Dehydroascorbic = MUCH higher blood levels of VitC ?

[OxC]

I'm always excited when I see brand new, peer-reviewed scientific articles concerning DHAA that are open source, meaning you can read the full text without having to subscribe to the journal. Here's a link to one just published in May 2014. It is focused on vitamin C uptake and recycling in the brain. An understanding of these mechanisms helps in understanding why DHAA has been investigated as a potential therapy for stroke and Alzheimers.

[ofonorow]

I finally watched the entire video, and while interesting, I came away wondering what evidence there was or is that DHAA provides health benefits. (When iron oxidizes, we get rust. When an apple oxidizes, it turns brown.) I don't understand why I would want an oxidant to enter my blood stream, even or especially at high levels, unless I was fighting a disease - such as Lyme?

The assumption in the video seems to be that because it is a form of vitamin C, that DHAA has all the same benefits of reduced ascorbate. The other assumption based on a single experiment is that the blood measurement (in red) was a) not an anomaly, and b) was reduced ascorbate in the blood.

So before going on lets review some of the proposed "facts" presented previously.

A simple list of facts:

• Reduced ascorbate is transported into cells, through the cell membrane, by SVCTs.
  

Even if we accept this, it does not explain how liposomal vitamin C, or even ordinary ascorbate reaches the blood stream. The claim is that ascorbate actually enters (and exits) intestinal cells called Enterocyte. (And since wikipedia was often cited, please note that there is no mention of ascorbate entering these cells in the enterocyte wiki discussion.) My training was that most nutrient transport is via intestinal villus http://en.wikipedia.org/wiki/Intestinal_villus. Little tubules that move nutrients from the intestines to the blood stream. So while the SVCT may transport AA through membranes, I do not think it is accepted that all ascorbate moves into and out of any cell prior to reaching the blood stream.

Furthermore, the Hickey/Roberts book RIDICULOUS DIETARY ALLOWANCE reveals that some (all, most?) of the ascorbic acid taken by mouth NEVER REACHES THE INTESTINES (if the stomach acid pH is low enough) because it is "assimilated" through the stomach wall into the blood stream.

DHAA, formed when reduced ascorbate is oxidized, is transported into cells, through the cell membrane, by certain GLUTs.

Dietary sources of reduced ascorbate include ascorbic acid (found naturally in foods, also in many dietary supplements), sodium ascorbate, calcium ascorbate, magnesium ascorbate (these salts are found in some dietary supplements, such as "buffered" vitamin C preparations), and even compounds such as ascorbyl palmitate (a fat-soluble compound added to some processed foods as a preservative, but when ingested the palmityl residue can be cleaved by esterase enzymes in the gut, releasing an ascorbate ion, and thus becoming a dietary source of vitamin C). There are others.

Dietary sources of DHAA include the DHAA found naturally in food, DHAA that is formed when the ascorbate in food becomes oxidized during processing or even chewing food, DHAA that is found in trace amounts in almost all dietary supplements (it is essentially impossible to have a large quantity of ascorbate that is not accompanied by a trace amount of DHAA due to some oxidation of the ascorbate), DHAA that is found in significant quantity in one brand of dietary supplement, and now, as demonstrated in the video http://youtu.be/YHKBhz7OCB4 DHAA that can be found in megadose quantities in a specially-prepared zucchini smoothie.

This is interesting and not something we usually think about, but as the video author points out, the ratio of AA to DHAA "in nature" is about 5 to 1."

When ingested, reduced ascorbate is absorbed and appears in the bloodstream at a particular rate; generally the peak value in the bloodstream occurs about 2 - 3 hours after ingesting it in typical supplemental or megadose quantities.

From our crude glucose meter measurements, this does sound like an alkaline ascorbate that has reached the intestines. High dose (5 grams) of Ascorbic Acid peaks around 20 minutes, which seems to confirm the Hickey/Roberts stomach entry mechanism. See:http://www.vitamincfoundation.org/forum/viewtopic.php?f=10&t=10603

It is clear that the more you eat in a single dose, the higher the peak blood values can get. But it is also clear that after consuming a dose of somewhere around 200 mg, absorption from the gut slows tremendously, and it requires multi-gram increases in dose to only slightly increase the resulting peak blood levels. This phenomenon is currently attributed to characteristics of the SVCT transporters.

