Dr. Bernstein for sure advocates for A1C’s in the 4’s. I do not feel that’s a realistic goal, but that’s what he writes and says. I think if you read past those unrealistic goals, he does have some good tips that will help real folks achieve more reasonable goals, as well as a mindset that good control is worth it which I think is true in so many ways.
Yup, Dr.B is one. A way to go before we get to “many”. 
Don’t get me wrong I agree with a lot of what he says. I just don’t consider his recommendations as medical guidelines.
I never said any such thing as that I feel I am entitled to an average A1c of four while others are not. It is not a question of ‘entitlement’ at all, but rather, of what the patient can achieve without endangering health or safety. Everyone should have whatever blood sugar value they are comfortable with. The whole point of my comments in response to the massive European study of the dangers of average blood sugars lower than 7% is that may well not even be a good idea.
The revolutionary import of that study has nothing whatsoever to do with what doctors recommend or with how many patients achieve what level of control, but rather, with the fact that it says that what all researchers, clinicians, endocrinologists, and diabetologists have regarded as an ideal goal if it could be safely achieved, that is, an average blood sugar value as close to normal as possible, is not even healthy for type 1 patients since it correlates with an increase in all-cause mortality. Since this is consistent with what was also discovered to be the case with type 2 diabetics in 2008, it is additionally scientifically supported by what Whewell would call ‘the consilience of inductions,’ that is, a similar result in a different case measured in a separate context, so that, along with the massive size of the study, lends it a lot of credibility.
The truly interesting question is why this should be so? Diabetics don’t seem to be a different kind of person from others, so normal parameters in all physiological values would seem to be sensible goals for them. Different mammals sometimes survive quite well with physiological values very different from human values, such as giraffes with an average blood pressure of 250/120 but no characteristic damage from this degree of hypertension, so we may ask how it is that their organs are so resistant to what would be harmful to other mammals, such as humans? Similarly, why do diabetics do better by not coming too close to normal with respect to blood sugar? The same sort of oddity appears in those who, because of cancer chemotherapy or dialysis, have to take erythropoietin to raise their hemoglobin levels. It turns out, much to the surprise of the medical profession when this was first discovered, that patients do much worse if you normalize hemoglobin, so they are better off being left seriously anemic, such as staying at a 110 level for males, for example, when normally anemic people are unwell.
This is a fallacy, making any subsequent arguments based on this fallacy invalid.
Whenever you quote a study, I highly recommend linking it. While you may think that you have legitimate arguments, others (including myself), may find your hypothesis/theories weak. You are not so omnipotent as to be capable to differentiate the legitimacy of the result of all studies.
While I welcome your contributions (regarding specific studies relevant to specific topics), you seem to misunderstand the implications of your posts.
As an individual with many years of experience- yet minimal amount of complications, I would hope you capable of inspiring others to also maintain their diabetes in such a way that they may also experience few limitations upon their person as a result of diabetes.
Well, why not email the authors of the study? They have a correspondence address author, as all such studies do. You can discuss with them their conclusion, which is:
“In conclusion, results from our study suggest an elevated mortality risk at both low and high HbA1c in type 1 diabetes patients. The higher risk of all-cause mortality at lower HbA1c levels found in our study might indicate that target HbA1c levels below a certain threshold may not be appropriate for all type 1 diabetes patients.”
The study says that other factors may be to blame for this though and that further evaluation is needed. It’s really hard to achieve a normal or close to normal a1c as a type 1 and the proportion of type 1s who can do it is minimal. I suspect there are not enough subjects with low A1Cs unfortunately to even draw meaningful conclusions. Plus, as everyone keeps pointing out, you yourself aim for a ridiculous level of control most of us on this forum would be unable or unwilling to achieve. Obviously you must see value in having a low A1C or you wouldn’t do this. I’m sorry for your frustrating experiences with the medical community. I was born in the 80s and diagnosed in the 00s, so I can’t speak for what doctors said in the 1960s, but my experiences with doctors have been mostly positive. The only doctor I know who advocates an a1c in the 4s is Dr. Bernstein, and he’d be the first to say that every other doctor is against him. I also had hypos that were more frequent, more intense and more unexpected before I worked towards tighter control, so your hypothesis isn’t even true for everyone.
These being the key words in the part of the conclusion you copied.
