Recommended Diabetes

Home | Fructose the starting point | Low Carb diet to treat type-2 diabetes | Bad Medicine Diabetes--Des Spence | Bad Medicine Diabetes--Des Spence | THE CAUSES: Fructose, insulin resistance, ascorbate, and collagen | More Jounral articles on COLLAGEN and its role in diabetic pathologies | Ascorbic acid diabetes studies | Journal articles on polyol pathway and ascorbate | Ascorbate role and not hyperglycemia is pathogenic | Explanatory letter recommending ascorbate supplement
THE CAUSES: Fructose, insulin resistance, ascorbate, and collagen

The pathway to diseases of the western diet:

The high sugar diet—mainly the reactive sugar fructose--overwhelms the liver’s repair system for glycation (attachment of sugar molecules to proteins, which hinders the functions of those proteins).  Frequent high levels of glucose exacerbate glycation by fructose in the liver.  This damage to the liver causes insulin resistance in the liver, and with insulin resistance comes through higher than normal levels of insulin and through de novo lipogenesis in the liver.  Since insulin promotes fat storage high levels of insulin promote excessive fat storage in the liver.  This results is a fatty liver, and that causes insulin resistance most significantly in the muscle and fat cell   A net result of the inflamed liver is a reduction of stored ascorbate which adversely affects the production of collagen.  One of the main functions of vitamin C is as an enzyme in the production of collagen.  The greater the insulin resistance the greater the negative effects upon the quality of the synthesize collagen.  Among the cells affect are the endothelial cells of the artery walls.  As gatekeepers (barriers) for blood borne substance, endothelial dysfunction promotes atherosclerosis.  Other tissues that have poorly synthesized collagen are more prone to the age related degenerative diseases associated with the western diet.   

Pharma being pharma promotes tobacco sciences that places the blame on high levels of blood glucose.  Thus their  sales reps, key opinion leaders, miss-educated physicians, and corporate media recommend tight glucose management through drugs (a low carb diet is a much better way to reduce blood glucose and dependence upon drugs).

I am not claiming that other factors aren't contributory, such as carbon monoxide, the reactive sugar galactose, to name but two.  I am claiming the based on a wide variety of evidence that the above is the leading cause.  And elsewhere I have set out the dietary fix for diabesity (the term that has been coined by others to name the interrelated conditions of diabetes and obesity).  New to my writings as of June 2017 is the role of defective synthesis of collagen and the role of ascorbate.  Earlier articles therefore on related topics are in need of modification. 

 


Rats synthesize ascorbate, thus a poor model. 


Testing for vitamin C is flawed since serum levels reflect current diet.  Testing should be done on tissues, specifically leucocytes which store about 100 fold the level of ascorbate.  Few hospitals/labs are equipped for such analysis and staff is not familiar with the procedure.   

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Couldn’t find INSULIN RESISTANCE and ASCORBATE in Google Scholar search, though in that search there were articles on collagen and diabetes (7/3/17)

 

Seems like pharma has research and treatment going down stream AGAIN, rather than dealing with the basic cause of low ascorbate and defective collagen and the effects upon insulin resistant and diabetic patients, pharma has framed the discussion to focus on glucose and glucose management with drugs (not diet).  Thus much of the research fails to measure the level in the cells that store for good reason between 10 and 100 fold the blood level of ascorbate.

 

Suspect is pharma in that the research into vitamin C’s role after 1998 is greatly reduced.   Pharma pushes the pro-drug high glucose theory for diabetic comorbidities.  Type 2 diabetes is a development of the precondition of insulin resistance.  Cells in the body, first starting with the liver and most significantly next occurring in the myocytes and adipocytes (fat and muscle cells) in which sensitivity of the glucose receptors on the cell walls to the as to the active transport of serum glucose is diminished.  The pancreas responds by secreting more insulin to cause a normalization of serum glucose.  Over often decades there is a gradual accumulation of fat in the pancreas which when sufficient causes a significantly diminished production of insulin.  This drop in production, typically over a period of 6 months, sometimes several years, will eventually produce symptoms of type-2 diabetes and show up on routine blood work which monitors fasting glucose.  Evidence: the conditions of western diet are strongly associated with insulin resistance, but not early stage diabetes.  It is held by researchers that the comorbidities associated with late stage (injecting insulin) are a result of the insulin and the accompanying obesity, and possible the accumulation of side effects from the cocktail of drugs given to lower glucose over the course of type-2 diabetes.  More evidence:  the 80% who are cured of type-2 diabetes through bariatric surgery subsequently have similar risk factors as those who never became diabetic (the remaining 20% of bariatric surgery patients).  Third evidence comes from those who are cured of type-2 diabetes through low carb diet with fasting, their risk factors return to a level similar to those who aren’t diabetic.  Both these show that the elevated insulin and glucose have not resulted in permanent damage.  A fourth bit of evidence comes from the tight management of glucose with drugs, it causes an increase rather than decrease in conditions associated with type-2 diabetes.  A fifth bit of evidence is that peoples on a high carb diet but with low sugar don’t get the conditions associated with the western diet, and this includes the oriental populations such as the Japanese who get the majority of calories from the refined carbohydrates white rice and noodles (around 70% of calories) because they average 14 grams of sugar daily.  The upland natives of Borneo, and those on the Island of Katava have an even higher percentage of carbs, yet their elderly living on the traditional diet have a very low incident of the conditions associated with the Western diet.  On this diet the Japanese and Okinawans are the longest lived of peoples from the developed nations.  The introduction of high sugar foods in all these peoples who had a high carb diet is producing in them the diabesity and obesity.  Thus for these and other reasons, the high starch diet—thus high periods of serum glucose--is not pathogenic.  All this and more supports the belief that exposure to dietary glucose is NOT pathogenic.  This support the research that defects in vitamin C utilization as an enzyme in the production of collagen is what causes the conditions associated with the western diet, and that mere insulin resistance is like type-2 diabetes a cause for these conditions. 

Unfortunate, as of this date (7/6/17) I have not found on point study on collagen and insulin resistance.  I will shortly be off the a university medical library to access their more extensive data base.  Corporate greed has made medical research a burden upon medical libraries, and explains why even large public library don't subscribe to the only line medical journal.  Several corporations have bought on most of the medical and other academic journals, and have placed a huge burden upon our university libraries.   Like all things in our corporatist world profits is the measure.  Impediments to learning and science are well documented, including medical research, but that is not a issue to be raised by politicians and our corporate press.  In 2007 I reviewed this issue at http://www.skeptically.org/id12.html 


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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.”

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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