Do you have a GCK mutation or another MODY? Because if the latter, none of this applies to you.
Yep, heart attacks are a (the?) key macrovascular complication, absolutely included.
It’s amazing what a bad rep medical research has. I’ve been guilty of that at times, too, but it’s hard to sustain when I engage with actual medical researchers.
Or lead them profoundly astray. 
But thank you.
niccolo,
I've been at this for 17 years. The people I've known over that time period who have concentrated on controlling their blood sugars to those normal limits, whatever their diagnosis and whatever the tools they have used, are complication free.
My dad, who carried our family's diabetes gene, religiously ate a low carb diet (around 100 g a day) starting at age 38 and lived to be 100. His 5 younger siblings who did not eat that way all had heart attacks starting in their 50s. My thin diabetic grandmother was just a few years away from death from kidney failure when she was the age I am now. My kidneys are completely normal.
Physicians have had their judgment fatally affected by the widely quoted but highly inaccurate, reporting on the ACCORD study where people with Type 2 lowered their A1cs using a toxic combination of oral drugs which included Avandia and sulfs. There were a handful of more deaths in the group taking the Avandia. Both drugs do things that damage the heart. More to the point, though, it turned out that the people who had the heart attacks were in the group that was supposed to lower their A1cs but who had personally not succeeded. They had over 7% A1cs.
Yet because of the way this study was reported I have heard from so many people whose doctors have told them, based on this study, "It's dangerous to lower A1c." This includes one high profile endo who edits a specialist newsletter. He refused a patient any meds to help them lower a 7% A1c telling her it would be "dangerous."
If doctors like that are that ignorant of the subsequent subanalyses of that research that they are literally ordering patients to RAISE their A1cs, you have to be very careful taking any advice about the safety of high blood sugars.
Doctors don't have time to read the actual research. They are up to their necks in alligators all the time. They rely on summaries and the summaries miss things. A lot of things.
So you really have to ask yourself the question that is usually called "Pascal's wager." What happens if you're wrong with either choice. If lowering post-meal blood sugar is useless, and you did it what have you lost? If lowering post-meal blood sugar prevents heart attack etc and you didn't do it, what have you lost? Which is worse.
I've followed Bernstein since 2006 variously between 30g and nearly 100g/day of carbs. It has not had any affect on my fastings. I even asked Bernstein on one of his teleseminars about my chronic high fasting blood sugars. All he did was recommend insulin. I'm not sure what a high carb diet would do to my fastings but I suspect they would be higher. I just checked my fasting right now on my regime of Levemir and Invokana and it was 97 mg/dl. I would never have seen a reading like that before.
I’m not unsympathetic to much of this. But generalizing between T1, T2, and MODY isn’t straightforward. I would absolutely advise stringent BG control to a T1, the T2 also but lipids and BP are just as important. But if treating MODY2 makes only minor differences in BGs, and doesn’t correlate with reduced complications, that’s a harder pitch to make, especially for interventions that themselves have consequences. But a lowish carb diet seems like a no-brainer.
I’ve been unimpressed by a lot of doctors, so we’re on the same page there. Much more so by various researchers, though.
And does your A1c budge?
My A1c has been consistent in the low 5s since starting insulin. But for other reasons I have little faith in my meter and A1c accuracy.
How does that compare to your pre-insulin A1c?
It is an HbA1c improvement of 1-1.5%. But also remember, this is while following a low carb high fat diet and pre-insulin I was on a triple medication regime.
ps. I never found any medications that demonstrated notably better blood sugar control
That’s great, and probably suggests you’re not MODY2, lots of evidence, and my experience, suggests the A1c just doesn’t budge much even with fairly aggressive control. Of course, I suppose you can be MODY2 and classic Type 2, no reason they can’t coincide.
I know just enough about statistics to find a lot of medical research horrifying. Doctors as a group tend to be borderline math-illiterate and they are impressed by findings that are very poorly supported by the statistics they choose to produce. Often they seem to be dazzled by the features of the software they employ without understanding GIGO.
