6 replies to this topic

[brosci]

I've read that vitamin C is beneficial for reducing advanced glycation end-products.  Would it be useful to supplement ascorbic acid before a carbohydrate-rich meal?  (I've read the half life is only around 30 minutes and glucose competes for absorption.)  Are there better natural supplements / timing for this purpose?

Edited by brosci, 07 August 2015 - 02:48 AM.

[OneScrewLoose]

I really doubt this. I would need to see multiple, high impact factor studies to back this up.

There is a supplement known to do this though. It's called Benfotiamine.

[brosci]

I've also read pomegranates help to reduce glycation?  (Although, it seems like that would add extra sugar to the fire?)

 

http://www.ncbi.nlm....pubmed/24433074

 

These results demonstrate that pomegranate juice and two of its major constituents are potent inhibitors of fructose-mediated protein glycation.

 

Benfotiamine looks interesting, although I'd prefer something a bit less synthetic:

 

http://www.longecity...ncer-risk-quit/

[pamojja]

I've read that vitamin C is beneficial for reducing advanced glycation end-products.  Would it be useful to supplement ascorbic acid before a carbohydrate-rich meal?  (I've read the half life is only around 30 minutes and glucose competes for absorption.)

 

In my experience I found it useful to supplement high-dose ascorbic acid only before a low-carb meal - if giving any value to the measurements of postprandial blood-glucose.

 

Though the full text isn't anymore found at the journal of the New Zealand Medical Association, had it pasted in an other thread and repasted it here:
 

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.

 

Despite being on a moderately low-carb diet (~70 g) since measuring 6 years, my average blood-glucose (once fasting, and twice postprandial after my 2 meals each day) has been 117 mg/dl. Which should give an average HbA1c of about 5.7%. Mine, while having been supplementing 20 g/d of ascorbic acid, has actually been 5.1% only (even including the once off value of 6.2% while for 6 weeks in a high-carb country and experimenting with Metformin).

 

I really doubt this. I would need to see multiple, high impact factor studies to back this up.

There is a supplement known to do this though. It's called Benfotiamine.

 

We'll never see multiple, high impact factor studies for non-patentable nutrients, the less with higher doses. They'll continue to become less..
 

[Supierce]

Glycine is a potent attenuator of post-prandial glucose response:

http://ajcn.nutritio.../76/6/1302.full

[brosci]

Glycine is a potent attenuator of post-prandial glucose response:

http://ajcn.nutritio.../76/6/1302.full

 

Very interesting, I found this article as well: http://www.sciencedi...878331713000508

 

I'm curious if there's an ideal approach timing?   (Glycine on an empty stomach 30m before a carb-rich meal?  Glycine with the meal?  After?)  Or, perhaps the timing is irrelevant if these types of foods / supplements are regularly consumed daily.  It feels a little counter-intuitive to consume a pure-protein supplement with a sugar/carb rich meal to prevent the formation of protein/sugar bonds.

Edited by brosci, 07 August 2015 - 11:21 PM.

[Kevnzworld]

The standard antiglycation supplements are :
Carnosine
Benfotiamine
B6
Vitamin C
Glycine