control group. The study involved 16 HIV patients with painful neuropathies, and 10 of them observed improvements after completing a 3 week ALCAR treatment. In yet another study, 20 patients who had antiretroviral-induced neuropathy were administered with 2gm/day of oral ALCAR for 4 weeks, and their mean pain intensity scores were observed to fall significantly but had no impact on any of the neurophysiological parameters that were measured. In a placebo-controlled, double-blind trial involving 90 HIV patients who had symptomatic distal symmetrical polyneuropathy, 1000mg/day of ALCAR were administered via intramuscular injections for two weeks. The results showed no differences in the intention-to-treat analysis compared to the placebo, although ALCAR was observed to offer some pain relief in the 66 patients who completed the clinical trial.

A number of studies have also been conducted to examine the effects of L-carnitine supplementation on physical performance. A series of uncontrolled studies have shown that acute doses administered an hour before exercise session or short-term administration ranging between 2-3 weeks of L-carnitine treatment at doses of 2-4gm/ day was linked to a rise in maximal oxygen uptake and decreases in plasma lactate. A recent trial that was double-blind, placebo-controlled examined 32 healthy adults who were administered with 1gm/day or 3gm/day for eight weeks, and no improvements were observed in aerobic and anaerobic exercise performance. It has also been noted that carnitine supplementation boosts the levels of plasma carnitine although studies have not suggested that supplementation with carnitine can boost the levels of carnitine in the cardiac or skeletal muscle. Theoretically, carnitine supplementation can boost performance but so far statistical data indicates that carnitine has no effect on athletic performance when administered in healthy individuals.

In a recent study, young adults aged between 22-27 years were administered with ALCAR supplements for one month. After they had completed the one-month treatment, they were evaluated using a video game maze. The subjects were observed to have improvements in efficiency with about 3 to 4 time's higher efficiency when navigating the video game maze in contrast with the control group.

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