When you get used to reading scientific studies, especially in the field of medicine, you’ll find that such language is typical. Physics has its decisive experiments that change everything overnight (e.g., irregularities in the orbit of mercury and Einsteinian relativity), but medicine, since it generally operates with statistical correlations in which it is difficult to eliminate all the variables, is traditionally tentative. Also, it has an excessively hesitant, conservative approach to everything, stemming from its ‘primum non noscere’ or ‘first do no harm’ philosophy, developed at a time before scientific medicine when doing anything was more likely to cause harm than good, and also from its concern to enforce institutional discipline and keep everyone practicing the same type of dogma all the time. As a result, when you suggest a new line of treatment today all you hear is a chorus of thalidomide warnings, as though the only thing that can happen as a result of getting a new idea is something bad. This is why medicine is stagnating for so long, as you can find in many online articles (see for example Gordon, who says the stagnation has been underway since 1984).
If you look at other schools of thought in medicine, where practice regulations are freer than in Anglo-Saxon countries, you’ll find that medical thinking is much more open to new ideas. Listen to German doctors and you’ll find them constantly laughing at the Anglo-American ‘Resignationsphilosophie,’ or ‘philosophy of resignation,’ which is, in their view, overly prepared to give up when it encounters a difficulty and consign the patient to some horrible fate, rather than actually make use of all the information gained during medical education about abnormal physiology and pharmacology to try to come up with something new.
Odd, it seems the (almost all?) reference links to the ACCORD study are no longer. I did find the following.
http://stanfeld.com/is-evidence-based-medicine-based-medicine-the-holy-grail/
“The Action to Control Cardiovascular Risk in Diabetes (ACCORD) study was abruptly halted in 2008 when researchers noticed an increase in deaths in the group of Type 2 diabetics being intensively treated to bring their blood sugar levels down to near-normal levels.”
Termination of the study received wide coverage by the traditional media. No one critiqued the design of the study or the reasons for its statistical outcome.
Two years later the investigators have realized the errors in the study.
“ A new analysis of data from that study has concluded that a rapid lowering of blood sugar (glucose) levels was not the cause of the increased risk of mortality.
However, even though the researchers were able to exclude intensive diabetes management from their list of suspects, they still aren’t clear what factors may have played a role.”
I applaud study author Dr. Matthew Riddle, a professor of medicine at Oregon Health and Science University in Portland, for further analyzing the data.
“The original question underlying the study was, would rapid lowering of blood glucose be an explanation for the excess mortality rates?”
“The answer was no. People who rapidly lowered their A1c didn’t have excess deaths,” Riddle said. In fact, “it was the ones who couldn’t bring their A1c’s down that had increased mortality.”
Tapestry - first of all THANKS SO MUCH for finding these more recent results. I myself had googled for them but not found anything past the early termination in 2008.
The lowest A1C categories in this and other studies often have very few statistics. I am not an expert in all the fancy statistics that medical studies do. But my experience from nuclear statistics - e.g. how many Unobtanium-239 particles decayed while you were counting - is that it’s super hard to draw meaningful statistical conclusions from the histogram bins with very low counts. Error bars on low-statistics bins are in fact quite asymmetrical (because the number can only be zero or positive) and the skewness can trick you. into wrong conclusions if you use mental or statistical models of symmetric error bars:

I think I experience this quite a bit. Have some very noticeable symptoms; go to doctor or even specialist; run a bunch of tests; go back to the doctor; tests don’t match short list of possibilities or match possibilities but don’t fall in the standard measurements for diagnosis; get told there is nothing wrong; continue living with issues unresolved.
Of course the medical community, which hates to be deprived of their whips and loves to blame the patient for non-compliance whenever their nostrums don’t work, scrambled to undermine the 2008 study showing such a dramatic increase in mortality among type 2 patients lowering their A1cs that it was deemed unethical even to complete the study, so it was halted to avoid criminal sanctions. There are countless studies searching for an escape route from the 2008 study, and while some found some flaws in it, others have reconfirmed it.
At the very least, we have evidence that lowering A1cs is not helpful, whether or not it is actually killing people, and since it is extremely stressful for patients and cultivates a serious risk of lethal hypoglycemia to struggle for low A1cs, even just conceding that there is no evidence that doing this lowers the death rate is evidence enough that it should not be a goal. We also know for certain that rapid lowering of blood sugars worsens retinopathy, and while the usual cant is that this leads to an improvement if it is maintained long-term, in patients with highly variable blood sugar levels trying to lower blood sugar may just produce a series of short-term worsenings of retinopathy and no compensatory improvement from long-term improvement in blood sugar control.
