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BENEFITS OF ACETYL CARNITINE: Experimental studies indicate that there is a decrease in the level of cardiolipin, a key lipid in the mitochondrial membrane, responsible for the membraneÕs electrical potential, causing reduced utilization of oxygen and increased production of oxygen radicals. Studies in rats show that young rats have 24,000 oxidative lesions in DNA per cell, increasing to 67,000 oxidative lesions per cell in older rats.
Animal studies from Italy report that old rats fed acetyl carnitine (ALC), the transporter that carries the fatty acid "fuel" into the mitochondria, have less mitochondrial damage and less DNA damage than old rats not fed ALC.
Acetyl-L-carnitine (ALCAR) is the molecule which transports fatty acids across the mitochondrial membrane so that they can be burned to produce energy. If one lacks sufficient ALCAR, the fat cannot be metabolized, so it will be stored, which is what body fat is. It appears that people produced less ALCAR naturally as they age. That would explain why children have lots of energy (they burn fat effectively), and older people tend to get fat and feel more tired (they store fat because they don't burn it effectively). Dr. Bruce Ames did a study with animals, feeding one group of old ones ALCAR and ALA (alpha-lipoic acid, also necessary to burn fat). The old animals fed the supplements were as vigorous and learned mazes as effectively as young animals. The effect has not been reproduced yet in humans, though the supplement is available in a company formed by Dr. Ames and is called Juvenon.
1. Balz Frei, Natural Antioxidants, pg. 81-2
2. "The purpose of this study was to determine if amino acid supplementation influences blood and muscle lactate response to exercise and the time course of the metabolic adaptations to training. Two groups of untrained males (n = 7 each) were given (double-blind) a daily supplement (2.9 g.day-1) containing a mixture of leucine, isoleucine, valine, glutamine, and carnitine (EXP) or 3 g.day-1 of lactose (CON). Following 7 days of supplementation there was no significant change in VO2peak, time to exhaustion (TTX) at 120% VO2peak, or muscle and blood lactate in either EXP or CON. Subjects then initiated 6 weeks of combined aerobic and anaerobic training on a Monark cycle ergometer. It was found that amino acid supplementation had no effect on either blood or muscle lactate accumulation during exercise, while supplementation resulted in a faster adaptation in buffer capacity. Performance during intense exercise was not improved with amino acid supplementation.""Effects of a low-dose amino acid supplement on adaptations to cycling training in untrained individuals", Vukovich MD; Sharp RL; Kesl LD; Schaulis DL; King DS, Int J Sport Nutr 1997 Dec;7(4):298-309
3. "We studied the influence of Etomoxir on fat and carbohydrate oxidation, and the influence of these changes on insulin sensitivity in type 2 diabetic patients. Etomoxir .. specifically inactivates carnitine-acyltransferase I (CAT I, EC: 126.96.36.199), the key enzyme for the transport of long-chain acyl-CoA compounds into the mitochondria. Thus, oxidation of fatty acids should be reduced by this drug and glucose utilisation be increased ... Twelve type 2 diabetic patients were treated ... for 3 days in this placebo-controlled, randomized, double-blind study. Treatment resulted in a significant increase in carbohydrate oxidation (from 72 to 113 g/24 h...), decrease in fat oxidation (from 139 to 114 g/24 h...), and decrease of the glucose appearance rate (RA) in the basal state (from 1.85 to 1.70 mg/kg min....). ... Thus, we could demonstrate a decrease in fat and increase in glucose oxidation by etomoxir" "Effects of the carnitine-acyltransferase inhibitor etomoxir on insulin sensitivity, energy expenditure and substrate oxidation in NIDDM," Hubinger A; Knode O; Susanto F; Reinauer H; Gries FA, Horm Metab Res 1997 Sep;29(9):436-9
4. "We tested the hypothesis that glucose plus insulin determine the rate of fat oxidation in humans by controlling the rate of fatty acid entrance into the mitochondria. ... Intracellular acylcarnitine concentrations were measured.... Oleate, but not octanoate, requires carnitine binding to gain access to the mitochondrial matrix; hence, if glucose and/or insulin limit long-chain fatty acid entrance into the mitochondria, then, ... long-chain acylcarnitine formation should be decreased, causing a decrease in oleate, but not octanoate, oxidation. Oleate oxidation decreased from the basal value of 0.7+/-0.1 to 0.4+/-0.1 micromol x kg(-1) x min(-1) (P < 0.05). In contrast, octanoate oxidation remained unchanged. Long-chain acylcarnitine concentration decreased... We conclude that glucose and/or insulin determine fatty acid oxidation by controlling the rate of long-chain fatty acid entrance into the mitochondria.""Glucose plus insulin regulate fat oxidation by controlling the rate of fatty acid entry into the mitochondria", Sidossis LS; Stuart CA; Shulman GI; Lopaschuk GD; Wolfe RR, J Clin Invest 1996 Nov 15;98(10):2244-50