There are multiple factors determining blood levels. Rate of absorption into the blood, and high dosages are immediately lowered by the kidneys (30 minutes half life). The idea of 200 mg is tied to the ascorbate absorption (per your model) into white blood cells, but has little to say about general blood levels. Again refer to RIDICULOUS DIETARY ALLOWANCE lulu.com/ascorbate.

When ingested, DHAA is absorbed and appears in the bloodstream (as reduced ascorbate) more quickly than when reduced ascorbate itself is ingested.

This would be amazing if true, but assuming the model presented is accurate then those poor enterocyte cells are undergoing severe oxidative stress! (If the C is being reduced in these cells, then other parts of these cells are oxidizing. The only way to provide the necessary electrons to reduce the oxidative stress is by an antioxidant.)

The peak levels occurs somewhere around 30 to 90 minutes after ingestion. The peak blood level achieved by ingesting 5 grams DHAA was twice as high as the peak level achieved by the same individual when he ingested 5 grams of reduced ascorbate. More rapid uptake and higher intracellular levels from exposing cells to DHAA as opposed to reduced ascorbate has been demonstrated in many in vitro studies. This phenomenon is currently attributed to characteristics of the GLUT transporters.

The one fact that supports the idea is the very short half-life of DHAA.

Here's some speculation:

• The term "bioavailable" is usually defined (in reference to vitamin C) as the amount of an oral dose that appears in the bloodstream, as compared to the same amount infused directly into the bloodstream. Blood levels are monitored over time to produce curves, and area-under-the-curve analyses are used to compare the estimated total amount of vitamin C in the blood from a single dose given orally versus the same dose given IV. The value is stated as a percent. When 200 mg reduced ascorbate is given orally, such calculations show that this dose is almost 100% bioavailable. When larger doses are given orally (say, 2 grams) such calculations show that this size dose is maybe only 20% bioavailable. The rapid and extremely high blood values achieved by ingesting DHAA suggest that the oral bioavailability of DHAA is much greater, although I'm not aware of any such calculations ever being done. Nevertheless, I speculate that doses of DHAA of 1 or 2 grams, or even 5 grams or more, may be very close to 100% bioavailable.

What about a 200,000 mg daily "bowel tolerance" dosage for mono or other high-powered virus? How would this dose pass through the enterocytes? The Cathcart theory is that any ascorbate which is not absorbed into the blood stream reaches the rectum causing diarrhea. See http://vitamincfoundation.org/pdfs/Vitamin_C_Dosage_in_Disease.pdf So where did the 200 grams of ascorbate go, if not into the blood and immediately into the ascorbate depleted tissues?

And Cathcart's theory is that at these dosages, we are no longer dealing with the "vitamin" property of ascorbate - the ability to make collagen and avoid scurvy - instead, we are using the antioxidant property to quench free radical fires caused by the virus.

That is not to say there couldn't be significant beneficial properties to the oxidant DHAA.

A forum poster wrote and article published in the Townsend Letter providing evidence that it is DHAA that is ultimately responsible for ascorbate's anti-viral properties. (At these 200,000 mg levels, probably 20% breaks down to DHAA and that may be what creates much of the benefit).

I know doctors who use the anti-malaria oxidant MMS to treat diseases like Lyme. They use the oxidant property on purpose. I do not want to rust myself, so I will not take 5 grams of DHAA to merely repeat the blood measurement shown in the video, but if I had Lyme disease, that would be a different matter, and I would then be willing to try high doses of DHAA. (With something like 5 times the amount of AA - later)

[OxC]

A forum poster wrote an article published in the Townsend Letter providing evidence that it is DHAA that is ultimately responsible for ascorbate's anti-viral properties. (At these 200,000 mg levels, probably 20% breaks down to DHAA and that may be what creates much of the benefit).

I'm not sure there is any evidence to support an assumption that "probably 20%" of a 200 gram dose of AA is converted to DHAA, but maybe it is true. Maybe, for that matter, the conversion of AA to DHAA is responsible for most of the perceived benefits of taking megadoses of AA. As you have pointed out, there remains a great deal that is unknown as to the fate or function of large doses of AA.

[OxC]