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Explanatory letter recommending ascorbate supplement

Dr. XXXX I find you first among authorities on obesity, diabetes, and how to reverse them.  I have a medical website since 2004, 11 years of university studies in science and philosophy, over 4 years of full-time investigation into issues associated with diabetes, I counsel several diabetic to follow your dietary management of type-2 diabetes, and I strongly recommend that they buy your two books, watch your lectures, and become your outpatient.  My examination of journal articles and books, prior to discovering your lectures on YouTube, has lead me to the same major conclusions as yours.  Your work was one more confirmation of my hypothesis to which you added important details and evidence.  Recently I have come across in my research of the diabetes pandemic the role of low ascorbate which causes defective collagen that causes diabetic angiopathy and thus the comorbidities associated with diabetes.  What is your opinion thereon?  Assuming the correctness of my piecing together the evidence and that you too are aware of this analysis, do you recommend supplementation, which supplementation and what dose?  Do you check with your patients for low ascorbate in tissues that store very high levels rather than serum ascorbate?—serum ascorbate reflects dietary intake.    

As you know pharma which is in the business of treating illness, and this leads them to create a guideline protocol for treating a chronic with patented drugs.  Their fiduciary model causes the industry to prefer treating 1) symptoms, 2) down-stream abnormalities, 3) to create chronic conditions through their medication, and 4) not to cure the condition.  In my search of the results of their tobacco science, I have come across in May that diabetics have reduced amounts of ascorbate, that the measure of serum ascorbate only reflect recent dietary intake, that to uncover this shortage requires doing an assay of tissues/cells which store ascorbate such as lymphocytes, that ascorbate is essential involved in 7 biosynthesis processes, of particular importance is the production of collagen, that the production of defective collagen is very possible the major causal factor in the development of diabetic angiopathy, and the development of diabetic angiopathy is the major cause for the comorbidities associated with diabetes; thus low cellular ascorbate is what physicians ought to be treating and scientists researching.  Given that the tight management of serum glucose has failed in clinical trials to produce a reduction in the comorbidities associated with diabetes, the causal explanation that the diabetic’s higher level of serum glucose with its higher rate of glycation and the production of advanced glycation end products (AGE) is suspect.  Other evidence goes to debunk the putative key role of the pharma-favored role of serum glucose with its profitable tight management of serum glucose.  One journal article entitled 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 (J Clin Invest. 1997 Aug 15; 100(4): 839–846) doubts the role of glycation.  Below is part of that article’s abstract.  The article found that oxidative stress—looking at skin samples--is not the cause of uniquely high for the diabetics, and thus not the cause for collagen vector in the pathologies associated with diabetes.  There are hundreds of articles, 85% before the year 2000, that are on low ascorbate and its consequences, of which some favor pharma’s oxidative stress theory caused by low ascorbate, while other stress a much different role of ascorbate and collagen.  Unfortunately I have not found a seminal article that pieces together the journal articles, I have copied about a dozen such articles—see attachments. 

            I could pursue the topic further, but for the other demands of research and goals.  I am gathering together my research into a single volume like Prof. Peter Gotzsche recent books.  Assuming the correctness of this line of analysis ascorbate or diabetics of supplements, like that of taking CoQ10 if on a statin.  Do you advise increasing ascorbate intake, and how much?    

From abstract (  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.

Another abstract:  Abstract

The plasma and tissue concentration of ascorbic acid (AA) is reduced in diabetes. This study was designed to investigate the mechanism and significance of this phenomenon. The low plasma AA concentration of diabetic rats can be normalized by dietary AA supplement (20–40 mg/day), a dosage approximately equal to the maximal synthetic rate of this substance in the rats. Treatment of diabetic rats with this regime prevented the decrease in activity of granulation tissue prolyl hydroxylase (PRLase), an AA-dependent enzyme required for maintaining the normal properties of collagen. The decreased plasma AA concentration and granulation tissue PRLase activity in diabetes can also be normalized by the aldose reductase inhibitor tolrestat. We conclude that in diabetic animals there is a true deficiency of AA that may be responsible for some of the changes of collagen observed in diabetes. Treatment with AA or an aldose reductase inhibitor may prevent some of the diabetic complications with underlying collagen abnormalities.

From my notes:

Dietary myo-inositol supplementation was effective in normalizing plasma AA levels

aldose reductase inhibitor tolrestat.


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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]



Harvard Prof. Marcia Angell, MD., former Chief Editor of NEJM wrote: “We certainly are in a health care crisis, ... If we had set out to design the worst system that we could imagine, we couldn't have imagined one as bad as we have.”


The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment