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 lipo C vrs oral 
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Joined: Thu Apr 05, 2012 1:40 am
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Post lipo C vrs oral
With all the buzz around liposomal Vit C, I’ve been producing my own homemade Lipo C and taking a 2 gram dose a day. In line with the buzz, I’ve been expecting this to equal 5 times the oral dose, or a 10 gm equivalency, at least.

But this is not so, it would seem.

This is the first time I’ve seen a graph with actual measured data points, taken from:
Pharmacokinetics of oral vitamin C
STEPHEN HICKEY, HILARY J. ROBERTS, & NICHOLAS J. MILLER

This very clearly shows NO difference between oral and Lipo at 5 gm doseage. I don’t see why I should continue with producing Lipo C when oral does just as well at this maintenance level of intake.
Interesting, no?


Sun Apr 22, 2012 6:55 am
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Vitamin C Expert
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Post Re: lipo C vrs oral
robr wrote:
This very clearly shows NO difference between oral and Lipo at 5 gm doseage.

It merely shows little difference in the plasma level. It doesn't tell us what is happening at the intra-cellular level.

If the lypo-C is mostly being released first in or around the cells throughout the body then this could have dramatically greater efficacy than regular C first "hitting" the body via the digestive system.

Plasma levels are merely one small part of the big picture.

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Sun Apr 22, 2012 7:55 am
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Post Re: lipo C vrs oral
Quote:
I’ve been producing my own homemade Lipo C and taking a 2 gram dose a day


If this is your only source of vitamin C then you may be better off using the homemade vs the commercial product
as homemade encapsulation is roughly 70% if done right. Meaning the other 30% could be available extracellularly (outside the cell)

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Sun Apr 22, 2012 10:00 am
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Ascorbate Wizard
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Post Re: lipo C vrs oral
Can you remind me about that graph. (I cannot locate my copy of the Hickey/Saul book at the moment.) I remember a different graph, and I wonder about this one. Were both lines 5 grams of vitamin C? Meaning 5 packets of Lypo-C??

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Mon Apr 23, 2012 2:26 am
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Post Re: lipo C vrs oral
This is all they say - no reference to Live On Lipo C specifically:

"Figure 1 shows the response of the female subject to single 5 g doses of liposomal and
standard formulation vitamin C; both produced similar response curves. These results are
comparable in form and magnitude to those expected for oral vitamin C in previously
depleted subjects. However, peak values exceeded 220 mM L
21
, which has been reported as
the maximum value attainable with repeated oral doses of 3 g six times daily [8]. The
subjects were experienced users of high-dose vitamin C and neither suffered any
gastrointestinal effects at this dose level.5 "
This study was published in "Journal of Nutritional and Environmental Medicine" 2008, no month mentioned. I have it in pdf form.


Mon Apr 23, 2012 3:38 pm
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Joined: Thu Apr 05, 2012 1:40 am
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Post Re: lipo C vrs oral
VanCanada wrote:
robr wrote:
This very clearly shows NO difference between oral and Lipo at 5 gm doseage.

It merely shows little difference in the plasma level. It doesn't tell us what is happening at the intra-cellular level.

If the lypo-C is mostly being released first in or around the cells throughout the body then this could have dramatically greater efficacy than regular C first "hitting" the body via the digestive system.

Plasma levels are merely one small part of the big picture.

I'm not really sure what happens to lipoproteins absorbed through the lymph. I thought they had a short journey to the liver, where those little packages get ripped open and the contents spilled out. In any case that big part of the big picture isn't measurable, right? So would it be fair to say that what may or may not be happening with liposomal delivery intracellularly is based more on a conceptual model of expected behaviour than any quantitative information?


Mon Apr 23, 2012 3:54 pm
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Vitamin C Master
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Post Re: lipo C vrs oral
Quote:
"Figure 1 shows the response of the female subject to single 5 g doses of liposomal and
standard formulation vitamin C; both produced similar response curves. These results are
comparable in form and magnitude to those expected for oral vitamin C in previously
depleted subjects. However, peak values exceeded 220 mM L which has been reported as
the maximum value attainable with repeated oral doses of 3 g six times daily [8]. The
subjects were experienced users of high-dose vitamin C and neither suffered any
gastrointestinal effects at this dose level.5 "

Image

Increasing the dose of liposomal vitamin C to 20g gave a broader response, with
a delayed maximum, as shown in Figure 2. In this graph, the 20g liposomal dose is
compared with a 5g standard dose (male subject). With a 20g intake, the peak plasma
level was delayed and the response was broader, indicating a greater absorption of
vitamin C. The 5g data set shows a marked outlier (peak): this is attributed to the fact
that one of the (5g) blood samples was difficult to extract, with inflammation at the
puncture site, providing only a small sample. The subject experienced no bowel
tolerance effects at either of these intakes.

Image

Figure 3 shows plasma levels following a 36g dose of liposomal vitamin C, for
both subjects. This resulted in peak plasma levels, in the region of 400 µM/L. A 95%
interfractile range (34-114), which contains 95% of the distribution with a mean of 74
corresponds to a calculated standard deviation of 17.4. We note that, under these
conditions, an outlier measurement of 400 µM/L would correspond to a deviation of
10.3 σ with a theoretical p value of 1.6x10 -13 (i.e. P<0.0000000000001). With this high
dose, both subjects exceeded their bowel tolerance, leading to diarrhoea. This
intolerance presumably arose from the high intake of phospholipid, without food
buffering, in fasting individuals. However, our observations using hourly doses suggest
that daily intakes of this magnitude are tolerable without bowel effects, as long as the
dose is spread throughout the day.


