Can someone explain… why T2 and Pre can’t go back to a normal diet once…

[nonethewiser]

Wife, although only diagnosed prediabetic lost a lot of weight & reversed diagnosis, since then she eats near enough normal diet including carbs but is mindful of putting weight back on.

 

[harbottle]

Wife, although only diagnosed prediabetic lost a lot of weight & reversed diagnosis, since then she eats near enough normal diet including carbs but is mindful of putting weight back on.

It's generally though the point where the hba1c goes from 'prediabetic' to 'diabetic' is the point at which the pancreas stops producing enough insulin to keep levels normal.

 

[Burylancs]

Where can I find a reasoned explanation of how genetics caused the weight gain that led to my T2D, and not my diet?

Where can I find a reasoned explanation of how genetics caused the weight gain that led to my T2D, and not my diet?

Genetics of type 2 diabetes

Type 2 diabetes (T2D) is the result of interaction between environmental factors and a strong hereditary component. We review the heritability of T2D as well as the history of genetic and genomic research in this area. Very few T2D risk genes were identified ...

www.ncbi.nlm.nih.gov

 

[AndBreathe]

Sounds like you’ve made some very positive changes @Exflex

It seems to me from reading the forum over many years, that those with T2 who have successfully reduced their HbA1c through weight loss tend to focus on a maintenance menu that keeps their weight on target and that helps maintain their glucose levels.

While those with T2 who have used a lower carb approach to reduce their Hba1c (and lost weight in the process) tend to focus on maintaining a lower carb approach to help keep their glucose levels on track, and that seems to help maintain weight.

Good luck with finding a maintenance approach that works for you, once you’ve approached your goals.

With both scenarios there, I think we’re in chicken<>eg territory.

Like so many other things in life, when the chips are down, we each have to Mack our choices, lay our bets and own them.

 

[AndBreathe]

It's generally though the point where the hba1c goes from 'prediabetic' to 'diabetic' is the point at which the pancreas stops producing enough insulin to keep levels normal.

I find it hard to believe there is any universal point at which a pancreas moves from fine to producing insuffient levels. We’re that the case, prediction models would be way better at gauging outcomes. As it stands we can have folks well into the diabetes ranges, still producing oooooodles of insulin, but are equally so insulin resistant.

 

[harbottle]

I find it hard to believe there is any universal point at which a pancreas moves from fine to producing insuffient levels. We’re that the case, prediction models would be way better at gauging outcomes. As it stands we can have folks well into the diabetes ranges, still producing oooooodles of insulin, but are equally so insulin resistant.

There probably isn't an exact value, but this is what has been observed and why there's a so-called 'pre diabetic' or 'impaired' state where levels are elevated (It's lower in the USA, around 6.0% hba1c, as it's also been seen that things like the first phase of stored insulin is lost before the disease fully develops). It's also been seen that beta cell dysfunction precedes insulin resistance, probably due to genetics and elevated fatty acids. As glucose levels rise, insulin resistance gets worse.

The so called 'oodles' is there because it's being constantly produced, not because there's a lot of it being produced.

 

[JITR]

https://www.nature.com/articles/s41586-024-07019-6

This is very technical. but highlights just how complex the condition is.

Thank you for this. Yes, it indicates why 'everyone is different' in their body's response to their T2D condition. It's so complex that I'd say all those who can (the many) are well advised to aim for 'full' remission to avoid T2 and its complications. I'll elaborate when I have a bit more time.

 

[AndBreathe]

There probably isn't an exact value, but this is what has been observed and why there's a so-called 'pre diabetic' or 'impaired' state where levels are elevated (It's lower in the USA, around 6.0% hba1c, as it's also been seen that things like the first phase of stored insulin is lost before the disease fully develops). It's also been seen that beta cell dysfunction precedes insulin resistance, probably due to genetics and elevated fatty acids. As glucose levels rise, insulin resistance gets worse.

The so called 'oodles' is there because it's being constantly produced, not because there's a lot of it being produced.

The thing is, insulin is so vary rarely tested, in UK. Of course some of the issue is insulin is dynamic, and reacts to whatever we do or don’t eat.

I think it is a great shame the HOMA-IR isn’t used in UK at diagnosis or beyond. I found it very interesting when I had it done. (my results suggested very little IR, but the. I’d been in remission some time by then. I might repeat it this trip.

