Vitamin C appetite? light headed?

[NiacinVC]

I have noticed I get light headed and hit with fatigue lately. At first I thought it was from megadosing VC but this has just started happening the last couple days. So I go eat and drink gatorade and feel instantly better. I think what is happening is that Vitamin C is curbing my appetite so sometimes I have to force myself to eat more because I am not taking in enough calories.

Anyone else have any similar experiences?

[scottbushey]

Absolutely. You will have a change in eating habits. Your body will not need to gourge due to the need to replace all the nutrients lost form the repair that is going on if you weren't on VC. The VC will begin to repair your body and as time passes, you will require less food. I lost about 20 lbs on VC and another 10 on Paleo.

[majkinetor]

On the other hand, maybe your genetics require sugar for functioning more then for other people and megadoses of C prevent sugar from entering the body.

There are also few studies about C delaying insulin secretion.

Maybe you should try to switch your body to use fat as proffered fuel instead glucose and see how it goes, just as scotty did.

[ofonorow]

On the other hand, maybe your genetics require sugar for functioning more then for other people and megadoses of C prevent sugar from entering the body.

Interesting twist, but I know of little or no scientific support for this speculation.

It would be nice if vitamin C blocked insulin as it would then be a great substance to use for weight loss!

[majkinetor]

Interesting twist, but I know of little or no scientific support for this speculation.

Thats not speculation. Glucose and DHAA compete, so the more DHAA you have in the gut, the less glucose can enter.

As for insulin, there are several studies about it, here is one. The reason may very well be the same.

Megadose of vitamin C delays insulin response to a glucose challenge in normoglycemic adults
http://www.ajcn.org/content/60/5/735.full.pdf

The physiological consequence of this is not clear. The same holds without megadoses (another study I have lists 1g per day oral dose)

Vitamin C is great substance for weight loss, but probably more for other reasons (like carnitine synthesis)
Notice that it delays, not attenuates.

[ofonorow]

Interesting twist, but I know of little or no scientific support for this speculation.

Thats not speculation. Glucose and DHAA compete, so the more DHAA you have in the gut, the less glucose can enter.

What is the "gut" reference? (Glucose/Ascorbate antagonism generally refers to the insulin mediated tunnel through the cell membranes into cells.)

First of all, the life of DHAA in the blood is a matter of minutes. (I still am skeptical about the DHAA argument that it is the normal way vitamin C enters cells.)

More importantly, the amount of glucose in the blood is generally 100 times that of vitamin C! Two orders of magnitude. Fasting blood sugar is around 100 mg/dl. After meals, glucose is generally much higher.

The renal threshold of vitamin C is 1.5 mg/dl. (Reference: http://www.news-medical.net/health/What-is-Vitamin-C.aspx

At high dietary doses (corresponding to several hundred mg/day in humans) ascorbate is accumulated in the body until the plasma levels reach the renal resorption threshold, which is about 1.5 mg/dL in men and 1.3 mg/dL in women. Concentrations in the plasma larger than this value (thought to represent body saturation) are rapidly excreted in the urine with a half-life of about 30 minutes; concentrations less than this threshold amount are actively retained by the kidneys, and half-life for the remainder of the vitamin C store in the body increases greatly, with the half-life lengthening as the body stores are depleted.

)

If not speculation, then it is an error. As a matter of probability, I do not see how vitamin C can "block" glucose.


added. Regarding the affect of AA on insulin.

Ascorbic acid (AA) is oxidized to dehydroascorbic acid (DHAA) when utilized in vivo. This metabolite is then rapidly taken up by blood cells or other tissues and reduced back to AA
by a glutathione and/or NADPH-dependent DHAA reductase ( I ). This cycle serves to save DHAA from rapid hydrolysis to diketogulonate, which cannot be recycled to AA and supplies AA for cellular metabolism. Hence, impaired cellular uptake of DHAA would accelerate vitamin C depletion. Cellular uptake of DHAA shares a common transport system with glucose, and, in vitro, glucose inhibits cellular transport of vitamin C in a dose dependent
fashion (2-4).

The claim is hard to accept, (or at least for me to understand) because it implies that the only way vitamin C can enter cells is to become oxidized (AA) or when it is in the form of sodium ascorbate (via the the sodium transporters, but in this case, SA shouldn't compete with glucose?)

I am trying to picture how the oxidative process of AA is controlled so that it has an equal chance of reaching all our trillions of cells through the blood stream.

I know that Jay Patrick, vitamin C expert and founder of Alacer, believed that vitamin C in the blood was sodium ascorbate.

However, Sherry Lewin, author of VITAMIN C: ITS BIOLOGY AND MEDICAL POTENTIAL wrote that vitamin C in the blood was AA, which entered cells, and that vitamin C was expelled from cells after attaching to sodium, and then traveled through the lymph as SA.

Lewin does point out that DHAA, while short lived, can more easily penetrate membranes, both cell and the blood brain barrier, than ordinary ascorbic acid.

It might make sense if the oxidative conversion to DHAA happened just as AA reaches a cell and is about to be "tunneled" through the GLUT transporter. Losing an electron as part of the membrane absorption process. (And what happens to those electrons "released" as vitamin C is absorbed into the cell?)

[majkinetor]

The claim is hard to accept, (or at least for me to understand) because it implies that the only way vitamin C can enter cells is to become oxidized (AA) or when it is in the form of sodium ascorbate (via the the sodium transporters, but in this case, SA shouldn't compete with glucose?)

At 1994 I think SVCT existance was only speculated and its not even mentioned in this study.
SVCT isn't blocked by glucose, however we talk here about GLUT2 which is expressed in beta cells of pancreas. Since glucose enters the body via portal vein that passes next to pancreas, blood glucose levels in that region are much higher postprandialy then what are normal, fasting blood glucose levels. Kidnies come later in this pathway when C is already distributed around...

Vitamin C doesn't have to be in SA format as sodium is abundant in the body. In the gut however, situation is different so little sodium probably helps - maybe Pauling sensed this and used half of the dose as SA, or maybe he just did it to prevent gerd.

You need to understand that gut region is different then other regions of the body. First, immune system is very active there which means that ROS damage is huge as body constantly controls pathogens that enter with food and local microbiota, and this means that DHAA concentration is not the same as in blood. Location is very important in the body.

Anyway, this phenomena is measurable, you don't have to guess if it exists, you just need to test it up and explain the findings. If insulin is delayed after C, and it is, then there is big probability that competition in pancreatic region is really big.

I am not sure myself about explanations and I need to recheck the references one day. I was reading lot of this stuff when I was C newbee...

[ofonorow]

I am beginning to understand (I think) the confusion. Our ideas of vitamin C transport are different.

I am only connecting (SVCT and GLUT) to the transport of vitamin C from the blood through the lipid cell membrane into cells.

I do not believe there is any role of a "vitamin C transporter" from the gut into the blood stream, and I think this confusion is why we seem to have vastly different takes on these things

I agree the Internet does not make this any easier to understand.
.