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r-ALA experiment
- Thread starter th'wolf
- Start date
Ceebs, you will find that almost ALL so called anti-oxidants also exhibit pro-oxidant activity too. ALA, much like glutathione, is more of an oxidant "buffer" than a true anti-oxidant (involved in redox cycling). And don't forget that your body also has an absolute requirement for anti-oxidants, especially the immune system.
Interesting thread. Wislon6, I don't have sodium cravings at all. Just thirsty and peeing a lot. Could be the glycerol, but since my intake hasn't changed in a long time, I can't figure out why ALA would suddenly cause the glycerol to have this effect, especially given the reports of the other ALA users who also report the thirst/peeing/dehydration (who are presumably not eating much glycerol).
MR BMJ, I haven't speculated much (just observing at this stage), but if I WERE to speculate, I would tend towards macros theory regarding reduced insulin secretion (hopefully temporary). After all, I did go through a patch of hypoglycemic symptoms when I first started th r-ALA, so it's not to hard to imagine that my body has somehow 'learned' that it doesn't need as much insulin from taking the ALA chronically. No need to invoke downregulation of GLUT4. But as I mentioned, things get pretty screwy when you start looking at variation in insulin secretion and glucose disposal in non-diabetic eumenorrheic women. You're trying to measure small differences against and ever changing background of hormones!
The rat soleus study is interesting, but without reading the whole paper it's hard to conclude much. Glycogen synthesis may be resistant to insulin stimulation during periods of acute starvation in muscles with fiber compositions similar to the epitrochlearis, but NOT in muscles with fiber compositions similar to the soleus. Partial reversal of the resistance observed in vitro for epitrochlearis muscles from starved rats may be due to the loss of factors which suppress the effect of insulin in vivo. So it makes big difference (in rats) if you're looking at soleus versus epitrochlearis, and whether you're looking at starved (glycogen depleted) versus well fed muscles. They should have looked at the epitrochlearis too, and stated whether the muscles were fed or depleted......
In any events, I don't think MY calves have any glycogen synthase activity at all. Thy're strong, but never grow, with or without ALA.
Interesting thread. Wislon6, I don't have sodium cravings at all. Just thirsty and peeing a lot. Could be the glycerol, but since my intake hasn't changed in a long time, I can't figure out why ALA would suddenly cause the glycerol to have this effect, especially given the reports of the other ALA users who also report the thirst/peeing/dehydration (who are presumably not eating much glycerol).
MR BMJ, I haven't speculated much (just observing at this stage), but if I WERE to speculate, I would tend towards macros theory regarding reduced insulin secretion (hopefully temporary). After all, I did go through a patch of hypoglycemic symptoms when I first started th r-ALA, so it's not to hard to imagine that my body has somehow 'learned' that it doesn't need as much insulin from taking the ALA chronically. No need to invoke downregulation of GLUT4. But as I mentioned, things get pretty screwy when you start looking at variation in insulin secretion and glucose disposal in non-diabetic eumenorrheic women. You're trying to measure small differences against and ever changing background of hormones!
The rat soleus study is interesting, but without reading the whole paper it's hard to conclude much. Glycogen synthesis may be resistant to insulin stimulation during periods of acute starvation in muscles with fiber compositions similar to the epitrochlearis, but NOT in muscles with fiber compositions similar to the soleus. Partial reversal of the resistance observed in vitro for epitrochlearis muscles from starved rats may be due to the loss of factors which suppress the effect of insulin in vivo. So it makes big difference (in rats) if you're looking at soleus versus epitrochlearis, and whether you're looking at starved (glycogen depleted) versus well fed muscles. They should have looked at the epitrochlearis too, and stated whether the muscles were fed or depleted......
In any events, I don't think MY calves have any glycogen synthase activity at all. Thy're strong, but never grow, with or without ALA.
Yes, but in my case I know for sure (thanks to the glucometer) that I do not have hyperglycemia.
Without a doubt in my mind, the thirst/peeing side effect is mainly due to reduced insulin. What is hard to figure out is why I'm not losing weight. For a comparison, in the first week of a traditional bodybuilding diet where I reduce carbs and sodium while increasing protein, I can expect to develop increased thirst and more frequent urination BUT I LOSE 3-4 KILOS of fluid as well. With the r-ALA I have the exact same symptoms WITHOUT the weight loss. It is obvious to me that the r-ALA is somehow repartitioning fluid as well as carbs.
As an update, I have reduced my daily r-ALA dose by 50%, and the dehydration isn't as bad as it was. I actually slept the whole night last night without a single trip to pee
But then again, that was after a nice big salty/carby/fatty pizza feed.......and my glucose AUC was a lot higher this time around (prolly not enough r-ALA). So maybe more sodium will do the trick. I'll try doubling my sodium for the next week and let you know how that goes.
