• Guest, the forum is undergoing some upgrades and so the usual themes will be unavailable for a few days. In the meantime, you can use the forum like normal. We'd love to know what you think about the forum! Take the 2025 Survey »

Carbs-independent remission

Maybe I'm misunderstanding, but my target was, and remains, to keep my bg low.
My weight loss was a welcome side effect of that.
Equally maintaining my bg at under the prediabetic level requires eating low carb and subsequently my weight is remaining stable
Am I alone in not concentrating on weight, but on bg?
 
Now that’s a very interesting perspective on the tradeoffs we need to consider, I shall remember this, thank you.
Low bg is the shared goal of us all, yes. Interesting that you see your weight loss as an incidental, not as the fundamental and inescapable imperative that enabled you to get the bg lowered in the first place.
 

My endocrinologist years ago said if I kept my weight low and exercised 30 minutes most days I should be okay . I had horrendous gestational diabetes. Ok so I did. But even very slim now and fit, I still got into high numbers lately . It is not just about visceral fat, it’s about genetics.
 
So they're suggesting compromised pancreatic beta cells regain some function with enough weight loss?
There's early research showing promise for beta cell regeneration with fasting - still rodent studies at this stage I think. Those studies were using a fasting mimicking diet so I guess if a diet was using any of the core FMD principles (IE: low sugars, low calories, low protein - specifically leucine, and some other amino acid tweaks) then something more than a "poor man's" remission might be attainable.
Before I was confident enough to try water fasting, I followed a fasting mimicking diet a few times. It was not difficult and I was surprised to be able to eat 60ish grams of carbohydrates each day, spread out over three meals and still get into a decent level of ketosis.
 
Yes, the genes have their role too. How much and for how many people is unclear.
 
There many reason why we are insulin resistant and develop T2, I have polycyclic ovary syndrome so my chances of developing T2 were always high, it’s also on both sides of my family with my dad and his siblings all developing T2 in their late 40s - all very skinny. My mum never developed it but 6 of her siblings did, all normal weight.

I was slim until a few years before diagnosis then I pilled on weight at a rate of knots without any change in my lifestyle, no one would believe me that I wasn’t overeating etc - T2 made me fat not the other way round. I have lost a huge amount of weight but I’m still very much diabetic. 13 years on keto diet with metformin only I would never try to introduce more carbs after all my hard work, why would I? I know what got me here today why mess with what works
 
chrisjohnh said:
Interesting that you see your weight loss as an incidental, not as the fundamental and inescapable imperative that enabled you to get the bg lowered in the first place.
Click to expand...
My blood sugars stabilised and I achieved remission before the largest part of my weight loss.
That is precisely why I think that Taylor's hypothesis.. (and it really is nothing more than that) is severely flawed.
My HbA1c hovers around 30 mmol/mol after 7 years..I have passed an OGTT test without recarbing beforehand.

Am I "cured" .. not if I go back to eating what made me sick in the first place but as I no longer consider carbs to be "food" then I don't see that happening.
 
Off topic, sorry, but with so many T2's in the family, have any of you had genetic testing for MODY?
 
I would prefer to say that Taylor’s hypothesis is not only that. It sits above decades of highly educated and dedicated thinking and scientific discourse on his part as well as experimentation. Its status would exceed, for example, my hypothesis that T2D is caused by wearing my socks inside out - that’s what “just a hypothesis” looks like. But, it may well be the case that his hypothesis is incomplete or less universal than proposed.
 
chrisjohnh said:
I would prefer to say that Taylor’s hypothesis is not only that. I
Click to expand...
But in the early days of his diet studies they tested for ketones in the trial participants.
If they got into ketosis by eating fewer carbs then it could be that causing the weight loss and remission.

That they failed to do this whilst carrying out DiRECT was interesting in itself.
 
I would add that it’s a pity that the complete picture of what the DiRECT remitters were eating during their second year has not been fully published, and may not have been even fully ascertained. This gap so far makes it hard for the rest of us to make an incisive assessment of the trial and of its implications for our own future T2D management. But I may do my own little experiment as I mooted earlier in the thread.
 
I agree there, yes it left that ambiguity in interpretation.
 
Certainly they believe that functional beta cell mass almost fully recovers once the pancreatic fat has been dispersed; but not necessarily all its former efficacy, which is a different thing.
 
chrisjohnh said:
Low bg is the shared goal of us all, yes. Interesting that you see your weight loss as an incidental, not as the fundamental and inescapable imperative that enabled you to get the bg lowered in the first place.
Click to expand...
Yes, my meter is my guide, not my scales.
I'm sure all the slim T2s don't see weight loss as fundamental and imperative. There are lots of posts from people who feel they need to put on weight, or who drop too low.

If I start increasing carbs I know my meter would rise beyond safety. I'm not prepared to take that risk just to see if my weight remains the same.
I shall be interested to see how you get on.
 
I think I'm in this camp. My priorities were firstly stop the nasty symptoms I'd had for ten years - neuropathy, oedema, kidney problems, wounds not healing etc. etc.

To achieve that I had to reduce my BG.

To reduce my BG I went (and have stayed at) ~20g carbs/day. Took four months. I was somewhere over 120kg when I started, and was still about 110kg when my A1c was back at 36 (down from 50).

I've lost a further >15kg since, still losing, and my BG has stayed around 36-38 in the intervening two and a half years. Weight loss (fat loss, strictly speaking) is to my mind a by product, not the cause, of my BG reduction.
 
chrisjohnh said:
Interesting that you see your weight loss as an incidental, not as the fundamental and inescapable imperative that enabled you to get the bg lowered in the first place.
Click to expand...
Easiest experiment validates thinking weight loss is not a fundamental and inescapable imperative to lower BG:

Day 1:
Take a diabetic.
Feed it carbs.
Measure BG.

Day 2:
Take a diabetic.
Feed it no or fewer carbs, same calories.
Measure BG.

Et voilá, BG lowered in a day without weight loss.
Mind, this doesn't prove anything long term, but it is a strong incentive to eat to your meter, weight loss or no.
 
Mmmm … sample size a little on the low side perhaps !
 
If you look at the nutrient listing for the Optifast shakes used in the original Newcastle study, or the Exante and Cambridge Diet plan shakes used in the DIRECT study, then the ND intervention is not only VLC diet, but is also low carb as in LCHF but without the HF part. So it is indeed a starvation diet.
 
The latter para misinterprets my intent, which is to see whether raising carbs will raise my A1c. My weight will remain constant because I will make it so by other adjustments.
 
chrisjohnh said:
Mmmm … sample size a little on the low side perhaps !
Click to expand...
Works with any diabetic not in remission (and many in remission as defined by hba1c), regardless of type.
Just find a random one to experiment on and I'll guarantee their BG will be higher after a high carb meal than after a low carb meal.

It's why T1's calculate their insulin doses based on carbs.
 
You must log in or register to reply here.
Menu
Log in
Register
Cookies are required to use this site. You must accept them to continue using the site. Learn More.…