Moderate/high-carb, low-fat members?

B

beating_my_betes

Well-Known Member
Relationship to Diabetes
Type 2
Is there anyone here, currently or otherwise, that has used a moderate/high-carb, low-fat diet to achieve weight-loss, with subsequent remission?
 
beating_my_betes said:
Is there anyone here, currently or otherwise, that has used a moderate/high-carb, low-fat diet to achieve weight-loss, with subsequent remission?
Click to expand...
I think many people if Type 2 find a low carb normal fat successful as it is carbs that convert to glucose so eating more carbs than the body can tolerate will increase blood glucose not reduce it. Low carb will also lead to weight loss in many.
The other way is low calorie which some have found successful and that generally is low fat and higher carb, much like the Slimming World or WW way.
 
beating_my_betes said:
Is there anyone here, currently or otherwise, that has used a moderate/high-carb, low-fat diet to achieve weight-loss, with subsequent remission?
Click to expand...
Pretty much, if I translate "low fat" as "low saturated fat". I zapped my T2D by cutting calories & losing weight. Kept the weight off, glucose regulation normal for about 6 years now.

I care about eating for cardiovascular health, which means minimal saturated fat, lots of unsaturated fat, lots of fibre, no refined carbs but lots of fruit and wholegrains, low sodium.

Everyhting gets converted to glucose eventually, not just carbs.

With T2D, usually a big thing is reduced liver insulin sensitivity due to visceral fat. This results in deranged gluconeogenesis, the process by which the liver constructs glucose from bit of fats and proteins; nothing to do with carbs. The liver keeps chugging out glucose, whch keeps BG high and is the prime reaon for high waking levels, regardless of how many carbs you ate. These background constantly elevated BG levels are generally more important than acute rises from eating carbs.

Which is one way of saying that weight loss => reduced visceral fat => restored liver insulin sensitivty (and pancreas insulin production) is a better route to remission than a narrow focus on carb control, to the extent that you can maintain the weight loss, which of course is the biggest challenge.
 
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Leadinglights said:
I think many people if Type 2 find a low carb normal fat successful as it is carbs that convert to glucose so eating more carbs than the body can tolerate will increase blood glucose not reduce it. Low carb will also lead to weight loss in many.
The other way is low calorie which some have found successful and that generally is low fat and higher carb, much like the Slimming World or WW way.
Click to expand...
Thanks! I'm not concerned about raised BG as a normal response to eating carbs. The stage I'm trying to get to will hopefully bring those levels down within the expected time-frame, given insulin is able to do its job correctly.
And people can lose weight eating any type of food or diet. It's all about creating a deficit between energy consumed and energy burnt 🙂
 
Eddy Edson said:
Pretty much, if I translate "low fat" as "low saturated fat". I zapped my T2D by cutting calories & losing weight. Kept the weight off, glucose regulation normal for about 6 years now.

I care about eating for cardiovascular health, which means minimal saturated fat, lots of unsaturated fat, lots of fibre, no refined carbs but lots of fruit and wholegrains, low sodium.

Everyhting gets converted to glucose eventually, not just carbs.

With T2D, usually a big thing is reduced liver insulin sensitivity due to visceral fat. This results in deranged gluconeogenesis, the process by which the liver constructs glucose from bit of fats and proteins; nothing to do with carbs. The liver keeps chugging out glucose, whch keeps BG high and is the prime reaon for high waking levels, regardless of how many carbs you ate. These background constantly elevated BG levels are generally more important than acute rises from eating carbs.

Which is one way of saying that weight loss => reduced visceral fat => restored liver insulin sensitivty (and pancreas insulin production) is a better route to remission than a narrow focus on carb control, to the extent that you can maintain the weight loss, which of course is the biggest challenge.
Click to expand...
Thanks! Everything you've written comports with the many cases I've seen online, regardless of protocol. My aim is to lose enough weight to clear out the ectopic fat and to restore insulin sensitivity. This of course presumes I haven't gone too far for too long, and destroyed my ability to bounce back. Second week of cgm use suggests I still have some juice left in the ol' Beta cells 🙂

So glad to hear you've managed to get on the other side of this, and will add it to the many other similar references that let me know I'm on the right track.

