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r-ALA experiment
- Thread starter th'wolf
- Start date
OK, I'll post something on Tuesday (I'm doing some more Pizza tests this weekend OUCH).
As for gender differences, I think that is premature.....I'm just one female and my r-ALA results may be very different to the next female. But someone's gotta get the ball rolling. It is pretty difficult to make sense out of it all, and I think the fluctuating hormones really do cause a large variation for me. Either that, OR r-ALA is addictive (causes insulin resistance???) in the sense that my baseline glucose levels were very much higher after stopping r-ALA for a few weeks compared to before I started the r-ALA. In other words, my glucose response before I started the r-ALA was much lower than it is now after 4 weeks on r-ALA followed by 2 weeks off.....scary!
As for gender differences, I think that is premature.....I'm just one female and my r-ALA results may be very different to the next female. But someone's gotta get the ball rolling. It is pretty difficult to make sense out of it all, and I think the fluctuating hormones really do cause a large variation for me. Either that, OR r-ALA is addictive (causes insulin resistance???) in the sense that my baseline glucose levels were very much higher after stopping r-ALA for a few weeks compared to before I started the r-ALA. In other words, my glucose response before I started the r-ALA was much lower than it is now after 4 weeks on r-ALA followed by 2 weeks off.....scary!
macrophage69alpha
New member
if this is the case (ms scenario) it is more likely due to less secreted insulin.. if you come off of r-ala.. a taper may be in order.. or taking supps that enhance insulin secretion... quercetin, etc...
macrophage69alpha said:
If I remember correctly, R-S-ALA resulted in a higher plasma insulin level than that of the R-enantiomer correct?
What if you switched/cycled the two.
I've been locked up studying non-science classes at school
, and I am sort of in a different frame of mind lately. SUX. Had to say that in case I totally missed the mark on this one.That's okay, because next semester I will be back on the science route...
BMJ
btw...I have access to blood glucometers, maybe i'll start keeping track as well. I have to use the r,s-enantiomer right now because of the ol' budget though.
MS
This is coming from long-term memory.
We did a glycerol study years ago with endurance athletes, looked at many variables (blood glucose, lactate, insulin, etc.) as well as markers of hydration, urine output, etc., cycling performance and thermoregulation.
I do remember from the early lit on glycerol that is causes dehydration particularly at the brain level. One of the reasons that people get headaches when they use it particularly if they are already dehydrated. The reason you may be having the sodium cravings despite normal intake is that there may be another sensory mechanism driving that craving at the central level due to the glycerol. Normally the hypothalamus will sense blood osmolality and drive thirst and sodium appetite, as sodium is necessary for whole body rehydration. It may be that while blood osmolality/whole body hydration is OK, some area of the brain is still sensing dehydration as a function of glycerol and continuing to drive the thirst/Na mechanism.
Back off on the glycerol and see what happens.
W6
This is coming from long-term memory.
We did a glycerol study years ago with endurance athletes, looked at many variables (blood glucose, lactate, insulin, etc.) as well as markers of hydration, urine output, etc., cycling performance and thermoregulation.
I do remember from the early lit on glycerol that is causes dehydration particularly at the brain level. One of the reasons that people get headaches when they use it particularly if they are already dehydrated. The reason you may be having the sodium cravings despite normal intake is that there may be another sensory mechanism driving that craving at the central level due to the glycerol. Normally the hypothalamus will sense blood osmolality and drive thirst and sodium appetite, as sodium is necessary for whole body rehydration. It may be that while blood osmolality/whole body hydration is OK, some area of the brain is still sensing dehydration as a function of glycerol and continuing to drive the thirst/Na mechanism.
Back off on the glycerol and see what happens.
