Acetyl L Carnitine

Reference: Calabrese V, Giuffrida Stella AM, Calvani M, Butterfield DA. Acetylcarnitine and cellular stress response: roles in nutritional redox homeostasis and regulation of longevity genes. J Nutr Biochem. 2006 Feb;17(2):73-88. Epub 2005 Oct 18. Review. PMID: 16413418

Summary: How we understand aging will depend on the physiological model we employ to explain cellular development and deterioration. On one hand, aging is associated with a reduced ability to cope with physiological challenges. On the other hand, aging is seen merely as inevitable deterioration. This study takes as its premise the ability of cells to bounce back and it explores the mechanisms by which brain cells in particular do this. To survive different types of injuries, brain cells have evolved networks of responses, which detect and control diverse forms of stress. Although the mechanisms underlying age-related alterations in stress tolerance are not well defined, many studies support the validity of the oxidative stress hypothesis, which suggests that lowered functional capacity in aged organisms is the result of an increased generation of reactive oxygen and nitrogen products. Under this hypothesis, acetyl L carnitine (ALCAR) is proposed as a therapeutic agent to increase the density of neurotransmitters. In other words, this vital nutrient will bulk up brain cells as a way to insulate them against further damage under potentially threatening circumstances. Under normal circumstances, ALCAR already acts as a modulator of cellular stress response. Effective normalized modulation produces an ability increase in short term memory; as a result, one can imagine ALCAR's capabilities to protect under duress. Nutrition and carnitine metabolism are addressed, and acetyl L carnitine supplements for brain cell boosting is recommended.