Also, the medical profession tends to ignore the extremely severe iatrogenic disease of ‘hyper-controlled diabetes,’ which is my term for the massive reduction in quality of life that can occur in diabetics striving for lower blood sugar values, since it has been demonstrated that this triples the frequency of severe hypoglycemic episodes. Is this new, doctor-caused disease really worth the gains that come with improved blood sugar control? It would be very difficult to quantify this, but someone should try, and the fact that no one has bothered speaks volumes about attitudes in the profession toward the burden of care on the patients. Any of us can die in the next few hours from hypoglycemia, but hyperglycemia doesn’t even begin to produce complications until a decade after onset of type 1 diabetes in children. So is it any wonder that so many patients opt for hyper- rather than hypoglycemia?
By the way, the latest study on the effects of intensive blood sugar control in diabetics suggests that there may be some genetic oddity that accounts for the negative impact of near-normalization of blood sugar in diabetics. This is consistent with the idea that in the large cluster of genes involved in predisposing people to developing diabetes, some may have genes making it dangerous for them to have normoglycemia, so their hyperglycemia may be partially protective.
Diabetes Care. 2018 Feb;41(2):348-355. doi: 10.2337/dc17-1638. Epub 2017 Nov 28.
Modulation of GLP-1 Levels by a Genetic Variant That Regulates the Cardiovascular Effects of Intensive Glycemic Control in ACCORD.
Shah HS1,2, Morieri ML1,2, Marcovina SM3, Sigal RJ4, Gerstein HC5, Wagner MJ6, Motsinger-Reif AA7, Buse JB8, Kraft P9, Mychaleckyj JC10, Doria A11,2.
OBJECTIVE:
A genome-wide association study in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial identified two markers (rs57922 and rs9299870) that were significantly associated with cardiovascular mortality during intensive glycemic control and could potentially be used, when combined into a genetic risk score (GRS), to identify patients with diabetes likely to derive benefit from intensive control rather than harm. The aim of this study was to gain insights into the pathways involved in the modulatory effect of these variants.
RESEARCH DESIGN AND METHODS:
Fasting levels of 65 biomarkers were measured at baseline and at 12 months of follow-up in the ACCORD-Memory in Diabetes (ACCORD-MIND) MRI substudy (n = 562). Using linear regression models, we tested the association of the GRS with baseline and 12-month biomarker levels, and with their difference (Δ), among white subjects, with genotype data (n = 351) stratified by intervention arm.
RESULTS:
A significant association was observed between GRS and ΔGLP-1 (glucagon-like peptide 1, active) in the intensive arm (P = 3 × 10-4). This effect was driven by rs57922 (P = 5 × 10-4). C/C homozygotes, who had been found to derive cardiovascular benefits from intensive treatment, showed a 22% increase in GLP-1 levels during follow-up. By contrast, T/T homozygotes, who had been found to experience increased cardiac mortality with intensive treatment, showed a 28% reduction in GLP-1 levels. No association between ΔGLP-1 and GRS or rs57922 was observed in the standard treatment arm.
CONCLUSIONS:
Differences in GLP-1 axis activation may mediate the modulatory effect of variant rs57922 on the cardiovascular response to intensive glycemic control. These findings highlight the importance of GLP-1 as a cardioprotective factor.
Have you considered that quality of life can be much worse for people when their diabetes isn’t well-controlled? Just because someone isn’t striving for a low A1C doesn’t mean they don’t have frequent hypos or don’t have to manage their disease as much. I know you’re anti all diabetes technology but CGMs have improved quality of life in many cases. As I said, I had more frequent, severe and unexpected hypos before I learned what was going on and strived for tighter control. My dad was on the 2-3 shot/day regimen in the 90s and had horrible hypos that seemingly came out of nowhere. Plus, remember there were no CGMs or insulin analogs at the time of the DCCT. Perhaps the frequency of hypos wouldn’t have been as severe if the participants were tightening control with modern insulins and technology. Your hypothesis is flawed.
I see this as significant. If the DCCT were run today with the intensive group comprised of CGM-savvy type 1 diabetics using analog insulin would lead to far fewer hypos in my estimation. I firmly believe that reduced BG variability enables a safer lower average and A1c.
I welcome all the advances and agree that it makes handling my diabetes easier. However, more accuracy in the tools we are currently using would help. i.e. bubbles are a problem in my Tandem t:slim cartridges no matter how carefully I load them. This throws off all my careful control even though it’s not my fault.
