Glucose Modulates Vitamin C Transport

[majkinetor]

Well, we knew that glucose competes with DHAA, but not with AA.

It looks like we were wrong. It competes with DHAA and directly inhibits SVCT transporter "from inside"

http://jn.nutrition.org/content/130/1/6 ... nsion.html

Low Carb Diet anyone ?

[VanCanada]

Do you think the competition works both ways?
A low(er) carb diet would be best for most of us, obviously, but to what extent do you think megadosing vitamin C could compensate for the deleterious health effects of a diet as high in simple carbohydrates as the Standard American Diet? If my memory is right I think the SAD is up to a daily average intake of 150 grams of sugar?? Linus Pauling recommended a maxiumum daily intake of 50 grams of sugar.

I'm thinking of this as a thought experiment for those hypothetical people willing to megadose vitamin C but not willing to change their typical SAD consumption of Frosted Flakes and Slurpees...a rare breed of person indeed, but perhaps useful for exploring these concepts more fully.

[majkinetor]

[majkinetor]

Actually, I found reference for higher concentration of AA in the gut (is it supraphisiological, I don't know):

http://www.sciencedirect.com/science/ar ... 299090727A

1. Concentration of ascorbic acid present in the gastric or intestinal secretion of fish, dogs and humans is several times higher than in plasma.

[ofonorow]

I'm lost

if AA and DHAA block glucose transport by all means they should be diabetogenic

Who is claiming this? How can 1/10 the volume in the blood (15 mg/dl versus 100 mg/dl) block out the higher concentration?

According to Dr. Ely, probably due to the fight-or-flight evolutionary response, the transports favor glucose. Glucose no doubt crowds out vitamin C, not the other way!? (I am learning that much of this F-o-F response is due to cortisol release, which rapidly elevates blood sugars.)

[majkinetor]

But continuous infusion could do it, perhaps.
But generally you are right. Nobody claims that, I provided research above from 1950. Also, there is higher concentration of C near the pancreas which delays insulin secretion (there are few studies about it) so glucose hang out more in the blood.

But I guess its not that important.

[jaamzg]

Here's a question. Would taking chromium (gtf) along with VC help in getting it into the cells, along with the glucose? We know it's first on the list to help transport glucose into the cell, but since the chemical structure of VC is similar, would it help transport it into the cells, also?

This also led me to think a little bit about the lypo-c which is theoretically helping by getting the VC into the cell via contact with the cell membrane. What if someone who was ill (not necessarily diabetic, flu for example) were to take AA along with Chromium, would that maybe produce better results by helping provide a bridge for the AA into the cells?

I wonder if taking chromium would raise titration levels as the body might be able to push more AA into the cells?

What do you all think?

[VanCanada]

There seem to be two elements to this experiment.

1. Does bowel tolerance (BT) increase for healthy individuals? (BT is expected to increase for those with the flu, etc., therefore testing this element with sick individuals quickly becomes too complicated for us amateurs.)

2. Are flu symptoms ameliorated more at a given level of vitamin C supplementation when chromium is co-administered?


And to take this line of thought into other related tangents, I have two other questions.

Would chromium work like vitamin K3 in helping vitamin C to induce apoptosis in cancer cells?

Would the serum levels of vitamin C be predicted to increase or decrease (compared to the same AA supplementation without any co-administered chromium) if chromium acts like you are saying it might?

[jaamzg]

Here would be my thoughts on this from a purely theoretical basis.

1) AA bowel tolerance, we assume, is a function of AA plasma levels and the osmotic pressure differential in the GI moves the AA into the body and halts further absorption until the AA gets utilized. If Chromium were to help move the AA into the cells from the plasma, I would assume that the plasma levels would drop and allow for greater bowel tolerance levels in a healthy individual.

2) On the flu symptoms, that would be the experiment. But if we are to work off the assumption given by Levy for the increased efficacy of Lypo-C being from being able to get the AA (SA for Lypo-c) INTO the cells instead of just bathing the cells, then another mechanism that assists in AA delivery into the cell may produce enhanced efficacy over AA alone. Chromium being that supplement that helps in glucose transfer maybe can also assist in AA transfer?

I have some chromium, I may try it one of these days soon to see if there is an increase in bowel tolerance. It would be interesting to also test it with homemade lypo-c, being that if it works as theorized, the undissolved VC in the homemade solution could still be transported into the cells and increase the bt levels. It might provide a double effect?

On the cancer cell apoptosis, my understanding was that cancer cells have a ravenous appetite for glucose and would uptake the VC due to it's similar chemical structure. The k3 is somewhat of a "booster" in the internal cell reaction bringing about a greater percentage of apoptostic cells. I'm not sure how chromium would affect a cancerous cell.