All the best 🙂
 
I achieved my initial weight loss on a moderate carb, low fat, moderate protein diet. Bagels, wholegrain toast, some rice, some pasta, baby potatoes - carbs with almost every meal, but not big portions. Pretty much all about calorie counting, and reducing things like cheese, butter fatty ready meals etc. were an easy win. Started taking calcium supplements once I realised I might not be getting enough with practically no dairy in my diet. I lost somewhere in the region of 14Kg on that diet. I achieved a very big drop in HbA1c (89 mmol/mol in October down to 39 in late January) coming up to around the 12Kg loss mark, though was taking Metformin and Dapagliflozin. I'm not sure when exactly I got my fasting levels down to normal levels as I wasn't testing often enough but maybe early January at maybe 9 to 10 Kg lost by that point.

I started investigating a lower carb diet in February and reduced my carb intake considerably, though not drastically, while maintaining the calorie deficit, and the weight loss proceeded as before. I put on a CGM at the time I was planning the change as was shocked at what even weight-loss portions of rice and pasta looked like on a graph. In retrospect, some low carb changes like swapping normal pasta with edamame pasta, and switching to a lower carb, higher protein bread product, could have been done sooner. In the beginning I was mostly focussed on losing weight and trying to find a diet that was as close as possible to what I was used to in the hope that it would make it easier to keep up the weight loss. So yes - big improvement and weight loss on moderate carb, though likely higher BG levels for a couple of months than I might have achieved if I went lower on carbs sooner. Still not in remission though - still taking the meds. HbA1c at 32 mmol/mol and I quite like it that way. Doctor's appointment next month so maybe that will change.
 
Thanks @PerSpinasAdAstra for sharing. Your situation is exactly as I would've predicted i.e Lose weight (More importantly, ectopic fat), leading to improved insulin-sensitivity, increased time-in-range and a remission-level lower a1c as a result. My personal opinion is that what you ate to achieve those results is entirely irrelevant. You reduced your caloric intake, forcing your body to start burning the reserves that created the insulin-resistance in the first place.

As concerns the cgm? I would be very surprised that had you worn a cgm from diagnosis you would have seen higher BG rises, that lasted for longer. Of course, that would likely have convinced you to immediately switch to low-carb/keto. But if you persisted with the plan that you did, in time, and commensurate with the weight/fat-loss, you'd likely have noticed the rises were no longer so high and would be much shorter-lived. I'd also speculate that with a bit of tinkering to get over the plateau, that if you continued with the original plan you'd also be at a similar a1c, simply by virtue of the extra loss and increasing insulin-sensitivity.

How people react to this point-of-view will very much depend on their beliefs around blood-sugar rises etc. and how much they are or are not responsible for the diabetic condition.

I'm not trying to argue you away from low-carb. But it can be a self-reinforcing trap. And should you ever feel like it is too restrictive for you, I believe there're ways to incorporate any food you want, without compromising where you're currently at.

All the best 🙂
 
To be fair, pretty much all weight loss will result from reduction of calorific intake (whichever route is chosen).
I averaged approx 100g carbs a day and 35g fat, so I guess low carb combined with low fat?
I lost 13.6 kg since 30 jan doing that

I needed to reduce cholesterol, particularly triglycerides, and carbs contribute to triglycerides. Once my weight is at target and blood results have improved I can reassess daily foods
 
beating_my_betes said:
Thanks @PerSpinasAdAstra for sharing. Your situation is exactly as I would've predicted i.e Lose weight (More importantly, ectopic fat), leading to improved insulin-sensitivity, increased time-in-range and a remission-level lower a1c as a result. My personal opinion is that what you ate to achieve those results is entirely irrelevant. You reduced your caloric intake, forcing your body to start burning the reserves that created the insulin-resistance in the first place.

