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Glucose uptake by skeletal muscle within the contexts of type 2 diabetes and exercise

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Whatever ..... not everyone reacts the same to anything and we all know that and so did Prof Taylor even before he even tried to prove that it would work. It certainly motivated one helluva lot of T2 people to have a go at losing weight one way or the other, to see if it helped. Of course - it usually does help.
 
Whatever ..... not everyone reacts the same to anything and we all know that and so did Prof Taylor even before he even tried to prove that it would work. It certainly motivated one helluva lot of T2 people to have a go at losing weight one way or the other, to see if it helped. Of course - it usually does help.
It absolutely motivated me in a massive way. I'm even considering buying a few copies of Taylor's books and gifting them to the doctors at my GP practise. 'Don't go mad on the internet' my GP said the day he diagnosed me. 'It'll just make your head spin. The nurse will give you some booklets'. Then, yesterday when giving me my new HbA1c results: 'Such a big drop so fast is unprecedented!'. I had to fight the urge to tell him that he should maybe go a bit mad on the internet himself. 😉
 
The counterbalance study showed that it worked for 100% of those who recovered pancreas function. Maintaining that weight loss is the weakest link.
Not true. There are plenty of anecdotal stories of people who lost the “required” % of weight and didn’t recover the ability to eat as normal. I’m one of them. I lost the weight and more immediately on diagnosis at just over the diagnostic level. As long as I kept the carbs (not calories) very low I was ok. As soon as I increased carbs (not calories) blood glucose began to rise and weight gain then followed. I’ve spoken with quite a number of others who have a similar response. Taylor hypothesis works for some. Not all. My surgery were shocked at my progress too.
 
The Newcastle diet is good in that it's simple, can be delivered by a health service, and clearly works, at least for a time. The downside is that it does nothing to help build new eating habits. I can cook, enough, I am currently motivated enough to plan my diet and lose weight week after week, and I'm committed to trying to do all I can to prevent or at least delay the onset of diabetic complications including trying to read scientific papers and whatnot. That said, I know how easy it would be for me to slip, buy some wine, some chocolate, order a large pizza, and watch a couple of movies. A few nights like that and my plans might all fall apart. Just like the way I went back to smoking cigarettes, twice, after having been off them for years at a time - it's just so easy to forget how hard it was to give them up and fall back into old habits.

If the prospect of keeping to a healthy diet for the rest of my life is daunting for highly-motivated me. I can only imagine how hard it might be for a group of people picked at random, put on a crash diet for a short time, advised to change their entire way of eating, then left largely to their own devices. I think it unfair to judge the value of Taylor's research and achievements based on the success or otherwise of a bunch of random people in staying out of McDonalds.
I lost 10kg to get to "remission" and then I lost another 20kg just because I could & because being skinny is fun 🙂 I've maintained the weight loss for 5+ years now. I got lucky with my peptides and that part of my CNS architecture responsible for hunger and satiety, but also I think that substantial, chronic aerobic exercise has played a big part: averaging 120 min - 150 min fairly brisk walking per day.

I doubt this is a universal panacea but there is a reaonable body of evidence to support it as a weight loss maintenance strategy. Not because of the calories burned (which would be expected to just result in more consumption all else being equal, together with metabolic adaption as a confounder), but more due to its effect on hunger/satiety.

As one entry point to this, I'd recommend Kevin Hall's revisit of his classic "Biggest Loser" study: https://onlinelibrary.wiley.com/doi/epdf/10.1002/oby.23308

The original study followed contestants from that awful Bigest Loser TV show over several years, looking at their weight, energy consumption/expenditure, metabolic etc trajectories. The people who managed to sustain substantial weight loss were those who maintained the most physical activity. They also had large sustained *reductions* in resting metabolic rate beyond what would be expected as a result of their change in weight and body composition, which Hall now interprets as being a consequence of their high levels of physical activity in line with Herman Ponzer's constrained energy model work.

Despite what you see on the Internet, this kind of long-term metabolic adaption is not typical of weight-loss in general - you get reductions in RMR due to change in body weight/composition, and a short-term transient additional reduction from rapid weight loss, but not a long term change taking RMR below what would be expected given body weight & composition. For this long term adaption it appears that you need substantial sustained physical activity.

Given the adaption and given other work from Hall and others showing that appetitie has a strong homeostasis characteristic - sustained increases in appetitie in response to weight loss - you might expect the overall impact of physical activity to be minimal for weight loss maintenace, but this is not the case.

