Editing Acetyl L-carnitine (ALCAR)
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[https://en.wikipedia.org/wiki/Acetylcarnitine Wikipedia page] | [https://en.wikipedia.org/wiki/Acetylcarnitine Wikipedia page] | ||
| − | Acetyl-L- | + | Acetyl- L-carnitine’s (ALCAR) transport of the important metabolic factor Acetyl CoA into the mitochondria increases energy production. Similar in structure to acetylcholine, it also stimulates acetylcholine production and enhances cellular membrane health. |
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== Effects on ALS == | == Effects on ALS == | ||
| − | There are anecdotal observations of low ALCAR levels in ALS patients (see the [http://www.alstdi.org/forum/yaf_postst53060_low-acetyllcarnitine-levels-and-alshuge-piece-of-the-puzzle.aspx discussion thread]), but so far no systematic study has been made about the issue. In an August 2013 Phase II double-blinded study | + | There are anecdotal observations of low ALCAR levels in ALS patients (see the [http://www.alstdi.org/forum/yaf_postst53060_low-acetyllcarnitine-levels-and-alshuge-piece-of-the-puzzle.aspx discussion thread]), but so far no systematic study has been made about the issue. In an August 2013 Phase II double-blinded study [1], ALCAR showed signs of slowing down progression in human patients between 40-70 years and on Riluzole. Dosage was 3 g/day for 48 weeks. |
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| − | ALCAR | + | Bioavailability of oral ALCAR decreases with increased dose [2], so it is more effective to take several small doses at a few hours' intervals. Insulin helps drive carnitine into the muscles [3]. |
| − | + | Choline appears to help carnitine economy by reducing excretion and promoting uptake by the muscles (see: http://examine.com/supplements/L-Carnitine ). A couple grams of choline daily is another good adjunct to oral carnitine supplementation. | |
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== Discussion threads on the ALSTDI forum == | == Discussion threads on the ALSTDI forum == | ||
[http://www.alstdi.org/forum/yaf_postst53060_low-acetyllcarnitine-levels-and-alshuge-piece-of-the-puzzle.aspx Low Acetyl-L-Carnitine levels and ALS - Huge piece of the puzzle?] | [http://www.alstdi.org/forum/yaf_postst53060_low-acetyllcarnitine-levels-and-alshuge-piece-of-the-puzzle.aspx Low Acetyl-L-Carnitine levels and ALS - Huge piece of the puzzle?] | ||
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== Pubmed link collection at Studies on ALS == | == Pubmed link collection at Studies on ALS == | ||
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| − | == | + | == References == |
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| + | [1] | ||
| + | <bibtex>@article{Beghi2013, | ||
| + | abstract = {Our objective was to assess the effects of acetyl-L-carnitine (ALC) with riluzole on disability and mortality of amyotrophic lateral sclerosis (ALS). Definite/probable ALS patients, 40-70 years of age, duration 6-24 months, self-sufficient (i.e. able to swallow, cut food/handle utensils, and walk), and with forced vital capacity (FVC) > 80\% entered a pilot double-blind, placebo-controlled, parallel group trial and were followed for 48 weeks. ALC or placebo 3 g/day was added to riluzole 100 mg/day. Primary endpoint: number of patients no longer self-sufficient. Secondary endpoints: changes in ALSFRS-R, MRC, FVC and McGill Quality of Life (QoL) scores. Analysis was made in the intention-to-treat (ITT) and per-protocol (PP) population, completers and completers/compliers (i.e. taking > 75\% of study drug). Forty-two patients received ALC and 40 placebo. In the ITT population, 34 (80.9\%) patients receiving ALC and 39 (97.5\%) receiving placebo became non-self-sufficient (p = 0.0296). In the PP analysis, percentages were 84.4 and 100.0\% (p = 0.0538), respectively. Mean ALSFRS-R scores at 48 weeks were 33.6 (SD 10.4) and 27.6 (9.9) (p = 0.0388), respectively, and mean FVC scores 90.3 (32.6) and 58.6 (31.2) (p = 0.0158), respectively. Median survival was 45 months (ALC) and 22 months (placebo) (p = 0.0176). MRC, QoL and adverse events were similar. In conclusion, ALC may be effective, well-tolerated and safe in ALS. A pivotal phase III trial is needed.}, | ||
| + | author = {Beghi, Ettore and Pupillo, Elisabetta and Bonito, Virginio and Buzzi, Paolo and Caponnetto, Claudia and Chi\`{o}, Adriano and Corbo, Massimo and Giannini, Fabio and Inghilleri, Maurizio and Bella, Vincenzo La and Logroscino, Giancarlo and Lorusso, Lorenzo and Lunetta, Christian and Mazzini, Letizia and Messina, Paolo and Mora, Gabriele and Perini, Michele and Quadrelli, Maria Lidia and Silani, Vincenzo and Simone, Isabella L and Tremolizzo, Lucio}, | ||
| + | doi = {10.3109/21678421.2013.764568}, | ||
| + | issn = {2167-9223}, | ||
| + | journal = {Amyotrophic lateral sclerosis \& frontotemporal degeneration}, | ||
| + | keywords = {Acetylcarnitine,Acetylcarnitine: therapeutic use,Adult,Aged,Amyotrophic Lateral Sclerosis,Amyotrophic Lateral Sclerosis: drug therapy,Disease Progression,Double-Blind Method,Drug Therapy, Combination,Excitatory Amino Acid Antagonists,Excitatory Amino Acid Antagonists: therapeutic use,Female,Humans,Male,Middle Aged,Nootropic Agents,Nootropic Agents: therapeutic use,Pilot Projects,Quality of Life,Riluzole,Riluzole: therapeutic use,Treatment Outcome,Vital Capacity}, | ||