As concerns the cgm? I would be very surprised that had you worn a cgm from diagnosis you would have seen higher BG rises, that lasted for longer. Of course, that would likely have convinced you to immediately switch to low-carb/keto. But if you persisted with the plan that you did, in time, and commensurate with the weight/fat-loss, you'd likely have noticed the rises were no longer so high and would be much shorter-lived. I'd also speculate that with a bit of tinkering to get over the plateau, that if you continued with the original plan you'd also be at a similar a1c, simply by virtue of the extra loss and increasing insulin-sensitivity.

How people react to this point-of-view will very much depend on their beliefs around blood-sugar rises etc. and how much they are or are not responsible for the diabetic condition.

I'm not trying to argue you away from low-carb. But it can be a self-reinforcing trap. And should you ever feel like it is too restrictive for you, I believe there're ways to incorporate any food you want, without compromising where you're currently at.

All the best 🙂
Click to expand...
You make some good points here about the CGM and perhaps I would have gone lower carb than was really necessary had I gotten an earlier, bigger fright. My guess is that BG rises earlier on would probably have reached higher levels though. I don't imagine they would have lasted any longer. I think of my fasting level as a baseline, and a specific meal will push levels up to a similar degree above that baseline, regardless of what that baseline is. The rate of glucose coming in pushing up the line vs insulin knocking it down again - a similar curve every time, with the base under the curve being the fasting level, more or less. The rise would look smaller on the graph, relatively speaking, with a taller base under it, but I imagine the change between the before-meal reading and the 2 hour later reading would not be very dissimilar shortly after the weight loss brought my fasting levels down. I have no way to test that now though of course.

Having looked into a few things in an effort to decide my long-term approach to carbs I decided that HbA1c might not be the only metric to be concerned about in the long run. Everyone thinks of diabetic complications in terms of being caused or associated with high average BG levels exclusively, perhaps because HbA1c is the blood test used to quantify what's going on - the severity of diabetes - and incidence and progression of complications are associated with that test as a metric. If the test is roughly based on average levels, then everything is studied in the context of averages, and that's what doctors look at. If you look at retinopathy risk for example there is this study - Link - it states that significant risk starts at a fasting BG level of around 6.6 mmol/L and a HbA1c of 46 mmol/mol, and risk rises in a mostly linear association with these metrics beginning at roughly those points. This suggests risk is all about average levels. However, the researchers note that very low levels of risk begin quite a bit below that point, as low as 6 mmol/L. If the risk really is entirely about averages, why would any risk at all below the 'substantial risk' threshold be easily detectable? My thinking is perhaps, below those thresholds, a person might spend time with BG levels in a 'danger zone' after they eat, but only after they eat, and perhaps only after specific meals. Spikes. Could a person with a fasting level of 6 mmol/L occasionally see their BG levels spike up to a level that a person with 6.6 mmol/L has begun to hit very much more frequently. I can imagine a quite narrow range of fasting BG values, where as a person passes through this range, they might go from spiking up to a specific level a couple of times a week to hitting that level after almost every meal of every day. Perhaps this is the risk threshold - not about average levels exactly, at least not initially, but about average time spent above the lowest boundary of a risky BG level threshold. Perhaps spikes are important.

That's retinopathy risk, but there are very many complications associated with diabetes. What if different risks have different BG level thresholds associated with them? My primary concern is atherosclerosis. I smoked for 20 years, didn't get enough exercise, was overweight, proceeded from normal glycaemia through prediabetes up to Type 2 levels over a span of many years. I have metabolic syndrome, and spent a long time, perhaps years, with high blood pressure and insulin resistance. Who knows how long I had elevated cholesterol levels. With all of those factors put together, I think it next to impossible that I'm not well on my way to a heart attack or stroke. I am very concerned about arresting the progression of my likely atherosclerosis to the greatest extent that is possible.

