Not sure how significant the effect was – but it’s disheartening that even regular physical activity doesn’t seem to mitigate this mitochondrial dysfunction. Although maybe it does and they just haven’t figured out the right way to exercise to prevent this.
Anyone have access to the original paper?
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They provided this link at the end of the article: https://link.springer.com/article/10.1007%2Fs00125-018-4602-6
“Physically active, young adults (men and women) with type 1 diabetes (HbA1c 63.0 ± 16.0 mmol/mol [7.9% ± 1.5%]) and without type 1 diabetes (control), matched for sex, age, BMI and level of physical activity, were recruited (n = 12/group) to undergo vastus lateralis muscle microbiopsies. ”
It’s an interesting study, but when the participants are athletes that have an average A1c well outside the target range, I’m more skeptical of their conclusions. It’d be nice to see studies that also included a group of pwds with an average A1c in the 6-6.5% range.
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This is always my issue with these studies. They are studying people who have high blood sugar much or all of the time. And granted, this is more reflective of most of the T1D population. But is the situation the same for people who keep their A1c within the 5% to low 6% range? In other words, is this because of T1D itself or is it because of high (or fluctuating) blood sugar?
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yes, that’s a limitation.
But I’ve yet to see a single study where someone who has T1D and a lower A1C is completely exempt from the higher risk of complications associated with T1D – they just have them to a lower degree. And some things, like heart disease, don’t seem to be tightly linked to A1C at all. So I can’t imagine that this mechanism just doesn’t happen at all in people with lower A1C, it’s probably just less severe.
They’re also saying that the mitochondria are producing higher levels of reactive oxygen species as part of their metabolism – the idea that I worry about is whether higher exercise levels, which increase metabolism, wouldn’t just increase the production of ROS. then again, maybe it does in the short-term, but in the long-term it induces long-term changes that make the body better able to cope with it or something?
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Over the years I have been turned down for so many research studies. Can’t even count how many.
This is how it goes:
Eric: Hi Mr. Researcher. I would like to apply for the research study you are doing on muscle mitochondria damage in T1D’s.
Researcher: Great! Can you please fill out this application for the study?
Eric: […write, write, write…]
Researcher: I am sorry, you do not qualify for the study. Your control is too good. We are only looking for candidates with an A1C of 9-11 %.
Eric:
[months later…]
Researcher: Our research was successful! We have demonstrated a link between diabetes and “Bad Factor X”!
This is great news for me personally, because it means I will be able to get more research grants from University!
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I think the bottom line here is that “some t1D’s, for unknown reasons, are subject to a higher degree of complications. We are fairly certain that it’s A1c dependent.” Now, where are my millions of $?
Mr. Researcher!
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To be fair, when looking at many issues that a disease causes, looking at the outliers (bad control for instance) you often get to see the damage or issue in a higher concentration, so just because the research isn’t aimed at reassuring all you all, that you don’t have any issues, doesn’t mean the research won’t help you. Very little of the research funded today is going to try to prove that tight control means a better life, but rather will try and uncover some gem of information that will lead to a cure or additional treatment.
A broader range would require more participants, so the study would cost more.
But certainly looking at a broader range of A1C would provide even more useful information than only looking at a small range.
“Bad Factor X” is predominant in control range 1, nominal in control range 2, statistically insignificant in control range 3, etc.
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to be fair, the number of active young men in their 20s with Type 1 in Canada or wherever this study took place, and who are willing to go through the ouchy process of a muscle biopsy, and also willing to travel to the study areas, is sufficiently small that I’m guessing the researchers had enough trouble just getting the number of participants they did. Who knows if they specifically excluded people with lower A1Cs or if those were the people who replied.
Although I agree a ton of studies do a disservice to themselves when they exclude people like you with good control.
Ha, well, grand. I already have a mitochondrial myopathy that interferes with my muscles’ ability to get the energy they need! 
Diabetic mitochondtial metabolism is impaired regardless of A1C. Type 1s do not metabolize sugars or fats in mitochondria as efficiently as non-diabetics. Mileage may vary between Type 1s but nature of disease impairs proper/ideal mitochondrial function from the get go.
We use alternate biochemical pathways to burn same fuels.
Would you take beer instead of millions?
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