Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

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Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

Post Number:#1  Post by ofonorow » Sat Jun 30, 2018 7:30 am

The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

https://wholefoodsmagazine.com/columns/vitamin-connection/the-science-of-vitamin-c-research-on-optimizing-blood-and-cellular-levels/
Passwater: This appears to contradict NIH claims that oral vitamin C will not help cancer patients and IV is necessary.

Hickey: For fun we can use the NIH data to show once again that they are wrong. They provide a chart to indicate the killing of Burkitt’s lymphoma cells by increasing concentrations of vitamin C. (Please see figure 5.) It shows how a very short exposure to dynamic flow levels of vitamin C can kill cancer cells. The chart shows that 0.3 mM/L (300 µM/L in the units we are considering) kills these cancer cells. Importantly, adding some other supplements increases the selective cancer killing of vitamin C, for example alpha-lipoic acid enhances the effect by a factor of 5-10 times.
Owen R. Fonorow, Follow #OWENRFONOROW at twitter

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Re: Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

Post Number:#2  Post by zarfas » Sat Jun 30, 2018 8:24 am

couple questions that I get asked/havemyself:

1
how does vit C kill cancer cells and not harm normal cells

2 is IVC the only way to get vit C to the level needed to kill cancer cells

3
is diarreha the only downside to "tons" of vit C?

4
Why does lots of vit C make me have to pee more and not have much fluid when I do pee, drink more water?

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Re: Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

Post Number:#3  Post by tjohnson_nb » Thu Jul 05, 2018 1:34 am

My understanding is that high ascorbate concentrations cause H2O2 to accumulate in cancer cells because they lack catalase and so apoptosis is induced.
'Always' and 'never' are 2 words you should always remember never to use.

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Re: Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

Post Number:#4  Post by pamojja » Sat Jul 07, 2018 3:26 pm

Hickey: With standard ascorbic acid taken orally the maximum plasma level seems to be in the region of 250 µM/L.


Does anyone actually know the contact of Hickey to inform him that levels of 517 µmol/L have actually been measured with daily intakes of 20 g AA:


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.

Cheryl A Krone
Senior Research Scientist
John TA Ely
Director
Applied Research Institute
PO Box 1925
Palmerston North

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....al/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.


(red emphasis by me)

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Re: Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

Post Number:#5  Post by Ralph Lotz » Thu Aug 09, 2018 10:26 pm

pamojja wrote:
Hickey: With standard ascorbic acid taken orally the maximum plasma level seems to be in the region of 250 µM/L.


Does anyone actually know the contact of Hickey to inform him that levels of 517 µmol/L have actually been measured with daily intakes of 20 g AA:


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.

Cheryl A Krone
Senior Research Scientist
John TA Ely
Director
Applied Research Institute
PO Box 1925
Palmerston North

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....al/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.


(red emphasis by me)



I'm sure that both Owen and Bill Sardi can contact Steve Hickey. He may be aware of this study from Ely and Krone.
Can you please completely spell out the URLs where the study is posted? Clicking on the links highlighted in your post didn"t work.
Thank You!
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Re: Steve Hickey: The Science of Vitamin C Research on Optimizing Blood and Cellular Levels

Post Number:#6  Post by pamojja » Fri Aug 10, 2018 5:13 am

Ralph Lotz wrote:Can you please completely spell out the URLs where the study is posted? Clicking on the links highlighted in your post didn"t work.
Thank You!


The original location where I found this study many years ago was:

Code: Select all

http://www.nzma.org.nz/journal/115-1160/156
http://www.nzma.org.nz/journal/115-1160/156

However, it has since a long time disappeared behind a paywall, the abstract seems to be found here now: https://www.ncbi.nlm.nih.gov/pubmed/14962639 (though with slightly different title and content)
Full text here: https://www.medical-hypotheses.com/article/S0306-9877(03)00313-X/fulltext


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