W6
Longtime viewer first time responder. Thought it was important to add my 2cents when I noticed that MS was experiencing higher baseline blood glucose readings while on ALA. I check my BG levels daily (upon waking and at diferent times during the day). When taking ALA my morning BG was consistently higher, and after a while I began noticing higher BG readings post meal. Now everyone has a different bodytype, so experiences will vary. But one other thing that concerns me is that so many posters complain about feeling tired after large doses of ALA and carbs. Unless they have a glucometer, hypoglycemia and hyperglycemia are hard to self diagnose. One simple rule that diabetics follow though is that shakiness, confusion, tension usually accompany hypoglycemia (verified this with my glucometer), while fatigue and tiredness usually accompany hyperglycemia (verified this with my glucometer).
This is off topic, but is a relatively new study worth pulling up. Thought i'd add it to this thread instead of opening a new one.
: J Nutr 2002 Oct;132(10):3001-6 Related Articles, Links
Alpha-lipoic acid inhibits glycogen synthesis in rat soleus muscle via its oxidative activity and the uncoupling of mitochondria.
Dicter N, Madar Z, Tirosh O.
Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel.
alpha-Lipoic acid (LA) is currently being investigated as a glucose-lowering agent for diabetes control; it is also considered a powerful dietary antioxidant. The objective of this study was to investigate the fate of glucose in isolated rat muscles incubated with LA and determine its effects on intramuscular redox status. Rat soleus muscles were incubated for up to 60 min with 2.4 mmol/L LA in the presence or absence of insulin. Intramuscular concentrations of LA were evaluated (uptake and reduction), and glycogen synthesis, glucose oxidation, intramuscular reactive oxygen species (ROS) production and mitochondrial membrane potential investigated. Insulin enhanced glycogen synthesis, whereas LA decreased rates by >50%. LA elevated ROS production and in combination with t-butylhydroperoxide, an oxidant, additively inhibited glycogen synthesis rates by 80%. Insulin acted as an antioxidant and attenuated ROS production by 30%. LA uncoupled the mitochondria and accelerated glucose oxidation 1.5-fold relative to the control. The glycogen synthesis pathway was found to be dependent on mitochondrial function because treatment with mitochondrial inhibitors eliminated the majority of glycogen synthesis. These data show that in this model, LA acts as a mild prooxidant, causing mitochondrial uncoupling and inhibition of glycogen synthesis. It appears that LA regulates glucose metabolism in the muscle differently than insulin.
PMID: 12368386 [PubMed - indexed for MEDLINE]
BMJ
: J Nutr 2002 Oct;132(10):3001-6 Related Articles, Links
Alpha-lipoic acid inhibits glycogen synthesis in rat soleus muscle via its oxidative activity and the uncoupling of mitochondria.
Dicter N, Madar Z, Tirosh O.
Institute of Biochemistry, Food Science and Nutrition, Faculty of Agricultural, Food and Environmental Quality Sciences, The Hebrew University of Jerusalem, Rehovot 76100, Israel.
alpha-Lipoic acid (LA) is currently being investigated as a glucose-lowering agent for diabetes control; it is also considered a powerful dietary antioxidant. The objective of this study was to investigate the fate of glucose in isolated rat muscles incubated with LA and determine its effects on intramuscular redox status. Rat soleus muscles were incubated for up to 60 min with 2.4 mmol/L LA in the presence or absence of insulin. Intramuscular concentrations of LA were evaluated (uptake and reduction), and glycogen synthesis, glucose oxidation, intramuscular reactive oxygen species (ROS) production and mitochondrial membrane potential investigated. Insulin enhanced glycogen synthesis, whereas LA decreased rates by >50%. LA elevated ROS production and in combination with t-butylhydroperoxide, an oxidant, additively inhibited glycogen synthesis rates by 80%. Insulin acted as an antioxidant and attenuated ROS production by 30%. LA uncoupled the mitochondria and accelerated glucose oxidation 1.5-fold relative to the control. The glycogen synthesis pathway was found to be dependent on mitochondrial function because treatment with mitochondrial inhibitors eliminated the majority of glycogen synthesis. These data show that in this model, LA acts as a mild prooxidant, causing mitochondrial uncoupling and inhibition of glycogen synthesis. It appears that LA regulates glucose metabolism in the muscle differently than insulin.
PMID: 12368386 [PubMed - indexed for MEDLINE]
BMJ
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