ALCAR and R-ALA complement each other as antioxidants, but the primary reason the two are recommended together is due to consistent synergistic effects that have been observed by Dr. Ames, namely these 3 studies:
Hagen TM, Liu J, Lykkesfeldt J, Wehr CM, Ingersoll RT, Vinarsky V, Bartholomew JC, Ames BN. Feeding acetyl-L-carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress. Proc. Natl. Acad. Sci. USA 2002;99:1870-5.
Liu J, Head E, Gharib AM, Yuan W, Ingersoll RT, Hagen TM, Cotman CW, Ames BN. Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: Partial reversal by feeding acetyl-L-carnitine and/or R-α-lipoic acid. Proc. Natl. Acad. Sci. USA 2002;99:2356-61.
Liu J, Killilea D, Ames BN. Age-associated mitochondrial oxidative decay: Improvement of carnitine acetyltransferase substrate binding affinity and activity in brain by feeding old rats acetyl-L-carnitine and/or R-α-lipoic acid. Proc. Natl. Acad. Sci. USA 2002;99:1876-81.
What has often gotten misconstrued is that ALA can prevent the pro-oxidative effects of ALCAR. And in fact, it can reduce ALCAR-induced ROS and has been proven to do so. So why is this not important? ALCAR was shown to generate ROS at high doses. You should be using 2g/day anyway so this should be a non-issue, especially if you are cycling off alcar every few months.
There are other studies that have examined the two in conjunction, but as is often the case, the research has not quite reached humans as of yet:
R-alpha-lipoic acid and acetyl-L-carnitine complementarily promote mitochondrial biogenesis in murine 3T3-L1 adipocytes.
Combined R-alpha-lipoic acid and acetyl-L-carnitine exerts efficient preventative effects in a cellular model of Parkinson's disease
From the latter study, check out the abstract:
Mitochondrial dysfunction and oxidative damage are highly involved in the pathogenesis of Parkinson's disease (PD). Some mitochondrial antioxidants/nutrients that can improve mitochondrial function and/or attenuate oxidative damage have been implicated in PD therapy. However, few studies have evaluated the preventative effects of a combination of mitochondrial antioxidants/nutrients against PD, and even fewer have sought to optimize the doses of the combined agents. The present study examined the preventative effects of two mitochondrial antioxidant/nutrients, R-alpha-lipoic acid (LA) and acetyl-L-carnitine (ALC), in a chronic rotenone-induced cellular model of PD. We demonstrated that 4-week pretreatment with LA and/or ALC effectively protected SK-N-MC human neuroblastoma cells against rotenone-induced mitochondrial dysfunction, oxidative damage and accumulation of alpha-synuclein and ubiquitin. Most notably, we found that when combined, LA and ALC worked at 100-1000-fold lower concentrations than they did individually. We also found that pretreatment with combined LA and ALC increased mitochondrial biogenesis and decreased production of reactive oxygen species through the up-regulation of the peroxisome proliferator-activated receptor-gamma coactivator 1alpha as a possible underlying mechanism. This study provides important evidence that combining mitochondrial antioxidant/nutrients at optimal doses might be an effective and safe prevention strategy for PD.
As you can see, a synergistic effect has been consistently reported between the two antioxidants, and thus I would recommend taking them together (though not at EXACTLY the same time because ALCAR will polymerize with Na-R-ALA; take the Na-R-ALA 30 minutes prior to ingesting ALCAR). Add agmatine to that stack as well, take it first thing in the morning, and reap the benefits.
. I personally would use 200mg Na-R-Ala + SS in her specific situation because she is using ALCAR (I know from PMs). As far as blood glucose control, I like to look at it from a Na-R-Ala dose per day rather than per meal due to its long half-life.
