when to take ALA?

[megazorro]

Only before high carb meals, right?
Today I ate pizza and took ala afterwards and later I felt strange, kinda hypo.

[Sixpack]

and postworkout w/ carbs

[PSKlifter]

i take mine w/ every other meal, which usually means all food meals + pwo shake.

[megazorro]

I found this here in another forum, what does this mean?

ALA's glucose disposal properties only work in the presence of high peroxide levels due to peroxidation through high stress mitochondrial respiration.

Best take it only during high oxidation periods... exactly why it worked for diabetics, since they have high peroxide levels from innefficient mitochondria.

High peroxide levels are produced during times of high mitochondrial stress (usually). Weight training and cardio will do this to you. Those are times considered high by me.

You all know that ALA will increase glucose uptake of muscle in insulin resistant rats right? This is mainly due to high oxidative stress produced by their insulin resistance. We see that high lipid peroxidation works to stimulate muscle glucose uptake in the second study. Although the lipid peroxidation comes from insulin resistance, it shouldn't matter which pathway. The only thing I am missing here is how exactly ALA's peroxide scavenging effects act upon the GLUT4. I doubt it's really sure right now. Layne Norton's new article will look into this. BTW he did a case study I want to tell you about:

With a blood glucose monitor Eric did Exercise training (ET) with no (-) ALA and with (+) ALA. Upon comparing his blood glucose levels to (-) ALA + ET, and 900mg's of ALA + ET, he had 40% lower blood glucose. I am unsure, but I believe there was insignificant changes during sedentary periods.

Heres a couple studies to clear up:


Protection against oxidative stress-induced insulin resistance in rat L6 muscle cells by mircomolar concentrations of alpha-lipoic acid.

Maddux BA, See W, Lawrence JC Jr, Goldfine AL, Goldfine ID, Evans JL.

Diabetes Research Laboratory, Mount Zion Hospital, San Francisco, California 94143-1616, USA. bmaddux@itsa.ucsf.edu

In diabetic patients, alpha-lipoic acid (LA) improves skeletal muscle glucose transport, resulting in increased glucose disposal; however, the molecular mechanism of action of LA is presently unknown. We studied the effects of LA on basal and insulin-stimulated glucose transport in cultured rat L6 muscle cells that overexpress GLUT4. When 2-deoxy-D-glucose uptake was measured in these cells, they were more sensitive and responsive to insulin than wild-type L6 cells. LA, at concentrations < or = 1 mmol/l, had only small effects on glucose transport in cells not exposed to oxidative stress. When cells were exposed to glucose oxidase and glucose to generate H2O2 and cause oxidative stress, there was a marked decrease in insulin-stimulated glucose transport. Pretreatment with LA over the concentration range of 10-1,000 pmol/l protected the insulin effect from inhibition by H2O2. Both the R and S isomers of LA were equally effective. In addition, oxidative stress caused a significant decrease (approximately 50%) in reduced glutathione concentration, along with the rapid activation of the stress-sensitive p38 mitogen-activated protein kinase. Pretreatment with LA prevented both of these events, coincident with protecting insulin action. These studies indicate that in muscle, the major site of insulin-stimulated glucose disposal, one important effect of LA on the insulin-signaling cascade is to protect cells from oxidative stress-induced insulin resistance.


In vivo effect of lipoic acid on lipid peroxidation in patients with diabetic neuropathy.

Androne L, Gavan NA, Veresiu IA, Orasan R.

Diabetes Center & Clinic, Cluj Napoca.

BACKGROUND: The diabetic state, in both humans and experimental animals, is associated with oxidative stress. Lipid peroxidation of nerve membranes has been suggested as a mechanism by which peripheral nerve ischemia and hypoxia could cause neuropathy. Lipoic acid (LA) is a powerful inhibitor of iron-dependent lipid peroxidation and reactive oxygen species. The treatment of diabetic peripheral and cardiac autonomic neuropathy with LA is based on good clinical and experimental evidence. MATERIALS AND METHODS: To investigate the magnitude of the oxidative stress, serum ceruloplasmin (Cp) and lipid peroxide (Lp) levels were measured in 10 patients with diabetic neuropathy, before and 70 days after treatment with single dose of 600 mg LA/day. For other 12 healthy age- and sex-matched control subjects the serum Cp and Lp levels were evaluated. RESULTS: Our results show that hyperglycemia is a factor for an increase in serum ceruloplasmin in patients with diabetic neuropathy compared to healthy subjects (p < 0.0001). High serum ceruloplasmin (Cp) level in patients with diabetes may be related to antioxidant defense. The treatment of diabetic neuropathy with LA does not affect significantly the serum Cp activity. The serum Lp levels after LA administration were significantly lower (p < 0.005) than those before treatment. CONCLUSIONS: The antioxidant therapy with LA improves and may prevent diabetic neuropathy. This improvement is associated with a reduction in the indexes of lipid peroxidation. Oxidative stress appears to be primarily due to the processes of nerve ischemia and hyperglycemia autooxidation.



Interesting note:

"Furthermore, all oxidized forms of LA (S-, R-, and racemic LA) stimulated glucose uptake, whereas the reduced form, dihydrolipoic acid, was ineffective."