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acetyl-L-carnitine

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Waldford recommends supplementation with 120mg of alpha-lipoic acid,

and 500mg of acetyl-L-carnitine daily (BT120YD p167, p191), but had

question marks on p. 167 indicating that he was not totaly convinced

of their anti-aging effects. His comments on p. 191 about acetyl-L-

carnitine said that additional research was needed as of the date of

publication (2000).

A recent article in Reader's digest mentioned that Dr. Ames was

recommending a similar combination for anti-aging. Below is a paper

published 2 years after BT120YD that seems to show that

hepatocellular ascorbate, which is supposedly a biomarker of aging,

was restored to more youthful by supplementation.

I would appreciate knowing how many people in this group follow this

recommendation and also whether they feel any positive effects from

the supplements, particularly the acetyl-L-carnitine.

Tony

===

Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):1870-5.

Feeding acetyl-L-carnitine and lipoic acid to old rats significantly

improves metabolic function while decreasing oxidative stress.

Hagen TM, Liu J, Lykkesfeldt J, Wehr CM, Ingersoll RT, Vinarsky V,

Bartholomew JC, Ames BN.

Department of Biochemistry and Biophysics, Linus ing Institute,

Oregon State University, Corvallis, OR 97331, USA.

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 ®-alpha-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 O(2) 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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