Hall hypothesizes: "One possibility is that increased physical activity expenditure attenuates the feedback signal controlling appetite ..."

Personally, that seems to have been the case for me. I hardly ever get food cravings these days, I find it easy to eat really well and pretty easy to maintain caloric balance, the usual aroma triggers are mildly interesting or sometimes just annoying, like olfactory ads etc etc.

Anyway, it's a fascinating topic and Hall's work is well worth checking out. He's kind of the field's rock-star experimentalist at the moment.
 
This is absolute nonsense.
There is a phenotype of people who are T2D without having any form of insulin resistance or visceral fat.
I've never heard of this. Please tell me more.
Or nobody is interested in; https://forum.diabetes.org.uk/boards/threads/something-to-think-about.107042/
I have literally written a book about this subject, that’s how big my document on it has grown by now.
Not only about glucose uptake by skeletal muscle but also by the brain which doesn’t require insulin from the pancreas; glucose is so important to the brain it produces it’s own insulin.


Prof. Taylor got popstar status, but according to his data the Newcastle diet doesn’t really work; https://www.ncl.ac.uk/press/articles/latest/2023/04/type2diabetesintoremissionfor5years/
After 5 years only 8% was still in remission, 11 extra motivated participants from his study that also still received support. Yet another issue nobody is talking about, what happened to the other 92%?


But that’s not on this interesting topic, which is relevant to all of us; daily exercise preserves beta cells in all types of diabetes and obviously sarcopenia is a major cause of diabetes. Including mine. Twice.
The process of getting and then maintaining significant weight loss is only the hardest thing in the entire world to do. The counterbalance study showed that it worked for 100% of those who recovered pancreas function. Maintaining that weight loss is the weakest link.
Or nobody is interested in; https://forum.diabetes.org.uk/boards/threads/something-to-think-about.107042/
I have literally written a book about this subject, that’s how big my document on it has grown by now.
Not only about glucose uptake by skeletal muscle but also by the brain which doesn’t require insulin from the pancreas; glucose is so important to the brain it produces it’s own insulin.


Prof. Taylor got popstar status, but according to his data the Newcastle diet doesn’t really work; https://www.ncl.ac.uk/press/articles/latest/2023/04/type2diabetesintoremissionfor5years/
After 5 years only 8% was still in remission, 11 extra motivated participants from his study that also still received support. Yet another issue nobody is talking about, what happened to the other 92%?


But that’s not on this interesting topic, which is relevant to all of us; daily exercise preserves beta cells in all types of diabetes and obviously sarcopenia is a major cause of diabetes. Including mine. Twice.
I think saying it didn't work is a radical interpretation of the text. My understanding is that those who recovered beta cell function AND maintained weight loss, maintained remission regardless of the difficulty.
Not true. There are plenty of anecdotal stories of people who lost the “required” % of weight and didn’t recover the ability to eat as normal. I’m one of them. I lost the weight and more immediately on diagnosis at just over the diagnostic level. As long as I kept the carbs (not calories) very low I was ok. As soon as I increased carbs (not calories) blood glucose began to rise and weight gain then followed. I’ve spoken with quite a number of others who have a similar response. Taylor hypothesis works for some. Not all. My surgery were shocked at my progress too.
I hate to contradict you, but anecdotes aren't science, nor is your personal situation. Dr Taylor has confirmed his results in 3 different studies. Of course it doesn't work in everyone, it doesn't even work in everyone who've only been diagnosed for less than 4 years.
 
I think it unfair to judge the value of Taylor's research
But I highly value that, it's also his research that shows the Newcastle diet doesn't work.

It seems the problem is not so much the weight, but the fat-to-muscle ratio.
Here are people with diabetes vs controls with the same BMI:

1707374930518.png

This study based on a large UK cohort is interesting:

Total and regional fat-to-muscle mass ratio measured by bioelectrical impedance and risk of incident type 2 diabetes

"Findings from two large prospective cohorts indicated that fat mass had a consistently stronger association with type 2 diabetes risk than BMI. Son et al. found that a low appendicular skeletal muscle mass index increased diabetes risk independent of general obesity in middle‐aged adults."

"Higher total and regional FMRs were associated with a higher risk of developing type 2 diabetes, independent of BMI."
 
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