OxC wrote:A simple list of facts:
- Reduced ascorbate is transported into cells, through the cell membrane, by SVCTs.
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. 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.
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.
When ingested, DHAA is absorbed and appears in the bloodstream (as reduced ascorbate) more quickly than when reduced ascorbate itself is ingested.
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.
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.
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.ofonorow wrote: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).
davea0511 wrote:AA, which is 99% of what you are using when you buy a bottle of regular vitamin C ... this form donates a bioavailable electron at the cellular level and provides an alternate pathway for aerobic ADP -> ATP synthesis (see http://crystal.res.ku.edu/taksnotes/Bio ... chp_17.pdf, pages 9-11), which is the main reason why vitamin C gives you energy.
The utilization of vitamin C for aerobic ATP synthesis is perhaps its most valuable asset…
...going from AA to DHA imparts energy to synthesize ATP ... the molecule responsible for energizing all cellular activity. So, again, consuming DHA is kind of like breathing in CO2, imnsho. Not doing you a whole lot of good filling your cells with spent fuel.
Summary of experiment:
1. Add β-hydroxybutyrate into the reaction cell → O2 consumption is increased.
2. Add rotenone or amytal into the reaction cell → O2 consumption is stopped (Complex I is inhibited).
3. Add succinate into the reaction cell → O2 consumption is resumed.
4. Add antimycin A into the reaction cell → O2 consumption is stopped (Complex III is inhibited).
5. Add TMPD + ascorbic acid into the reaction cell → O2 consumption is resumed.
6. Add CN- into the reaction cell → O2 consumption is stopped (Complex IV is inhibited).
”Hepatocytes prepared from 48 h starved animals are glycogen depleted, therefore the source of their glucose production is gluconeogenesis. Cells were incubated in the presence of various concentrations of ascorbate or dehydroascorbate for 30 min and their glucose production was measured. For comparison gluconeogenesis from alanine was also detected. Significant glucose formation from ascorbate was observed, which reached saturation at relatively low ascorbate concentrations. Dehydroascorbate-fueled glucose production showed a greater rate and saturation was reached at higher substrate concentrations. Gluconeogenesis from both substrates was surprisingly effective, its rate being comparable to that from alanine.”
Gluconeogenesis from Ascorbic Acid: Ascorbate Recycling in Isolated Murine Hepatocytes (1996)
“The major pathway of catabolism of ascorbic acid in the guinea pig is the oxidation of its lactone carbonyl carbon to CO2 with subsequent oxidation of the entire carbon chain to CO2.”
“The guinea pigs fed the massive amounts of ascorbic acid catabolized the vitamin at a faster rate than those animals fed the control amount. The total amount of radioactivity excreted by the experimental groups was significantly greater than the amount excreted by the control group… This was due to greater CO2 excretion in the experimental group.”
Catabolism and Tissue Levels of Ascorbic Acid Following Long-term Massive Doses in the Guinea Pig (1974)
” Volunteers were given a steady intake of various individually different daily dosages of ascorbic acid. After 3 weeks 1-14C-labelled ascorbate was given together with various amounts of unlabelled ascorbic acid (90-1000 mg). Regardless of the total daily dose, in cases where the carrier dose amounted to 180 mg or more, carbon dioxide was recovered from the breath. The amount recovered ranged from 1 to more than 30% of the given dose. The larger the amount of carrier the larger was the amount of label recovered as carbon dioxide.”
Formation of Carbon Dioxide from Ascorbate in Man (1985)
"1. Evidence is presented showing that progressive degradative changes occur in L-ascorbic acid dissolved in water and kept at 25°C for a 72-hour period. 2. When a human subject received 20 μc of freshly dissolved L-ascorbic-1-C14 acid solution, little or no C14 appears in his respiratory CO2. 3. Men who were given similar samples of L-ascorbic-1-C14 acid aged for 36 and 72 hours, respectively, excreted 30.6% of the ingested C14 as respiratory CO2."
Respiratory Catabolism in Man of the Degradative Intermediates of L-ascorbic-1-C-14 Acid (1963)
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