Without a doubt in my mind, the thirst/peeing side effect is mainly due to reduced insulin. What is hard to figure out is why I'm not losing weight. For a comparison, in the first week of a traditional bodybuilding diet where I reduce carbs and sodium while increasing protein, I can expect to develop increased thirst and more frequent urination BUT I LOSE 3-4 KILOS of fluid as well. With the r-ALA I have the exact same symptoms WITHOUT the weight loss. It is obvious to me that the r-ALA is somehow repartitioning fluid as well as carbs.
As an update, I have reduced my daily r-ALA dose by 50%, and the dehydration isn't as bad as it was. I actually slept the whole night last night without a single trip to pee
But then again, that was after a nice big salty/carby/fatty pizza feed.......and my glucose AUC was a lot higher this time around (prolly not enough r-ALA). So maybe more sodium will do the trick. I'll try doubling my sodium for the next week and let you know how that goes."Frequent urination could also be the result of ohter hormone abnormalties (lack of vassopresin)."
That's what I was thinking as I was reading through this. Sounds like diabetes insipidus, but why? Then again, onset can be acute and occur at any age.
You guys are all kicking around the hyperglycemia idea, well that would be osmotic diuresis but MS isn't hyperglycemic. But, she may have developed over time, very high blood glycerol concentrations for reasons unknown or a threshold concentration was finally achieved, or there may be interactive effects with menstrual phase. We found that glycerol was grossly elevated in the blood for 4 - 6 hours after a single feeding. High chronic glycerol intake could be causing the problem.
I know you've been taking the glycerol for some time MS, but renal clearance may have changed, perhaps there is some synergistic effect with ALA, who knows. I'd suggest cutting out all glycerol for about 5 days and see what happens. If the polyuria stops, then you have your answer. If not, then its time to get checked for DI.
W6
That's what I was thinking as I was reading through this. Sounds like diabetes insipidus, but why? Then again, onset can be acute and occur at any age.
You guys are all kicking around the hyperglycemia idea, well that would be osmotic diuresis but MS isn't hyperglycemic. But, she may have developed over time, very high blood glycerol concentrations for reasons unknown or a threshold concentration was finally achieved, or there may be interactive effects with menstrual phase. We found that glycerol was grossly elevated in the blood for 4 - 6 hours after a single feeding. High chronic glycerol intake could be causing the problem.
I know you've been taking the glycerol for some time MS, but renal clearance may have changed, perhaps there is some synergistic effect with ALA, who knows. I'd suggest cutting out all glycerol for about 5 days and see what happens. If the polyuria stops, then you have your answer. If not, then its time to get checked for DI.
W6
No problem W6. As it happens, I ran out of glycerol recently and have substituted honey in my recipe. It doesn't feel or taste as nice, but it does allow me an opportunity to "dry out" and clear the dietary glycerol from my body.
Aside from that, reduced vasopressin doesn't really explain why I haven't lost "fluid" weight. Judging from the mirror, I definitely have less subQ fluid and my muscles are still full, no change in weight. On the surface this is all good and is exactly what one would expect from a glucose partitioning agent like r-ALA. I was more puzzled by Ula's initial results where she lost 10lbs weight in 2 weeks without changing anything. Now THAT has gotta be a change in fluid balance.
There is definitely something interesting going on here, and it's not just me. It's all anecdotal for sure, but the other posters who have noticed similar symptoms must be in the same boat as me. Now if r-ALA in otherwise apparently healthy people can cause DI, that is worth knowing!! Aside from interrupted sleep, it's nice not to be a bloat bag for a change. I have always been prone to fluid retention most of my adult life.
Anyway, I only got up once last night, so it looks like cutting back on the ALA or glycerol is working
Aside from that, reduced vasopressin doesn't really explain why I haven't lost "fluid" weight. Judging from the mirror, I definitely have less subQ fluid and my muscles are still full, no change in weight. On the surface this is all good and is exactly what one would expect from a glucose partitioning agent like r-ALA. I was more puzzled by Ula's initial results where she lost 10lbs weight in 2 weeks without changing anything. Now THAT has gotta be a change in fluid balance.
There is definitely something interesting going on here, and it's not just me. It's all anecdotal for sure, but the other posters who have noticed similar symptoms must be in the same boat as me. Now if r-ALA in otherwise apparently healthy people can cause DI, that is worth knowing!! Aside from interrupted sleep, it's nice not to be a bloat bag for a change. I have always been prone to fluid retention most of my adult life.
Anyway, I only got up once last night, so it looks like cutting back on the ALA or glycerol is working
macrophage69alpha
New member
increase the sodium intake.. r-ala is pottasium sparing
OK, lots of good advice here. In the name of good research, I'm not going to increase my sodium just yet. If I change too many variables at once (I've already reduced my ALA dose and ditched the glycerol) then we'll never know what's going on. Maybe after a week of this, I'll start increasing my dose of ALA, then reintroduce glycerol, and THEN I'll try increasing sodium. One thing at a time.
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