Very important: More evidence that it isn’t high serum glucose that drives the pathologies and thus justifies the tight management of serum sugar, but rather supportive of low ascorbate and defective collagen that is driving those pathologies. It is the cholesterol myth all over again only this time it is blood sugar.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC508256/ J Clin Invest. 1997 Aug 15; 100(4): 839–846.

Age-dependent increase in ortho-tyrosine and methionine sulfoxide in human skin collagen is not accelerated in diabetes. Evidence against a generalized increase in oxidative stress in diabetes.

The glycoxidation products Nepsilon-(carboxymethyl)lysine and pentosidine increase in skin collagen with age and at an accelerated rate in diabetes. Their age-adjusted concentrations in skin collagen are correlated with the severity of diabetic complications. To determine the relative roles of increased glycation and/or oxidation in the accelerated formation of glycoxidation products in diabetes, we measured levels of amino acid oxidation products, distinct from glycoxidative modifications of amino acids, as independent indicators of oxidative stress and damage to collagen in aging and diabetes. We show that ortho-tyrosine and methionine sulfoxide are formed in concert with Nepsilon-(carboxymethyl)lysine and pentosidine during glycoxidation of collagen in vitro, and that they also increase with age in human skin collagen. The age-adjusted levels of these oxidized amino acids in collagen was the same in diabetic and nondiabetic subjects, arguing that diabetes per se does not cause an increase in oxidative stress or damage to extracellular matrix proteins. These results provide evidence for an age-dependent increase in oxidative damage to collagen and support previous conclusions that the increase in glycoxidation products in skin collagen in diabetes can be explained by the increase in glycemia alone, without invoking a generalized, diabetes-dependent increase in oxidative stress.

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Misses ascorbate role in production of collagen, and this is likely more of an issue that oxidative stress.

http://care.diabetesjournals.org/content/diacare/27/10/2491.full.pdf Diabetes Care, Vol. 27, Oct. 2004

Lymphocyte and Plasma Vitamin C Levels in Type 2 Diabetic Patients With and Without Diabetes Complications

Diabetes has been considered to be associated with oxidative stress. It has been suggested that increased free radicals and decline of antioxidant defense mechanisms induce diabetic micro- and macrovascular complications (1–3). Vitamin C is one of the major antioxidants and is detected in various blood components (4). However, measurements of vitamin C levels have shown inconsistent results, and the interpretation of vitamin C levels in diabetes as an antioxidant biomarker has not been clarified (5–8). In this study, we investigated the lymphocyte and plasma vitamin C levels in type 2 diabetic patients with and without diabetes complications.

CONCLUSIONS — Increased oxidative stress in diabetes could contribute to depletion of antioxidants such as vitamin C (2,3). In this report, we demonstrated that the lymphocyte vitamin C level is significantly lower in type 2 diabetic patients, but we could not observe such an association in plasma vitamin C levels. The plasma concentration of vitamin C is considered to be strongly correlated with transient consumption of foods such as fruit, supplements, and vegetables (4).

RESULTS — The lymphocyte vitamin C level in diabetic patients was significantly lower than in control subjects (18 4.5 vs. 28 7.9 nmol/mg protein, P

0.0001), whereas the plasma vitamin C level was not different (59 19 vs. 53 18 mol/l, P 0.17) (Fig. 1A and B). There were no significant linear correlations between the lymphocyte and plasma vitamin C levels in diabetic patients (r 0.011, P 0.95) as well as in control subjects (r 0.14, P 0.35). The lymphocyte vitamin C level in diabetic patients with complications was significantly lower than in those without complications (17 3.3 vs. 21 5.4 nmol/mg protein, P 0.011) (Fig. 1C), whereas the plasma vitamin C level was not different (59 18 vs. 59 21 mol/l, P 0.97). CONCL

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Testing for levels[edit] [Laboratory testing reflects recent dietary intake, not storage--jk].

Simple tests use dichlorophenolindophenol, a redox indicator, to measure the levels of vitamin C in the urine and in serum or blood plasma. However these reflect recent dietary intake rather than the level of vitamin C in body stores.^[45] Reverse phase high performance liquid chromatography is used for determining the storage levels of vitamin C within lymphocytes and tissue. It has been observed that while serum or blood plasma levels follow the circadian rhythm or short term dietary changes, those within tissues themselves are more stable and give a better view of the availability of ascorbate within the organism. However, very few hospital laboratories are adequately equipped and trained to carry out such detailed analyses, and require samples to be analyzed in specialized laboratories.^[109][110] https://en.wikipedia.org/wiki/Vitamin_C#Deficiency

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