As the the prediction, as I stated in 1), my assumption would be serum levels would decrease more rapidly with the chromium/AA combo, as the AA is transported into the cells, over the same given period of time for AA alone.

[majkinetor]

[jaamzg]

Quite a list of references, Majk! I'll have to spend some time going over it. Since I'm not really up to speed on the uptake and release of C into cells, maybe you can explain it a little more. I think I had read on another post that DHA and AA were taken into cells by different pathways. Once the C is used in the cell, does it just release DHA or is it releasing AA also? If all cells re-release the AA after uptake thereby keeping the plasma level elevated, where does the all the AA get used, since we know there has to be a constant supply to keep plasma levels elevated?

My thinking was that if it were going into the cells, as the lypo-c is supposed to do, then you raise your bowel tolerance level, just like you can do with the homemade lypo (unless the theory is wrong and it's just that the lipids being consume reduce the GI distress). If it is true that the C is getting into the cells, then I would assume a lower circulating plasma level, but that would depend, as you say, on it not being re-released.

I'm feeling another group self-experimentation coming on like when we stated the homemade lypo-c thread

[ofonorow]

I apologize, for the injection, I have not had time to digest all the arguments above, but I did notice:

then you raise your bowel tolerance level, just like you can do with the homemade lypo

Is this well known? Raise means you still hit bowel tolerance.

It is very hard to hit it with Lypo-C.

If this observation were generally true, it may confirm the notion that homemade lipos are just emulsifying C (and protecting the vitamin like kiwi or aloe vera gel would) and not creating sustainable liposomes such as those that are in Lypo-C.

[majkinetor]

I think I had read on another post that DHA and AA were taken into cells by different pathways.

GLUT transporters are bidirectional so DHA will go up and down. AA that is oxidized inside the cell can also get out via this mechanism. Currently it is not known how cells exactly push AA out of itself and this is subject of resarch AFAIK. I know Levy said similar thing in our lypo c thread related this route.

BTW, lipo c has higher BT not because it is absorbed more, but because it has different digestion route and is 100% absorbed in small intestines via lymphatic channels as chylomicron.


Should it bring higher BT ? I don't know, it doesn't seem very likely to me. I am not even sure how BT functions since I observed that many people who can't initially tolerate high doses (like 1,2g) can after some time tolerate 10x higher dose. This is inline to what Pauling speculated about enzimatic reactions that turn on once there is enough C, so body pushes more from GI tract after that (thats why you get rebound scurvy when you stop supplementation).

The only true way to test it is via biopsy I guess.
BTW, I accidentally doubled the references - I fixed it now.

[jaamzg]

Is this well known? Raise means you still hit bowel tolerance.

I would say that anything having to do with homemade lypo is not well known. From personal experience, in a healthy state, I am able to raise BT from around 3grams to around 8 grams with homemade lypo. I suspect it's due to lack of full encapsulation and that is why there is still a BT level that's hit. Maybe there really isn't a BT level with commercial Lypo since it's pure lypo without the extra unencapsulated VC floating around. But, at least for me, there is a BT limit on the homemade stuff. If I remember correctly, when running the tests on the homemade lypo c, I had created a batch and divided the emulsified solution, sonfied one half and not the other. There was less gas produced when mixing the baking soda in with the homemade lypo c than than there was when mixing it with the emulsified (non sonified) solution, but even the sonified solution produced some gas.

I know Levy said similar thing in our lypo c thread related this route.

Do you have a link to that thread, please?

I'll need someone to explain that powerpoint slide to me. Why would the cell be taking up DHA, reducing it, then sending the AA out? Doesn't that just negate the whole point of taking up AA for that electron? Why would it be using up energy to make AA and then get rid of it? And if the cells did this, then why not just take DHA and let the cells create AA for us? I'm missing something somewhere. I totally get that there may be a competition between glucose and AA if they have similar molecular structures and are using the same pathways but reducing the DHA to send on it's way just seems odd to me.

I'll probably give the chromium a try this next week and report back on any perceived changes in BT levels.

[majkinetor]

As far as I know DHA is excreted. So cell can take AA via SVCT, it gets oxidised to DHA which then gets excreted out via GLUT.

See this pic
http://www.biocarta.com/pathfiles/m_vitcbpathway.asp

However, some cells (all ?) must have mechanism to push out AA - at least liver, kidney and adrenals - to the blood. As I said its still new topic and not much is known so who knows if maybe all cells can do that. Why would cells do that? Who knows; there are reports that AA could serve as paracrine agent for instance.

Here is the page you requested:
viewtopic.php?p=23712#p23712