5. " A 1-year, double-blind, placebo-controlled, randomized, parallel-group study compared the efficacy and safety of acetyl-L-carnitine hydrochloride (ALCAR) with placebo in patients with probable Alzheimer's disease (AD). Subjects with mild to moderate probable AD, aged 50 or older, were treated with 3 g/day of ALCAR or placebo (1 g tid) for 12 months. Four hundred thirty-one patients entered the study, and 83% completed 1 year of treatment. ... Overall, both ALCAR- and placebo-treated patients declined at the same rate on all primary and most secondary measures during the trial. In a subanalysis by age that compared early-onset patients (aged 65 years or younger at study entry) with late-onset patients (older than 66 at study entry), we found a trend for early-onset patients on ALCAR to decline more slowly than early-onset AD patients on placebo on both primary endpoints. In addition, early-onset patients tended to decline more rapidly than older patients in the placebo groups. Conversely, late-onset AD patients on ALCAR tended to progress more rapidly than similarly treated early-onset patients. The drug was very well tolerated during the trial. The study suggests that a subgroup of AD patients aged 65 or younger may benefit from treatment with ALCAR whereas older individuals might do more poorly. However, these preliminary findings are based on past hoc analyses. A prospective trial of ALCAR in younger patients is underway to test the hypothesis that young, rapidly progressing subjects will benefit from ALCAR treatment." "A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease", Thal LJ; Carta A; Clarke WR; Ferris SH; Friedland RP; Petersen RC; Pettegrew JW; Pfeiffer E; Raskind MA; Sano M; Tuszynski MH; Woolson RF, Neurology 1996 Sep;47(3):705-11
6. " Muscle carnitine levels were examined in 31 younger [ MEAN, 27 years] and 27 older [49 years] men. .. No mean...differences in free...and total... muscle carnitine levels were found between the younger and older subjects, respectively... These findings suggest that muscle carnitine levels are similar between younger and older males, and there does not appear to be any relationship between muscle carnitine and markers of muscle oxidative potential (i.e., oxidative enzymes, % type I fiber). ""Relationships between muscle carnitine, age and oxidative status", Starling RD; Costill DL; Fink WJ, Eur J Appl Physiol 1995;71(2-3):143-6
7. "The effect of 6-week endurance training on mitochondrial ATP production rate was determined in 14 elderly men. Mean age... 63 +/- 6 yr,... Endurance training resulted in a significant increase in maximal oxygen uptake (L min-1) (P < 0.01)...carnitine palmitoyltransferase I activities remained statistically unchanged. A higher mitochondrial ATP production rate was observed after endurance training with the ... It was concluded that the increased mitochondrial ATP production rate of aged human skeletal muscle with training seems mainly to occur through an increased mitochondrial content, and in a way similar to those observed in young men.""Mitochondrial ATP production rate in 55 to 73-year-old men: effect of endurance training", Berthon P; Freyssenet D; Chatard JC; Castells J; Mujika I; Geyssant A; Guezennec CY; Denis C, Acta Physiol Scand 1995 Jun;154(2):269-74
8. "In a double-blind, placebo study, acetyl-L-carnitine was administered to 7 probable Alzheimer's disease patients who were then compared by clinical and 31P magnetic resonance spectroscopic measures to 5 placebo-treated probable AD patients and 21 age-matched healthy controls over the course of 1 year. Compared to AD patients on placebo, acetyl-L-carnitine-treated patients showed significantly less deterioration in their Mini-Mental Status and Alzheimer's Disease Assessment Scale test scores...This is the first direct in vivo demonstration of a beneficial effect of a drug on both clinical and CNS neurochemical parameters in AD." Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer's disease",Pettegrew JW; Klunk WE; Panchalingam K; Kanfer JN; McClure RJ, : Neurobiol Aging 1995 Jan-Feb;16(1):1-4
9. "Visceral obesity is strongly associated with insulin resistance. One potential cause is increased availability of FFA. Alternatively, it has been proposed that there is impaired oxidation of lipid in individuals at risk for obesity. The extent to which either concept involves skeletal muscle is uncertain. To examine these opposing hypotheses, 17 healthy lean and obese premenopausal women,..., participated in leg balance studies for measurement of FFA and glucose utilization during basal and insulin-stimulated conditions. .. During fasting conditions, however, rates of FFA uptake across the leg were negatively correlated with visceral adiposity as were activities of muscle carnitine palmitoyl transferase and citrate synthase. In summary, visceral adiposity is clearly associated with skeletal muscle insulin resistance but this is not due to glucose-FFA substrate competition. Instead, women with visceral obesity have reduced postabsorptive FFA utilization by muscle.""Skeletal muscle utilization of free fatty acids in women with visceral obesity", Colberg SR; Simoneau JA; Thaete FL; Kelley DE, J Clin Invest 1995 Apr;95(4):1846-53