| + | month = sep, | ||
| + | number = {5-6}, | ||
| + | pages = {397--405}, | ||
| + | pmid = {23421600}, | ||
| + | title = {{Randomized double-blind placebo-controlled trial of acetyl-L-carnitine for ALS.}}, | ||
| + | url = {http://www.ncbi.nlm.nih.gov/pubmed/23421600}, | ||
| + | volume = {14}, | ||
| + | year = {2013} | ||
| + | } | ||
| + | </bibtex> | ||
| − | == | + | [2] |
| − | + | <bibtex>@article{Harper1988, | |
| + | abstract = {The pharmacokinetics of single intravenous and oral doses of L-carnitine 2 g and 6 g has been investigated in 6 healthy subjects on a low carnitine diet. Carnitine was more rapidly eliminated from plasma after the higher dose. Comparing the 2-g and 6-g doses, the t1/2 beta of the elimination phase (beta) was 6.5 h vs 3.9 h, the elimination constant was 0.40 vs 0.50 h-1 and the plasma carnitine clearance was 5.4 vs 6.1 1 x h-1 (p less than 0.025), thus showing dose-related elimination. Saturable kinetics was not found in the range of doses given. The apparent volumes of distribution after the two doses were not significantly different and they were of the same order as the total body water. Urinary recoveries after the 2-g and 6-g doses were 70\% and 82\% during the first 24 h, respectively. Following the two oral dosing, there was no significant difference in AUCs of plasma carnitine. Urinary recoveries were 8\% and 4\% for the 2-g and 6-g doses during the first 24 h. The oral bioavailability of the 2-g dose was 16\% and of the 6 h dose 5\%. The results suggest that the mucosal absorption of carnitine is already saturated at the 2-g dose.}, | ||
| + | author = {Harper, P and Elwin, C E and Cederblad, G}, | ||
| + | issn = {0031-6970}, | ||
| + | journal = {European journal of clinical pharmacology}, | ||
| + | keywords = {Administration, Oral,Adult,Biological Availability,Carnitine,Carnitine: administration \& dosage,Carnitine: blood,Carnitine: pharmacokinetics,Diet,Female,Half-Life,Humans,Injections, Intravenous,Metabolic Clearance Rate,Middle Aged}, | ||
| + | mendeley-groups = {alcar}, | ||
| + | month = jan, | ||
| + | number = {5}, | ||
| + | pages = {555--62}, | ||
| + | pmid = {3234464}, | ||
| + | title = {{Pharmacokinetics of intravenous and oral bolus doses of L-carnitine in healthy subjects.}}, | ||
| + | url = {http://www.ncbi.nlm.nih.gov/pubmed/3234464}, | ||
| + | volume = {35}, | ||
| + | year = {1988} | ||
| + | } | ||
| + | </bibtex> | ||
| − | [ | + | [3] |
| + | <bibtex> | ||
| + | @article{Stephens2006, | ||
| + | abstract = {Increasing skeletal muscle carnitine content may alleviate the decline in muscle fat oxidation seen during intense exercise. Studies to date, however, have failed to increase muscle carnitine content, in healthy humans, by dietary or intravenous L-carnitine administration. We hypothesized that insulin could augment Na+-dependent skeletal muscle carnitine transport. On two randomized visits, eight healthy men underwent 5 h of intravenous L-carnitine infusion with serum insulin maintained at fasting (7.4+/-0.4 mIU*l(-1)) or physiologically high (149.2+/-6.9 mIU*l(-1)) concentrations. The combination of hypercarnitinemia (approximately 500 micromol*l(-1)) and hyperinsulinemia increased muscle total carnitine (TC) content from 22.0 +/- 0.9 to 24.7 +/- 1.4 mmol*(kg dm)(-1) (P<0.05) and was associated with a 2.3 +/- 0.3-fold increase in carnitine transporter protein (OCTN2) mRNA expression (P<0.05). Hypercarnitinemia in the presence of a fasting insulin concentration had no effect on either of these parameters. This study demonstrates that insulin can acutely increase muscle TC content in humans during hypercarnitinemia, which is associated with an increase in OCTN2 transcription. These novel findings may be of importance to the regulation of muscle fat oxidation during exercise, particularly in obesity and type 2 diabetes where it is known to be impaired.}, | ||
| + | author = {Stephens, Francis B and Constantin-Teodosiu, Dumitru and Laithwaite, David and Simpson, Elizabeth J and Greenhaff, Paul L}, | ||
| + | doi = {10.1096/fj.05-4985fje}, | ||
| + | issn = {1530-6860}, | ||
| + | journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology}, | ||
| + | keywords = {Adult,Carnitine,Carnitine: blood,Carnitine: metabolism,Carnitine: urine,Humans,Insulin,Insulin: blood,Insulin: pharmacology,Male,Muscle, Skeletal,Muscle, Skeletal: drug effects,Muscle, Skeletal: metabolism,Organic Cation Transport Proteins,Organic Cation Transport Proteins: metabolism,RNA, Messenger,RNA, Messenger: metabolism,Sodium,Sodium: metabolism,Transcription, Genetic}, | ||
| + | mendeley-groups = {alcar}, | ||
| + | month = mar, | ||
| + | number = {2}, | ||
| + | pages = {377--9}, | ||
| + | pmid = {16368715}, | ||
| + | title = {{Insulin stimulates L-carnitine accumulation in human skeletal muscle.}}, | ||
| + | url = {http://www.ncbi.nlm.nih.gov/pubmed/16368715}, | ||
| + | volume = {20}, | ||
| + | year = {2006} | ||
| + | } | ||
| + | </bibtex> | ||
