Allies Voice: Bad research endangering Type 2s and non-diabetics alike
I don't intend to create a revolt for treating Type 2 diabetes with analogues - but I do intend to raise a few questions to prevent unnecessary deaths like the loss of Tim Russert. The new trend Novo Nordisk is attempting to set in diabetes treatment for Type 2 is analogues first. The theory is scientifically unsound and the research was flawed, at best. A study recently published questioned the intensive treatment approach for Type 2 diabetes. Results of this study found tight blood glucose control offered no added protection against heart attack and stroke. Novo proceeded with their "catch it early" campaign despite another study published earlier this year that previously confirmed the same results from aggressive Type 2 treatment. Before entrusting your life to the promise of analogues - you deserve full disclosure.
First rule of proving the value of therapy is to have a fair "control group". In this particular study - the "control group" was TREATED with oral diabetes medications. If you're using a drug to "control" the situation - it is illogical to assume you have a control group. I'd settle for pseudo-control group for supporting the truth behind this research.
The other beef I have with this study is assuming the patient has diabetes. Was this a 1 time glucose check or was it a 3 month snapshot via HbA1c? For an explanation of why this matters - please watch the video. You'll also get a few though on the untimely and unnecessary death of Tim Russert.
Also - how did the physicians qualify the treatment for a participant? Was the patient was thoroughly evaluated (stimulated C-peptide, antibodies present, HbA1c, etc.)? If so - the choice of treatment would have a direct correlation to the outcome. If antibodies were present - it seems if you wanted to show a definite result of diabetes in 1 year - you would assign these patients to the oral med group. Although this is a legal violation of the Hippocratic Oath (prescribing a medication that would DO HARM) - I'm sure the payoff was worth it for Novo. After all - they are running that campaign to get all people in the whole wide worth on analogues.
My lay interpretation of this study is that 51% (possibly 92%) of the 381 patients were experiencing transient elevated glucose to begin with. This means that if they had remained "untreated" the approximate 4 to 7 days they spent on diabetes treatment would have produced the same outcome without treatment. The morning fasting blood glucose of 126 mg/dL is not a fair threshold to diagnose DIABETES.
Was there a true control group in this study? I.e.) no treatment whatsoever? I also wonder what the diagnosing HbA1c was - and what it was when the study ended.
This study without a control is nothing more than a RUSE to justify the new Novo Nordisk A/S campaign for analogue treatment for Type 2 - another diabetes marketing scheme. And by the way - the whole wide world needs to know this is NOT insulin. Eli Lilly, Novo Nordisk, and Sanofi-Aventis sells ANALOGUES. It is NOT just like human insulin. It is a confusing foreign protein that lowers blood glucose. Well get back to this - but when the body perceives glucose levels are too low - it attacks any endogenous insulin (first) because it knows how to create the homegrown insulin - it knows how to create the antibodies to destroy it.
When the body no longer has the ability to destroy what no longer exists (aka analogue-dependent diabetes) it begins to create resistance at the insulin receptor cells. This is why Type 2 diabetics start increasing their dose to override the resistance to the analogues. Please forgive my redundant reference - mo' analogue, mo' money, mo' problems (Tim Russert).
The hook, line and stinker of this fishy research is the fact that a patient starting insulin therapy is not likely to see his or her doctor for at least a month. It is likely he/she will continue on the analogue for 30 days before visiting their doctor. By that time - the body will have begun creating insulin antibodies or islet cell antibodies to assist in destroying any endogenous insulin production - therefore REQUIRING the analogue dose to increase. This foreign analogue will also create the insulin receptors to shut-down to prevent HYPOGLYCEMIA . Believe me when I tell you - HYPOGLYCEMIA is far more traumatic to the body than hyperglycemia. Remember - those who still have functioning beta cells have C-PEPTIDE TO PROTECT FROM COMPLICATIONS OF DIABETES.
It is a common phenomenon for many Type 2s to begin on a dose that gradually doubles and even TRIPES. This could be evidence that endogenous insulin production is overridden by analogue therapy. A stimulated C-peptide test could confirm this hypothesis. The bottom line here is: less endogenous insulin production means less C-peptide and more vulnerability to the complications of diabetes.
[On any given Sunday - a person who does not have diabetes can have a blood glucose of 50 mg/DL or 500 mg/dL. The reason they do not experience complications of diabetes is because their beta cells function! Analogues override and prevent the healthy function of beta cells.]