Think it very strange they compared 5 gram of regular oral ascorbic acid to 20g or 36g liposomal only!?

Especially with the resulting serum levels of equal oral doses (5g) almost identical I would be most curious if this hold true for higher dose regular C too.


Last edited by pamojja on Wed May 30, 2012 12:22 am, edited 1 time in total.

Tue May 29, 2012 11:46 pm
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Vitamin C Master
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Joined: Sun Jul 26, 2009 7:44 am
Posts: 220
Post Re: lipo C vrs oral
But then there is this study which already shows that serum levels as high as 517 µmol/L can be have with regular oral ascorbic acid!

Quote:
Journal of the New Zealand Medical Association, 23-August-2002, Vol 115 No 1160
23-August-2002, Vol 115 No 1160

Glycohaemoglobin and ascorbic acid

Copplestone et al1 (http://www.nzma.org.nz/journal/115-1157/25/) identified misleading glycohaemoglobin (GHb) results due to a haemoglobin variant (Hb D Punjab) and listed a number of other possible causes for such false results (ie, haemolytic anaemia, uraemia, lead poisoning, alcoholism, high-dose salicylates and hereditary persistence of foetal haemoglobin).

We have observed a significant "false" lowering of GHb in animals and humans supplementing ascorbic acid (AA) at multigram levels. Mice receiving ~7.5 mg/d (equivalent to > 10 g/day in a 70 kg human) exhibited no decrease in plasma glucose, but a 23% reduction in GHb.2 In humans, supplementation of AA for several months did not lower fasting plasma glucose.3,4 We studied 139 consecutive consenting non-diabetic patients in an oncology clinic. The patients had been encouraged as part of their treatment to supplement AA. Self-reported daily intake varied from 0 to 20 g/day. The plasma AA levels ranged from 11.4 to 517 µmol/L and correlated well with the reported intake. Regression analysis of their GHb and plasma AA values showed a statistically significant inverse association (eg, each 30 µmol/L increase in plasma AA concentration resulted in a decrease of 0.1 in GHb).

A 1 g oral dose of AA can raise plasma AA to 130 µmol/L within an hour and such doses at intervals of about two hours throughout the day can maintain ~230 µmol AA/L.5 Similar levels could also be achieved by use of sustained-release AA tablets. This AA concentration would induce an approximate 0.7 depression in GHb. The GHb assay used in our study, affinity chromatography, is not affected by the presence of AA.3 Thus, unlike the case with Hb D Punjab, our results were not caused by analytical method artifact. More likely, the decreased GHb associated with AA supplementation appears related to an in vivo inhibition of glycation by the elevated plasma AA levels, and not a decrease in average plasma glucose.3 If this is true, the effect has implications not only for interpretation of GHb but also for human ageing, in which glycation of proteins plays a prominent role in age-related degenerative changes.

A misleading GHb lowering of the magnitude we observed can be clinically significant. Current recommendations for diabetics suggest that GHb be maintained at 7, a level that is associated with acceptable control and decreased risk of complications; when GHb exceeds 8, re-evaluation of treatment is necessary.6 Moreover, relatively small increases in average blood sugar (ie, GHb) can accompany adverse reproductive effects. A difference in mean maternal GHb of 0.8 was found for women giving birth to infants without or with congenital malformations.7 In either of these circumstances, an underestimation of GHb could obscure the need for more aggressive intervention.

Vitamin usage is common in New Zealand and after multivitamins, AA is the most often consumed supplement.8 Moreover, diabetics are encouraged to supplement antioxidants, including AA. Thus, it seems prudent for primary care health providers to inquire regarding the AA intake of patients, especially diabetics, when using GHb for diagnosis or treatment monitoring.


References:

Copplestone S, Mackay R, Brennan S. Normal glycated haemoglobin in a patient with poorly controlled diabetes mellitus and haemoglobin D Punjab: implications for assessment of control. NZ Med J 2002;115(1157). URL: http://www.nzma.org.nz/journal/115-1157/25/
Krone CA, Ely JTA. Vitamin C and glycohemoglobin revisited. Clin Chem 2001;47(1):148.
Davie SJ, Gould BJ, Yudkin JS. Effect of vitamin C on glycosylation of proteins. Diabetes 1992;41(2):167–73.
Paolisso G, Balbi V, Bolpe C, et al. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll Nutr 1995; 14(4):387–392.
Lewin S. Vitamin C: Its Molecular Biology and Medical Potential. New York: Academic Press; 1976.
Kenealey T, Braatvedt G, Scragg R. Screening for type 2 diabetes in non-pregnant adults in New Zealand: practice recommendations. NZ Med J 2002;115(1152):194–6.
Rosenn B, Miodovnik M, Dignan PS, et al. Minor congenital malformation in infants of insulin-dependent diabetic women: association with poor glycemic control. Obstet Gynecol 1990;76:745–9.
Allen T, Thomson WM, Emmerton LM, Poulton R. Nutritional supplement use among 26-year-olds. N Z Med J 2000;113(1113):274–7.


Tue May 29, 2012 11:52 pm
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