There are no studies available based on large-scale gathering of CGM data, yet. I have no way to tell if BG spikes are or might be a risk factor for heart disease. There is this opinion piece written by a cardiologist - link - and similar materials out there, but nothing that you might call evidence. That article has sample CGM graphs from completely healthy up to prediabetic levels. At present, two slices of wholegrain toast with a small apple causes a spike that peaks at around 10 mmol/L, and I spend maybe 30 minutes above the 'magic' 7.8 mmol/L level pointed to by the cardiologist. I doubt doing that occasionally would do me any harm, but what if I did it after every meal, every day. Ten and a half hours per week with my BG in a 'danger zone', if 7.8 mmol/L were in fact some kind of risky threshold to pass. I doubt very much that 7.8 is such a level, but I do strongly suspect that such a level may exist. In the context of atherosclerosis, perhaps it is a level at which glucose in the blood becomes in some way an irritant to the artery walls, a cause of inflammation. Or something along those line. Perhaps an hour a week irritating my arteries is very much better than ten hours.

I have no way to evaluate this risk or even know if it's real, though I've decided to play it safe and try to stay below 8 mmol/L as much as I can, aiming to go above this level no more than two or three times in an average week. I can do that on the low-ish carb diet (with exercise after some meals) without eating too much saturated fat, while keeping my cholesterol well under control with 10mg Atorvastatin, and with a fairly considerable variety in my diet. I don't see any good reason not to continue what I'm doing. I'm hoping that in years to come someone will publish a study based on a massive amount of CGM data, analysed by an AI or whatever, which identifies whether or not BG spikes are associated with any health issues and, with any luck, provide me with guidance in future years. Until then, gonna test all my meal options with a CGM and stick mostly to those that keep me below a magic threshold I made up myself 😉
 
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PerSpinasAdAstra said:
You make some good points here about the CGM and perhaps I would have gone lower carb than was really necessary had I gotten an earlier, bigger fright. My guess is that BG rises earlier on would probably have reached higher levels though. I don't imagine they would have lasted any longer. I think of my fasting level as a baseline, and a specific meal will push levels up to a similar degree above that baseline, regardless of what that baseline is. The rate of glucose coming in pushing up the line vs insulin knocking it down again - a similar curve every time, with the base under the curve being the fasting level, more or less. The rise would look smaller on the graph, relatively speaking, with a taller base under it, but I imagine the change between the before-meal reading and the 2 hour later reading would not be very dissimilar shortly after the weight loss brought my fasting levels down. I have no way to test that now though of course.

Having looked into a few things in an effort to decide my long-term approach to carbs I decided that HbA1c might not be the only metric to be concerned about in the long run. Everyone thinks of diabetic complications in terms of being caused or associated with high average BG levels exclusively, perhaps because HbA1c is the blood test used to quantify what's going on - the severity of diabetes - and incidence and progression of complications are associated with that test as a metric. If the test is roughly based on average levels, then everything is studied in the context of averages, and that's what doctors look at. If you look at retinopathy risk for example there is this study - Link - it states that significant risk starts at a fasting BG level of around 6.6 mmol/L and a HbA1c of 46 mmol/mol, and risk rises in a mostly linear association with these metrics beginning at roughly those points. This suggests risk is all about average levels. However, the researchers note that very low levels of risk begin quite a bit below that point, as low as 6 mmol/L. If the risk really is entirely about averages, why would any risk at all below the 'substantial risk' threshold be easily detectable? My thinking is perhaps, below those thresholds, a person might spend time with BG levels in a 'danger zone' after they eat, but only after they eat, and perhaps only after specific meals. Spikes. Could a person with a fasting level of 6 mmol/L occasionally see their BG levels spike up to a level that a person with 6.6 mmol/L has begun to hit very much more frequently. I can imagine a quite narrow range of fasting BG values, where as a person passes through this range, they might go from spiking up to a specific level a couple of times a week to hitting that level after almost every meal of every day. Perhaps this is the risk threshold - not about average levels exactly, at least not initially, but about average time spent above the lowest boundary of a risky BG level threshold. Perhaps spikes are important.