So when you look at studies, you have to read the full text very carefully, look at what they say they were doing and then see if the methodology they used really does provide the answers. Did they ignore and fail to control for important variables? Were the matched groups really matched--I have seen many studies where two groups have significantly different makeups but are considered to be matched.
Then look at the way the results are presented. If all you see is a bunch of averages with large standard deviations, be wary when those are used to show one group had an important difference from another. If there are no subanalyses that break out different sub groups, be wary, too. And last, but not least, check out the statistical significance. I have seen quite a few studies where the results were not statistically significant reported to say that though the results didn't reach significance they showed the result "trending" towards whatever outcome the researcher hoped to find. That, of course, means as much as saying that the in a coin flip, the coin came up heads 7 times out of 10 so that was a "headsy" coin.
And yet though this is Statistics 101, I had a long discussion with a biology professor whose research has been featured in the media who was astonished to learn that statistically insignificant data "trending" in that way was actually meaningless, since she sees that all the time in research she reviews.
And that doesn't begin to get into the way that statistics are manipulated by those with agendas, like drug companies, to make a result seem more impressive than it is. Where the incidence of some disease is 5 in 100,000 and the drug cuts it to 4 in 100,000 and the research is titled "Drug lowers risk of Disease by 20% and doctors are urged to prescribe it on that basis, not understanding how "risk" statistics are calculated.
Epidemiology is all about statistics, but unfortunately, it is a field where they are often badly misapplied. And you probably didn't have trained epidemiologists analyzing that MODY2 data. So be cautious.
My guess is that people with blood sugars that reach into the mid 200s have the same health as other people whose blood sugar reaches those heights. We know for a fact that until very recently, a good chunk of all Type 2 diabetics were undiagnosed at the time when their blood sugars were in that range, and so they formed part of that "normal" comparator group.
Unless the study screened those normal people with OGTT (which never happens in big studies because it is too expensive), I'd be very cautious about any result that was based on "normal" vs something else. The high end of normal is full of people with undiagnosed diabetes. Some huge percent of people with Type 2 have diabetic complications on the day of diagnosis, which means they have had diabetes post meal for as long as ten years, but weren't diagnosed due to the reliance on FBS. The move to diagnose people with A1c probably makes this worse. All it takes is a little anemia or certain ethnic genes and you have a lovely A1c and very high blood sugars.
How much did your HbA1c change after you started insulin if you don't mind my asking?
Jenny, actually doctors are, as a group, the most highly educated and intelligent people in our society. Can I ask what your individual qualifications are to make such statements? I know you have a fairly popular diabetes website-- but how does that make you an expert of a level that you can ridicule the education and expertise of medical professionals worldwide?
What gives you the qualifications to evaluate studies to determine if they were done properly, or following sound scientific principle? and why should anyone be impressed or alarmed with your stamp of approval or lack thereof?
This is a legitimate question-- what is your background? You are presenting yourself as an expert in this forum on quite a few subjects, and at this point you are even telling a member to disregard the advice given to them by a medical doctor whose specific expertise a member sought out. so I think that's a fair question.
Actually, mine didn’t budge at all. Insulin certainly helped me curb excursions, and lower the equilibrium rate, too, but I guess on average it just didn’t make much difference. Of course, reducing variability might also be a good thing–we have much less data there.
I think you’re confused about how natural experiments, assuming that’s what we’re still talking about, work. You don’t have to screen out anybody. You simply find familial groups where some have the gene defect and some don’t, and you observe whether complication rates vary.
http://diabetesupdate.blogspot.com/2014/12/accord-final-analysis-lo...
jenny found the flaw in the data analysis in 2010. the lancet caught up with her in 2014. i put my stock in what jenny has to say.
so go ahead and get warm, fuzzy feelings from researchers being nice to you.What a weirdly passive aggressive final sentence. I know internet anonymity brings this kind of thing out in people, but come on. A little civility goes a long way, and doesn’t get in the way of feisty disagreement, either.