I’m a new guy around here. I got a Libre right after diagnosis, and just can’t live without it. It’s data has been invaluable, and I would never have gotten an A1C of 5.3% without it (that was 3 months after diagnosis, and I was brought in the hospital with DKA and an A1C of 13% back then).
I think CGMs (and FGMs like the Libre) are THE biggest improvement for diabetics (especially for T1’s) in the last 15 years. Even more so than pumps. And I think the next big thing are or will very soon be pumps with closed loop algorithms. The results I’ve seen from people who use Loop, OpenAPS, or AndroidAPS are incredible. This tech makes sub-6% feasible for a lot of T1’s, and more importantly, take away lot of the daily T1 worry. Activity like exercise also gets easier because of predictive basal reduction.
So I’m hopeful. I do think that a cure will be there in my lifetime (I’m 35 years old), but won’t be here “in 5 years”. Before the cure, my bet is on smart insulin becoming a reality. That is, glucose responsive insulin - insulin that is injected all in one daily dose, but is encapsulated, and gets out of its shell only if “triggered” by enough blood glucose presence. I think this will be the next best thing before a true cure, and I think it will be here within the next 10-20 years, because once a pharma company succeeds in creating a smart insulin, they completely own the market. Every diabetic will want that insulin, so it will sell like hot cakes.
Aside from that, I agree with Goldfish - improving existing tech would also be a big help. My #1 wish right now is a blood glucose sensor that is extremely accurate, does not need calibration, and lasts for a very long time (or better yet, is not a disposable item at all). #2 is a hyper fast acting insulin to use in closed loops. #3 is a hyper fast glucagon analogue for countering impending lows.
Add to that the idea that when low A1c are achieved via a low-carb diet in conjunction with whatever pharmaceutical approach is necessary, those A1c are NOT accompanied with increased hypoglycemia at all. In fact, I demonstrated this directly to my endocrinologist (albeit somewhat unintentionally). I’d been getting a near-normal A1c via low-carb with ZERO incidents of hypoglycemia. I then achieved the same A1c, though with some additional carbs added to the diet - the results were weight gain and multiple incidents of hypoglycemia.
The entire picture needs to be considered.
DCCT wasn’t concerned with the safety of lower HbA1c values; that was the ACCORD study, which was much later, well within the age of high tech diabetes devices, in 2008.
Obviously the issue is a balance, but my concern is that the enormous cost of strict glucose control in terms of the demands on the patient’s time, energy, vigilance, and worry is seldom taken into account in the uncritical praise of ever-lower blood sugar levels in many medical journal articles, and little weight is given to the tripling of severe hypoglycemia incidents under a strict control regimen or to the deaths from hypoglycemia that can occur. Even the disruption of a patient’s social and work life, or ability to hold a driver’s licence, is an important consideration to throw onto the scales against whatever physiological value there is in lower blood sugar levels, which in any case have to be discounted by the influence of genetics and continuing autoimmunity in causing or contributing to the etiology of the complications.
Also, even good blood sugar levels are a gamble, since for some people, they fail to pay dividends. A friend of mine, for example, who always had better blood sugar control than I did, was blind and on dialysis at age 32, but not me. So while patients pay a heavy price for good blood sugar values, the investment may not bring any benefits. Additionally, if metabolic memory is operative in the patient, the very high blood sugar levels from years before may continue to generate new complications even though the patient has now achieved perfect blood sugar control. In my case, for example, since I had type 1 diabetes for 20 years before the first home glucometers became available, I had a long history of hyperglycemia, which has caused me now, many decades later, to have had to have four laser photocoagulation treatments for retinopathy even though my A1c has been in the four-range for the last decade. So what is the use of strict control in my case and for the many others in my situation? Perhaps it is no use at all?
It is really a fine line-drawing exercise. Would you accept a life of constant, severe hypoglycemia incidents undermining your job, your social life, and your legal right to drive a car in return for delaying the onset of end-stage renal failure by a year, from 17 years after onset to 18 years? The answer will depend on your priorities in life. Some healthy people choose to smoke, so they would rather live with the pleasure of cigarettes and the risk of cancer, heart disease, and early death. Diabetics have the same variation in approaches to life, so perhaps some people would rather avoid hypoglycemia and a regimented life entirely and take their risks, while others would not. Answering the question of how you want to calibrate complication risks against lifestyle values is highly individual.