That's retinopathy risk, but there are very many complications associated with diabetes. What if different risks have different BG level thresholds associated with them? My primary concern is atherosclerosis. I smoked for 20 years, didn't get enough exercise, was overweight, proceeded from normal glycaemia through prediabetes up to Type 2 levels over a span of many years. I have metabolic syndrome, and spent a long time, perhaps years, with high blood pressure and insulin resistance. Who knows how long I had elevated cholesterol levels. With all of those factors put together, I think it next to impossible that I'm not well on my way to a heart attack or stroke. I am very concerned about arresting the progression of my likely atherosclerosis to the greatest extent that is possible.

There are no studies available based on large-scale gathering of CGM data, yet. I have no way to tell if BG spikes are or might be a risk factor for heart disease. There is this opinion piece written by a cardiologist - link - and similar materials out there, but nothing that you might call evidence. That article has sample CGM graphs from completely healthy up to prediabetic levels. At present, two slices of wholegrain toast with a small apple causes a spike that peaks at around 10 mmol/L, and I spend maybe 30 minutes above the 'magic' 7.8 mmol/L level pointed to by the cardiologist. I doubt doing that occasionally would do me any harm, but what if I did it after every meal, every day. Ten and a half hours per week with my BG in a 'danger zone', if 7.8 mmol/L were in fact some kind of risky threshold to pass. I doubt very much that 7.8 is such a level, but I do strongly suspect that such a level may exist. In the context of atherosclerosis, perhaps it is a level at which glucose in the blood becomes in some way an irritant to the artery walls, a cause of inflammation. Or something along those line. Perhaps an hour a week irritating my arteries is very much better than ten hours.

I have no way to evaluate this risk or even know if it's real, though I've decided to play it safe and try to stay below 8 mmol/L as much as I can, aiming to go above this level no more than two or three times in an average week. I can do that on the low-ish carb diet (with exercise after some meals) without eating too much saturated fat, while keeping my cholesterol well under control with 10mg Atorvastatin, and with a fairly considerable variety in my diet. I don't see any good reason not to continue what I'm doing. I'm hoping that in years to come someone will publish a study based on a massive amount of CGM data, analysed by an AI or whatever, which identifies whether or not BG spikes are associated with any health issues and, with any luck, provide me with guidance in future years. Until then, gonna test all my meal options with a CGM and stick mostly to those that keep me below a magic threshold I made up myself 😉
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Thanks!

Give me a 'minute' to chew through this. Will get back to you when I have a much clearer mind 🙂
 
PerSpinasAdAstra said:
You make some good points here about the CGM and perhaps I would have gone lower carb than was really necessary had I gotten an earlier, bigger fright. My guess is that BG rises earlier on would probably have reached higher levels though. I don't imagine they would have lasted any longer. I think of my fasting level as a baseline, and a specific meal will push levels up to a similar degree above that baseline, regardless of what that baseline is. The rate of glucose coming in pushing up the line vs insulin knocking it down again - a similar curve every time, with the base under the curve being the fasting level, more or less. The rise would look smaller on the graph, relatively speaking, with a taller base under it, but I imagine the change between the before-meal reading and the 2 hour later reading would not be very dissimilar shortly after the weight loss brought my fasting levels down. I have no way to test that now though of course.

