Am i taking too much r-ala?

[supplyed]

Sometimes take up to 15-20 a day, usually around 10 (one for every 30-40 carbs)... is this too much?

How long after it gets into your bloodstream will it be effective?

Does r-ala make you hungry? I can not go more than 2 hours without getting hungry no matter how much I eat in the previous meal... Often times I will get hungry 30 min later.

 

[hardrock]

I take one capsule per 30-50 g carbs. I seem to get hungry about every hour while taking it. Without I usually make it 2.

 

[INNOCENT]

take with 30-45g carbs.. is what i usually do, so it seems like ur on the right track bro

 

[Ulter]

It disposes of your carbs into your muscle so quickly that you may feel hungry for carbs again sooner than you normally would. But that's better than the alternative which is to have the carbs sitting there while your body just keeps putting out more insulin. Your body stops burning fat when the insulin is present. So you may not be hungry but you're not burning fat either. According to Dr Packer's study just published in Sept, Glucorell R also inhibits your bodies ability to make new fat cells.
That said, you should not need more than 10/day. It lasts a couple hours.

 

[supplyed]

Thanks for the fast replies... So lets say I plan on having a meal with 80 g carbs. I pop 2 pills, then half way through my meal I have to stop eating and can not continue until 1 hour later. You're saying the carb disposing properties will still be in effect at that time?

I often eat >400 carbs still 10 should be enough?

Any links to Dr Packers study?

Thanks

 

[Ulter]

If I understand your questions you mean your meal is interrupted and then you go back and finish in an hour, like you're a fireman and it's a false alarm? Yes the effect will still be there when you go back to your meal in an hour.

J Biol Chem. 2003 Sep 12;278(37):34823-33. Epub 2003 Jun 30.



Alpha-lipoic acid inhibits adipocyte differentiation by regulating
pro-adipogenic transcription factors via mitogen-activated protein kinase pathways.

Cho KJ, Moon HE, Moini H, Packer L, Yoon DY, Chung AS.

Department of Biological Sciences, Korea Advanced Institute of Science and
echnology, Daejeon 305-701, South Korea.

Obesity is associated with a number of pathological disorders such as non-insulin-dependent diabetes, hypertension, hyperlipidemia, and cardiovascular diseases. alpha-Lipoic acid (LA) has been demonstrated to activate the insulin signaling pathway and to exert insulin-like actions in adipose and muscle cells. Based on this similarity LA is expected to promote adipogenesis in pre-adipocytes. Here, however, we report that LA inhibited differentiation of 3T3-L1 pre-adipocytes induced by a hormonal mixture or troglitazone. Northern blot analysis of cells demonstrated that this inhibition was accompanied with attenuated expression of adipocyte-specific fatty acid-binding protein and lipoprotein lipase. Electrophoretic mobility shift assay and Western blot analysis of cells demonstrated that LA modulates transcriptional activity and/or expression of a set of anti- or pro-adipogenic transcription factors. LA treatment of 3T3-L1 pre-adipocytes also resulted in prolonged activation of major mitogen-activated protein kinase signaling pathways but showed little or no effect on the activity of the insulin receptor/Akt signaling pathway. These findings suggest that LA inhibits insulin or the hormonal mixture-induced differentiation of 3T3-L1 pre-adipocytes by modulating activity and/or expression of pro- or anti-adipogenic transcription factors mainly through activating the MAPK pathways.