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one thing i;ve always wondered about ALA...

danielson

Elite Mentor
Platinum
with say glucocorticoid (i think) steroids, if you take them for too long you can get atrophy of the adrenal glands due to long term negative feedback (i.e. because you are artifically introducing corticosteroids into the blood stream the adrenals produce less of their own and as a result shrink long term)

now i understand that the action of ALA is not that of insulin, it doesn;t act like a hormone but rather increases the insulin sensitivty of cells. but by doing so im curious as to whether the body realises that blood sugar levels are dropping faster than expected for the levels of insulin being secreted and thus reduces its pancreatic secreton of insulin

now im unaware of whether the pancreas will reduce its B-cells or if it even can but i am wondering whether it will reduce its insluin secreteons when taking ALA and whether it will bring them back up once it has finshed being taken.

i;ve not seen it anywhere in the readng i've done on the supplement which has been 100% postive (of R-ALA anyway), but i;d like to know if it is a concern.

it sounds like a great supp, and i really wanna shred up (having never got past 11%bf before) and this seems like the best way...any thoughts? be as technical as you need to....i have a science/bio background :)
 
doesn't biotin have a role in preventing ^
 
by what mechanism? im unsure how it can as i;ve never seen biotin mentoned as an essential co-enzyme for insulins actions
 
bump for an answer....if it can help me looked toned i'd love to try it
 
yup, i wanna take it when cutting

but the only thing stopping me and others i know from taking it is the long term effects it could have, since i have a genetic pre-disposition to developing diabetes.....

i;ve seen all the data about what it can do, but nothing about the long term effects on cells having the glut-4 receptor upregulated
 
I don't believe this would occur. Beta cells in the pancreas can be destroyed by autoimmune function (as in type 1 diabetes). However, that is a genetic defect. That is the only thing I know of that would cause beta cell destruction.

Ryan
 
bump again....i really wanna take it as do many friends but we're all concerned about any potential for reduction of insulin secreteion or action
 
what did you ever find out on the subject? I'm in the same boat you are diabetes runs in my family and i want to use ALA long term for weight loss maintenance.

there are diabetes drugs that already exist that increase insulin sensitivity called thiazolidinediones. I'm sure research has been done on them to detect for a negative feedback loop. My pharmacology book doesnt make any mention of negative feedback but studies may have been done on the subject.
 
i had thought about looking at the NIDDM medications as a reference point, but i have had 'teaching' in this area and it has never been mentioned as a side effect of them, and i;ve also not seen it mentioned in any pharmacology texts that i've read.

my pubmed searches have been fruitless as well, but i hate that damned thing anyway as i can never find what i want, so it left me wondering about ALA specifically

you turned up anything on the research front? you seem quite good at finding the net sources of info...and thanx for the bump
 
danielson said:
by what mechanism? im unsure how it can as i;ve never seen biotin mentoned as an essential co-enzyme for insulins actions

i believe biotin is an essential cofactor for lipoamide (ala in its amide form) during the pyruvate dehydrogenase step preceeding the creb's cycle. it's been a little while since i took biochem so i could be off. but i think i'm right.

and i've never heard biotin being required to mediate any of ala's actions in increasing insulin sensitivity.

it's more of ala depleting the body's store of biotin that is the reason you're supposed to take the 2 together.
 
i just talked to an endocrinologist on another board and he says that something like ALA will be better than using nothing for those at risk of type 2 diabetes. He also said that yes, the islet of langerhan cells will have a negative feedback loop which decreases insulin production but that that is a good thing as they will not have to work as hard to produce as much insulin and will therefore last longer. I am not sure where he stands on the risks of long term atrophy of Islet of Langerhan cells but i am trying to clarify that. He says the answer is too complex and he doesnt have time to explain it but that the risk of contracting type II diabetes is going to be lower on ALA.
 
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hmm

makes sense.....im not sure whether your beta-cell number wont decrease on the basis of something that improves the effects/actions of insulin

this is probbly enough for me, if i manage to corner an endocrinologist or pharmacologist i'll ask them, however the last one i asked had never heard of ALA (was also a diabetologist) and labelled it a 'homeopathic' herb or something similar :rolleyes:
 
bump.. Very interesting. I'm taking GlucorellR in large doses for 4 months straight. Was wondering the same effect. Also, if there's a crash after stopping using it.
 
This could be an interesting debate. However, I question the relevance of your inquiry to r-ALA. Are you worried about pancreas atrophy? You draw a parallel between adrenal gland and pancreas, yet the atrophy of adrenal gland results from exogenous administration of glucocorticoids. ALA is not insulin, insulin activates a pathway through which GLUT-4 is translocated from the intracellular compartment into the membrane, thus the cell surface becomes receptive to insuling and glucose uptake which results in synthesis of a few kinases which are responsible for translocation of GLUT-4 onto the membrane and glycogen synthesis. ALA acts in a few ways:
1) it increases insulin stimulating effects on the pathway to GLUT-4 translocation
2) increase the expression of GLUT-4 transporters in the membrane - larger surface=more uptake
3) ALA has anti-oxidative effects on free radicals (perroxides/reactive oxygen species) which even in small amounts can totally inhibit GLUT-4 expression and kinases responsible for glycogen synthesis (welcome diabetis)

Therefore ALA's action in the body is merely of a facilitator to insulin and glucose clearance, but i'm yet to see anything to mention that it reduces the serum/secretion of insulin. I think the confusion about ALA and pancreatic atrophy stems from a myth that ALA is an insuin mimic - but it is not.
 
yeah its why we had the confusion juve, when talking about it to my friends we realised the negative feedback in regards to the corticosteroids were due to the fact that exogenous steroid was being administered, we were unsure about the effects of something that increases/facilitates the action of insulin would have on the pancreas.
 
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