Having looked into a few things in an effort to decide my long-term approach to carbs I decided that HbA1c might not be the only metric to be concerned about in the long run. Everyone thinks of diabetic complications in terms of being caused or associated with high average BG levels exclusively, perhaps because HbA1c is the blood test used to quantify what's going on - the severity of diabetes - and incidence and progression of complications are associated with that test as a metric. If the test is roughly based on average levels, then everything is studied in the context of averages, and that's what doctors look at. If you look at retinopathy risk for example there is this study - Link - it states that significant risk starts at a fasting BG level of around 6.6 mmol/L and a HbA1c of 46 mmol/mol, and risk rises in a mostly linear association with these metrics beginning at roughly those points. This suggests risk is all about average levels. However, the researchers note that very low levels of risk begin quite a bit below that point, as low as 6 mmol/L. If the risk really is entirely about averages, why would any risk at all below the 'substantial risk' threshold be easily detectable? My thinking is perhaps, below those thresholds, a person might spend time with BG levels in a 'danger zone' after they eat, but only after they eat, and perhaps only after specific meals. Spikes. Could a person with a fasting level of 6 mmol/L occasionally see their BG levels spike up to a level that a person with 6.6 mmol/L has begun to hit very much more frequently. I can imagine a quite narrow range of fasting BG values, where as a person passes through this range, they might go from spiking up to a specific level a couple of times a week to hitting that level after almost every meal of every day. Perhaps this is the risk threshold - not about average levels exactly, at least not initially, but about average time spent above the lowest boundary of a risky BG level threshold. Perhaps spikes are important.

That's retinopathy risk, but there are very many complications associated with diabetes. What if different risks have different BG level thresholds associated with them? My primary concern is atherosclerosis. I smoked for 20 years, didn't get enough exercise, was overweight, proceeded from normal glycaemia through prediabetes up to Type 2 levels over a span of many years. I have metabolic syndrome, and spent a long time, perhaps years, with high blood pressure and insulin resistance. Who knows how long I had elevated cholesterol levels. With all of those factors put together, I think it next to impossible that I'm not well on my way to a heart attack or stroke. I am very concerned about arresting the progression of my likely atherosclerosis to the greatest extent that is possible.

There are no studies available based on large-scale gathering of CGM data, yet. I have no way to tell if BG spikes are or might be a risk factor for heart disease. There is this opinion piece written by a cardiologist - link - and similar materials out there, but nothing that you might call evidence. That article has sample CGM graphs from completely healthy up to prediabetic levels. At present, two slices of wholegrain toast with a small apple causes a spike that peaks at around 10 mmol/L, and I spend maybe 30 minutes above the 'magic' 7.8 mmol/L level pointed to by the cardiologist. I doubt doing that occasionally would do me any harm, but what if I did it after every meal, every day. Ten and a half hours per week with my BG in a 'danger zone', if 7.8 mmol/L were in fact some kind of risky threshold to pass. I doubt very much that 7.8 is such a level, but I do strongly suspect that such a level may exist. In the context of atherosclerosis, perhaps it is a level at which glucose in the blood becomes in some way an irritant to the artery walls, a cause of inflammation. Or something along those line. Perhaps an hour a week irritating my arteries is very much better than ten hours.

I have no way to evaluate this risk or even know if it's real, though I've decided to play it safe and try to stay below 8 mmol/L as much as I can, aiming to go above this level no more than two or three times in an average week. I can do that on the low-ish carb diet (with exercise after some meals) without eating too much saturated fat, while keeping my cholesterol well under control with 10mg Atorvastatin, and with a fairly considerable variety in my diet. I don't see any good reason not to continue what I'm doing. I'm hoping that in years to come someone will publish a study based on a massive amount of CGM data, analysed by an AI or whatever, which identifies whether or not BG spikes are associated with any health issues and, with any luck, provide me with guidance in future years. Until then, gonna test all my meal options with a CGM and stick mostly to those that keep me below a magic threshold I made up myself 😉
Click to expand...
There's nothing wrong with being cautious, but my own feeling is that these numbers that we are referencing are probably quite arbitrary. Just the fact that it is possible to keep changing the thresholds for a1c classifications etc. suggests that it might be all about hedging our bets.

