eDOC wrote:Dennyk, I'm assuming you are on oral VC and measuring the glucose readings using a meter...correct.
Generally, I recommend 1 hr prior or 2 hrs after a meal, but most of my patients never bother, take the required dose straight up, with none issues. Those on 30-60 mL/day to cover a flareup, take approx 3-5 liters of water per day, during that period.
eDOC wrote:I'm doing fine, very occupied, might not be frequent visitor till end March.
Dennyk wrote:Yes on the VC. I take 4 grams, 4 or 5 times/day. And I'm measuring Glucose, (blood sugar) with a finger prick and simple meter. I am certain my water intake has been lacking badly, but have really picked it up due to your comments/reminder. My thanks again. Have been back at 15 ml twice a day on DMSO, and feeling great.
Want to wish you well, and good luck on whatever your upcoming adventure might be.
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eDOC wrote:Dennyk, I'm glad your feeling better with fewer or non headaches. Hope your labs are better too.
I doubt that your sugar is high, but is rather low, if checked in a lab.
Dennyk wrote:My A1c went up to 6.3 from 6.0, but like I said I have not been following my low carb diet which can keep it under 6. Not sure why it didn't come down as expected from the DMSO. Does this back Owen's thoughts that VC is detected as glucose?
Journal of the New Zealand Medical Association, 23-August-2002, Vol 115 No 1160
Glycohaemoglobin and ascorbic acid
Copplestone et al1 (http://www.nzma.org....al/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.
HbA1c doesn't measure glucose directly, it measures glycated Haemoglobulin, which does of course gets glycated by the average glucose levels in the blood, but not by vitamin C at all. On the contrary, while measured blood glucose might give higher values due to vitamin C, Hb1Ac on the contrary is lowered by high enough vitamin C intake.
Dennyk wrote:I tried switching to a more alkaline diet, which included a lot more carbs, so I guess the higher number makes sense.
Dennyk wrote:I also noticed that while my total cholesterol, and LDL came down very nicely, my triglycerides went up from 181 to 253 mg/dl. Could this be from all the lecithin in my lipo C ? I'm trying to understand as much as I can, but It's still pretty confusing to me. So many trade offs, and so much conflicting info out there.
pamojja wrote:Dennyk wrote:I tried switching to a more alkaline diet, which included a lot more carbs, so I guess the higher number makes sense.
Why that? I'm on a low carb diet and my blood repeatedly showed alkalosis.
I guess I was trying to focus on a better diet for cancer.
Dennyk wrote: I'm stopping completely the Vitamin A, to see if lab results improve. My doctor has ordered for a repeat test in 30 days. If anyone sees flaws in my logic, I would appreciate the feedback.
In general, acute toxicity occurs at doses of 25,000 IU/kg of body weight, with chronic toxicity occurring at 4,000 IU/kg of body weight daily for 6–15 months. However, liver toxicities can occur at levels as low as 15,000 IU (4500 micrograms) per day to 1.4 million IU per day, with an average daily toxic dose of 120,000 IU, particularly with excessive consumption of alcohol. In people with renal failure, 4000 IU can cause substantial damage. Signs of toxicity may occur with long-term consumption of vitamin A at doses of 25,000-33,000 IU per day.
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