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Part 2

No argument that blood sugar must be lowered or that damage is being done as long as it is raised.  Is increasing blood insulin the only—or even the best way to lower blood sugar?
Should this protocol be examined?  If it is known that weight loss most often virtually reverses diabetes, why not treat the obesity first in a motivated patient?

From the brief history above—this seems to be working for me, whereas standard ADA guideline driven treatment simply did not. The ACCORD study results are interesting in this respect.   The following words were excerpted from the conclusions of this research:

“our study has identified a previously unrecognized harm of intensive glucose lowering in high-risk patients with type 2 diabetes mellitus and high glycated hemoglobin levels. This harm may be due either to the approach used for rapidly lowering glycated hemoglobin levels or to the levels that were achieved. Our findings highlight the importance of conducting trials with sufficient statistical power to assess commonly used approaches on clinically relevant outcomes”

In the methods section of this study, it will be seen that almost all of the pharmaceuticals used to achieve the “aggressively lowered” HgA1c goals were insulin or beta cell stimulants.  Could this “previously unrecognized harm” be high insulin levels?

There are new drugs on the horizon that, like Metformin, do not work by raising blood insulin levels.  SGLT2 blockers lower blood sugar by preventing re-absorption of glucose by the kidneys effectively lowering blood sugar directly and significantly.  These drugs are in the final stages of testing with the FDA.  There were some breast and bladder cancers in one experimental group, although overall cancers were the same in the control group.  Other similar drugs have had trials with no significant cancer differences between groups.
Another very important class of drugs are glucagon receptor antagonists.  These attach to hepatocytes at glucagon receptor sites, thereby making these sites unavailable to glucagon, thus preventing release of glucose.  Testing so far has demonstrated encouraging results as to safety and efficacy.

These drugs bring down blood sugar in a very substantial way without raising insulin to such high levels that it may be doing severe vascular damage aside from preventing the patient from losing weight.  The obesity alone is well known to cause serious health problems both in diabetics and non-diabetics.

The fact that the metabolism of sugar is only a part of metabolism in its entirety is a fact rarely, if ever acknowledged, let alone addressed in treatment planning.  I have never discussed my diet in terms of my metabolic rate, or my ability to adapt to a lower caloric intake at a visit with my diabeticion.

According to the generally accepted Harris-Benedict Equation for calculation of BMR, my daily resting requirement is 2410 calories, as a moderately active individual, around 2900.  During more than a year before beginning “insulin therapy”, I had consistently lost weight on a diet of around 2000 calories per day and also in the 4 months since discontinuing “insulin therapy”.  I virtually lost no weight during almost 2 years on the ADA regimen.

I believe that it is reasonable to ask the question: “Should the ADA, clinicians and the FDA critically review the treatment of the approximately 60 plus percent of type 2 diabetics who are obese?”

Can other than “insulin therapy”, be considered for use in lowering blood sugar? 

Might SGLT2 inhibitors and glucagon receptor antagonists with or without much lower doses of insulin or insulin producing drugs achieve ideal blood sugar goals with sharply lowered morbidity and mortality?  A large number of studies, including the ACCORD study, suggest this should be so.

Sulfonylureas (approved by the FDA) kill beta cells.  When already stressed, overworking beta cells are further pushed by drugs to release more insulin, some of the insulin released is not fully mature.  This pre-insulin is not nearly as physiologically active as insulin released under less stressed conditions. 

Is some of the “insulin resistance” really about impotent insulin?

It would be instructive to see a study having a control group treated with current ADA guideline insulin therapy and an experimental group treated with an FDA 3^rd phase approved SGLT2 blocker and an appropriate glucagon blocker.  Both groups would have Metformin available. Of course both groups would be controlled for similar diet and exercise habits as well as other important lifestyle factors.  Many completed studies would predict very different morbidity and mortality statistics between the groups.   Perhaps the FDA should consider fast-tracking a study having such a huge potential for reducing loss of life and limb.

Diabetes is an enormous burden on health care resources.  Some say it has the potential to bankrupt the health care system.  Same old, same old treatment isn’t cutting it.  The quicker we can start thinking out of the box, the quicker we can stop putting people in them.

This is very thought-provoking information. I feel we are on the cusp of a breakthrough that may equal Dr. Banting's discovery of insulin.

I have many patients who are on the sulfonylureas. I have known that secretagogues use up beta cells leading to beta-cell exhaustion but I had never heard of the higher death rates. If a person cannot tolerate metformin for whatever reason, is there a low-cost alternative that could be prescribed? It seems all the newer drugs are cost-prohibitive for many PWD.

Roxy

Drugs that move off patent protection become inexpensive.  That is the case with metformin and the sulfonylureas.  I always refused sulfonylureas, not only because of their reputation for heart attacks and excess mortality, but the evidence seems to suggest that they on average fail after 1-4 years.  Other medications, even metformin are much more durable.  And I don't know of any other oral medications that have moved to generic status in the US.

Yes, there is another protocol that has been in use by diabetics since the early 1980’s. There are three areas that are addressed immediately after the tests are done to determine the extent of complications already present that need to be addressed in addition to the diabetes. Area (1)”Preserve beta cells”,(2)”Treat the symptoms”,( 3)”Prevent or Reverse the complications”.  The treatment plan is tailored to the individual, but basically it includes diet, +/or  weight loss, +/or  exercise, +/or  oral sensitizing or insulin-mimetic agents, +/or  insulin and the goal is Normal Blood Sugars (70-100) over the course of the day and into the night.  There is no room for sulfas. The intent is to empower the patient through education, negotiating adjustments as needed, and giving them the skills needed to deal with future obstacles to maintaining normal numbers.

Because the diet only includes 6 carbs for breakfast, 12 for lunch, and 12 for dinner, and if you exercise strenuously or can handle it an additional 6-12, the beginning dose of insulin is quite small. The rule of thumb is: Small doses of medication results in small mistakes that are easily corrected. Since insulin is the most potent fat-building hormone, reducing the dosage can help with weight loss but even more important it is insulin that helps the cell receive important nutrients for survival. If you need insulin to cover the “Dawn Phenomenon” but the diet and exercise and medications normalize the rest of the day, that will go a long way towards saving those beta cells till the cure arrives at our feet. Many who begin on insulin titrate off it as weight and insulin resistance improves. Others will always need it due to autoimmune components of the disease. But the amounts are small doses compared to what is needed with 45-60% of calories as carbs, even if they ARE so full of fiber.

Small doses of carbohydrates results in fewer glucose spikes and takes advantage of the type 2’s slow-acting insulin’s (either endogenous or exogenous) ability to do its work. We don’t want more than the body needs because the fat cells with the help of insulin transform the rest into saturated fat we end up sitting on!