We know for instance that non-diabetics can often have very large BG rises, while still being very healthy, because it's not necessarily the rise, but the duration. I'm not suggesting that going from 4.5-25 mmol in one meal is a good thing, but I do think that as a community we might have been conditioned, even by ourselves, to fear too much about the expected rise that would accompany a meal containing glucose, fructose etc.

Again, I'm not telling anyone not to be cautious.

Here's an interesting video on the topic. Of course, when talking about non-diabetics it's easy to think none of this applies to us. However, if the 'spikes' were damaging in and of themselves, as many suggest (I think there is some grounding in the work of Jenny Ruhl) then we would expect to see a lot of problems occurring for non-diabetics who over-indulge...in the moment.

Anyway, I'm just offering this up as a point-of-interest. I'm not advising anyone to change what tehy believe and how they act:

 
Will have a look at the video - many thanks. My own thinking on the subject, specifically when it comes to atherosclerosis, is that there are so many risk factors associated with it, and it takes such a long time for health issues to manifest themselves, that any effect of BG spikes are effectively invisible at this time. It is known that people who appear to be entirely healthy do experience BG spikes. However, some level of atherosclerosis can be detected in around 42% of adults, most of whom do not show any outward signs (yet) of health problems. 'Healthy' people who are not in fact healthy, with no good data available to determine if BG spikes are, or are not, a risk factor. The incidence of heart disease in Type 1s illustrates that high average BG levels are definitely risk factor (Type 2 data is complicated by additional risk factors - insulin resistance, being overweight, metabolic syndrome). As such it's a 'nobody knows' thing at this time when it comes to having a HbA1c in the normal range, with problems with impaired glucose tolerance that result in frequent, high spikes, and whether this is anything to worry about. I'm not suggesting anyone follow me in my level of paranoia in this area though. I'm probably over-thinking it 😉
 
PerSpinasAdAstra said:
The incidence of heart disease in Type 1s illustrates that high average BG levels are definitely risk factor
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Do T1D have high average BG? Also, given much of the T1D population are just following their normal eating plan, and dosing insulin as required, how would we be able to distinguish between the effects of the diabetes and the effects of dietary pattern, when it comes to heart and other diseases?
 
beating_my_betes said:
Do T1D have high average BG? Also, given much of the T1D population are just following their normal eating plan, and dosing insulin as required, how would we be able to distinguish between the effects of the diabetes and the effects of dietary pattern, when it comes to heart and other diseases?
Click to expand...
Yes - a T1 will generally have quite a high HbA1c (certainly compared to healthy people). I imagine this is coming down over time with better technology, though I know next to nothing on that subject. It we assume that T1s tend to eat a diet that is similar to the population as a whole (I don't see why there'd be very much of a difference) then T1 is a known risk factor for cardiovascular disease, independent of other factors - Link It that's the case, the high average blood glucose levels are an indicator of the risk factor - unless injecting insulin is itself a risk factor, which I very much doubt.

That study notes that cardiovascular disease risk has been coming down over time in T1s, but has not converged with the 'control' - people without diabetes. I would guess that the reason risk is coming down over time is due to statins, and perhaps better tech (CGMs, pumps and such) which might result in better time in range.
 
PerSpinasAdAstra said:
Yes - a T1 will generally have quite a high HbA1c (certainly compared to healthy people). I imagine this is coming down over time with better technology, though I know next to nothing on that subject. It we assume that T1s tend to eat a diet that is similar to the population as a whole (I don't see why there'd be very much of a difference) then T1 is a known risk factor for cardiovascular disease, independent of other factors - Link It that's the case, the high average blood glucose levels are an indicator of the risk factor - unless injecting insulin is itself a risk factor, which I very much doubt.

That study notes that cardiovascular disease risk has been coming down over time in T1s, but has not converged with the 'control' - people without diabetes. I would guess that the reason risk is coming down over time is due to statins, and perhaps better tech (CGMs, pumps and such) which might result in better time in range.
Click to expand...
Thanks!
 
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