I guess I'm really surprised you were put on insulin, let alone a pump when your A1c was 5.8%. I was basically told by multiple doctors I didn't need insulin until I went out of control and an A1c of 7% was consider well controlled.
Yep, the insulin choice looks a bit odd in retrospect. I was briefly put on a sulphonylurea, but was concerned about beta cell burnout. I advocated for early insulin–the notion was this was progressive, and we could preserve beta cells–and the endos were supportive. First basal, but quickly bolus to curb excursions. Did that for 12 years, got tired of fighting my basal during exercise, went on pump a few months back. A1c was pretty stable throughout all of that. Will be interesting to see what the next one is!
I will respectfully point out that the reference you give is a different analysis then the original work done on Accord. The reference you give also mischaracterizes the conclusions of the original (and 2014 Lancet study). The Accord trial data used an intention to treat analysis. This is done in part to reproduce a more real world dynamics of treatment. The Accord trial methodology was more complicated then the reference you give suggests:
Design
The design and results of the ACCORD trial have been published previously.12 and 13 Briefly, 10 251 men and women aged 40–79 years with established type 2 diabetes (mean duration 10 years), a mean gHbA1c concentration of 67 mmol/mol (8·3%), and either previous cardiovascular events or risk factors for cardiovascular disease were recruited from 77 clinical centres in the USA and Canada. Participants were randomly allocated to either intensive glucose-lowering therapy, with a target HbA1c concentration of less than 42 mmol/mol (6·0%), or to standard glucose-lowering therapy, with a target concentration of 53–63 mmol/mol (7·0–7·9%). The medications used to achieve these targets were the same in the two groups and included metformin, short-acting and long-acting insulins, sulfonylureas, meglitinides, thiazolidinediones, acarbose, and incretins. Participants were concomitantly enrolled in either a blood pressure trial (intense vs standard reduction) 14 or a lipid trial (optimised statin therapy with or without fenofibrate vs placebo), 15 in a double two-by-two factorial design. Patients were followed up at least every 4 months to ensure therapeutic goals were met and maintained and to monitor outcomes and adverse effects. The study protocol was approved by the ethics committee of each study centre, and approved and monitored by an independent data safety and monitoring board. All participants provided written informed consent.
The conclusions of the 2014 Lancet revaluation of the data do not alter the overall Accord data. Again from the Lancet 2014 article:
---------------------------------------Panel.
Research in context
Systematic review
The effect of intensive glucose lowering on cardiovascular outcomes in people with type 2 diabetes remains unclear. Four large outcomes trials allocated people with type 2 diabetes to intensive versus standard glucose-lowering regimens and assessed the effects of the intervention on various cardiovascular outcomes. A meta-analysis of data from these trials reported that the incidence of fatal and non-fatal myocardial infarction was reduced by 15% (95% CI 6–24) during a mean follow-up period of 4·4 years.6 By contrast, the treatment approach had no effect on fatal or non-fatal stroke. The ACCORD trial involved intense versus standard glucose-lowering therapy in people with established type 2 diabetes and additional cardiovascular risk factors. Although no significant effect was found on the primary composite cardiovascular outcome, the incidence of non-fatal myocardial infarction decreased, whereas death, especially cardiovascular deaths, increased. We therefore decided to use the ACCORD data to assess the relation between glucose lowering and ischaemic heart disease.
Interpretation
Intensive glucose-lowering therapy was associated with reduced risks of any myocardial infarction, coronary revascularisation, and unstable angina, when assessed separately and in combination, during a mean treatment period of 3·7 years. Further reductions were seen during an additional follow-up period of 1·2 years after the intensive treatment had been stopped. Although this analysis was not prespecified, our findings suggest that further investigation of this relation could identify individuals in whom the benefit of glycaemic control would clearly outweigh any harm.
Basically it's a lot more complicated then many seem to want this all to be and no it wasn't simply a few 'lazy doctors who couldn't read simple statistics. Do take a look at the sophisticated statistics of both these trial...
Hope this helps.