I never said Big Pharma was stupid - in fact they're just brilliant at marketing studies to sell their products. I just hope this one doesn't dupe medical professionals the same way the "Humulin" insulin campaign did in 1983.
Increasing diagnosis, increasing complications, and higher costs -- who's benefiting here?
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Great post! I’m sure you recognize that the 3 stooges (3 amigos, 3 musketeers), our charitable representatives, most major universities, and even practicing medical personnel would castigate everything you have just presented. In fact, there are several blog sites which already have challenged unknowing diabetics to pay greater sums of money for treatment/management based on ‘arranged’ research results. They get a pat on the head (preferential treatment) for the excellent control they achieve/espouse, and elevate their standing to become ‘opinion leaders’ and oracles for the internet community. For example, treating people with insulin who (may) never have actually been ‘diabetic’ in the first place, gives the appearance of a wunder-cure. The kick in the ass for the patient comes later when they discover that rDNA insulin destroyed beta cell function and any hope for a return to normalcy. When these ‘newbies’ and ‘probies’ finally realize how they are being manipulated, they can join us (long-standing T1’s) in gazing at the horizon where a cure supposedly rests. When government, schools of higher education, the FDA, and all other influential parties have been BOUGHT by the pharmaceutical industry (3 stooges referenced above). There is no doubt this masquerade they so quietly employ is nothing more than a sham to drive up medical costs, and leave the patient without adequate information until it’s too late.
Most people don’t realize that the revered DCCT study results included the fact that only 5% of all participants could maintain “normal” HbA1c’s. Of course, the other results, like hypoglycemia unawareness, exacerbation of complications, sudden death, and diminished quality of life were not even factors playing into the approval of rDNA insulins and analogs for mainstream protocol. Additionally, one must marvel at the 3 stooges’ selection of patients for this study—they were ONLY the better candidates; those with ANY downside were dismissed from the study.
As you have stated, the first rule in a fair research design is to have a ‘control’ group—which represents the ‘normal’ population. Otherwise, when the control group is treated with oral meds (which are already known to cause serious problems), the ‘new’ treatment for comparison stands a much better chance to come out labeled “the winner.” In the case of rDNA insulins and analogs, they have not even been forced to make comparisons to anything except their own lesser rDNA insulin products—disregarding those factors which are most important in the daily life of a diabetic.
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actually, tim russert did not have diabetes. that was a rumor. additionally, he had a pre-existing condition (asymptomatic coronary artery disease) which he was managing with diet and exercise, so he did not, as you say, "drop dead." that is not to doubt the nature of such a tragedy, but diabetes doesn't seem to have played a part in his death.
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"Russert was known to suffer from atherosclerosis (aysymptomatic coronary artery disease)...He was also a diabetic." It was also reported that he successfully passed a stress test given in April.
http://www.lawyersandsettlements.com/articles/10773/avandia-sales-drop.html
Headline: Many Die Of Heart Attacks Without Prior History Or Symptoms
Link: http://www.sciencedaily.com/releases/2008/06/080616124938.htm
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While I agree that the study was flawed at best, I am a bit concerned about your belief that a fasting blood glucose of 126 is not "real diabetes". Our understanding of the human body is that damage occurs when fasting blood glucose levels are consistently over 100 mg/dl. Also, IIRC, cRp is only an effective measure when trying to distinguish between autoimmune diabetes and insulin resistance/IGT diabetes.
However, I do believe that patients presenting close to "non-diabetic" and "pre-diabetic" levels should be given a trial by intense lifestyle management before pharmaceutical intervention (of any sort) is introduced.
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Very little is in fact known about the effect of hyperglycemia in various ranges on the patient's morbidity and mortality. Since the human body is a machine which has been fine-tuned by over a million years of evolution to expend energy to maintain internal homeostasis only when necessary, the fact that in normal individuals the body is designed to allow blood sugar to rise to 130 after a meal is a strong indication that this level is not toxic. Conversely, if it is significantly toxic, then the whole strict control regimen for type 1 patients is pointless, since no amount of intervention can keep the blood sugar level under that limit in those patients.
Generally you will find that as the surplus of endocrinologists and diabetologists grows, the number of patients who, for purely economic reasons, have to be defined as having a 'diabetic' or a 'pre-diabetic' blood glucose range has to be correspondingly increased. This is most simply done by changing the goal posts and definining lower and lower blood sugar levels as 'diabetic.' The same trick is being performed in support of the AIDS industry, and when the rise of AIDS cases in Africa ceased to keep pace with what the media hysteria and drug companies required, the goal posts were shifted and a whole range of diseases were defined as symptomatic of AIDS as long as they occurred in Africa, from tuberculosis to chronic diarrhea.
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Sanktpauli--
Thank you for your eloquent, focused response (you saved me a bunch of keyboarding.) I particularly appreciate your spotlighting the shifting of goal posts, as I feel that this ploy is widely used by pharma and doctors, and not necessarily for 'humanitarian' reasons.
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I suspect you and your colleagues believe that you are more qualified than the "Maker" to decide at what level high blood glucose should be defined and determine who should get treatment. Early on, in my diabetes adventure (mid 1950s), when we only had urine strips and once-a-year fasting blood glucose testing, we were educated regarding a "renal threshold" where excess blood glucose would be filtered out by the kidneys. For most diabetic patients, glucose was not spilled into the urine until the bG level exceeded 180 mg/dL. Of course, any sugar in the urine reflected the amount of extra blood glucose above 180 that was 'filtered out' since the last elimination. Why didn't the "Maker" decide that 100 mg/dL was the line of demarcation for the kidneys to remove excess sugar?
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hey tmana - I'm with you 1000% on intense lifestyle management before drugs. Wish there was a 'do over' option for T1
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I think I have to agree. Remember me, Judy Sadler? I was really sick taking 6 shots a day and developed an allergy for my medication. I am 65 pounds lighter, doing much better but still have some allergic type reactions, flushing and terrible bouts with anxiety. The doctor said my AC1-A is 6.9 and that I do not need medication for my diabetes. I have problems with being resistant no matter what I try. I still believe that the medication caused all of my problems. I have to take Nexium and Zantac and Antacids after my family practitioner put me on Byetta and januvia together. I found out later this was a no no. To all who are suffering, my prayers are with you and know that you are not the only one. Just look at the statistics. The amount of Americans with disabling chronic diseases are rising at an alarming rate. If you can, buy or grow organic and put up your own food, just like back in the day that I remember being healthy. God Bless. Judy
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Dear Judy - The more we share with one another - hopefully the more we will all find safety in living with diabetes. Thank you for sharing your experience before meds and after.
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The great problem with the DCCT is that everyone takes it as the final word on diabetes, when in fact it only measured one factor, the relation between hyperglycemia and complications, among the many that can be measured in the complex picture of diabetes. Other studies conducted decades earlier have investigated the link between many different variables and diabetic complications and found more interesting results. The linkage between complications and hyperglycemia was NOT the most significant correlation noted, but rather, duration of diabetes, uric acid levels, and the amount of insulin needed to control blood sugar were all much better predictors of the development of complications. Duration of diabetes may just measure the influence of aging on physical decline, and uric acid levels probably just measure declining renal function or male gender. But the more interesting correlation is that patients who could achieve control by taking 0.5 units of insulin/day/kg of body weight had a much lower risk of complications than those requiring more insulin, regardless of the actual level of blood sugar control achieved. This suggests that residual insulin output, and thus c-peptide output, may be the decisive factor in minimizing complications. Better blood sugar control may then just measure higher natural insulin output, which in turn measures c-peptide levels, with only this latter factor being a genuine cause of lowered complication risk rather than just an incidental correlation of lower risk.
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Sanktpauli—
Your observations align rather closely with a study that was presented in a Diabetes Interview survey done by Scott King. If C-peptide activity and maintaining even a minimum activity level for beta cell production is the reason T1 diabetics reach the 50-year medalist category for Eli Lilly’s award, why isn’t this recognized in the medical community? In other words, why aren’t tests done regularly to see the effects of rDNA insulins, other protocols that are available, and even the possibility that diet may affect C-peptide levels. Of course, we also have to wonder why insulin antibody tests are not required as basic information to select the most compatible insulin for each diabetic’s needs and to maintain minimum C-peptide levels without causing antibody response and inflammation. It’s interesting to note that C-peptide has always been considered, by the medical profession, as nothing more than a throw-away polypeptide which was only a part of insulin formation during beta cell production of proinsulin, later resulting in insulin plus a breakaway C-peptide chain. It would appear to me that they have thrown away the baby and kept the bathwater.
Doesn’t C-peptide end up as a product going through the portal vein, ending up in the liver, where it is NOT sorted out as waste, but rather “used”?
It might interesting to do some comparison studies in Europe and UK where citizens have had access to both natural and rDNA products to define or explore different outcomes.
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