 

[JITR]

https://www.nature.com/articles/s41586-024-07019-6

This is very technical. but highlights just how complex the condition is.

Genetics of type 2 diabetes

Type 2 diabetes (T2D) is the result of interaction between environmental factors and a strong hereditary component. We review the heritability of T2D as well as the history of genetic and genomic research in this area. Very few T2D risk genes were identified ...

www.ncbi.nlm.nih.gov

Thank you for this. Yes, it indicates why 'everyone is different' in their body's response to their T2D condition. It's so complex that I'd say all those who can (the many) are well advised to aim for 'full' remission to avoid T2 and its complications. I'll elaborate when I have a bit more time.

I think any model of T2D must include diet and genetics as well as other factors. While the technicalities are beyond me, I came across this sentence in the article BuryLancs' cited, Somewhat to the surprise of investigators, most of the genes known to be involved in insulin secretion and action were not found to be associated with T2D in the population.

This fits in with what Roy Taylor and his team established in the Counterpoint study 15 odd years ago. Excess fat in the pancreas interferes with insulin secretion.

His partner in the DiRECT study, Mike Lean, considers the 40% of those with fatty liver who become T2D to have a genetic disposition to do so.

in other words diet and genetics go together in T2D like a 'horse and carriage'

 

[Exflex]

I must admit my original post was based on nativity. I have now come to understand I would be ill advised to go back to eating the way I did before. The changes need to be life-long, however long that is!

I found this by Zoe Harcombe extremely informative - kindly posted by one of the forum members:

What should we eat? – Zoë Harcombe

www.zoeharcombe.com

 

[Kreator]

Hi,

I'm now eating a 'Normal Diet' for me, which includes 'fish & chips' eg 'occasionally'

...I'm not eating anything like I was before I achieved remission though, as my diet has totally changed!

FYI, I still eat 'Carbs' in a 'normal' way as do i eat Protein, Fibre, fat etc...

...depends on how you look at it really...

PS. Apologies if I sound cryptic, but there is no definitive do or don't - it's entirely individual...

...Hope I've helped! 😉

 

[42istheanswer]

I'm not sure how well this fits into this discussion but...

I had suspected GD - not diagnosed but my first baby was big (over 4kg) and so I had automatic testing at 28 weeks in my second pregnancy (passed GTT) and again at 36 weeks due to repeated glucose in my routine urine tests (passed GTT again). Again a big baby but slightly under 4kg.

I suspected this was due to my grandparent :wink: maternal grandad diagnosed type 2 but underweight at diagnosis. Only had insulin following heart attack in line with recommendations for that, otherwise managed with tablets.

I was diagnosed type 2 at 41 at routine over 40s health check (a couple of months after covid-19 infection) and subsequently discovered that my father had been diagnosed type 2 about 18 months before. I don't think he's officially underweight but he's low end of normal weight (paternal family are all slim, maternal side the women are not slim unless ED).

I lost a lot of weight (though still classed as overweight) by going low carb low cal. I increased the calories once I hit my target dress size (heavier than when I was previously that dress size) but tried to keep the carbs down below 130g. I think they have crept up a little and i have gained a few lbs but still way below diagnosis weight (and still generally fitting in the size I had aimed for). My HbA1c is still good but my FBG has crept up, as has my total cholesterol. I'm not sure if that is carb creep, the few lbs weight gain, or something to do with liver/pancreas that is independent of those two.

 

[PerSpinasAdAstra]

I lost a lot of weight (though still classed as overweight) by going low carb low cal. I increased the calories once I hit my target dress size (heavier than when I was previously that dress size) but tried to keep the carbs down below 130g. I think they have crept up a little and i have gained a few lbs but still way below diagnosis weight (and still generally fitting in the size I had aimed for). My HbA1c is still good but my FBG has crept up, as has my total cholesterol. I'm not sure if that is carb creep, the few lbs weight gain, or something to do with liver/pancreas that is independent of those two.

Rising fasting blood glucose (FBG) and cholesterol may be a sign that fat is accumulating in your liver again. I'm very far from being an expert on anything though I have tried to read as much as I can about the possible mechanisms underpinning the various approaches to achieving remission. According to Prof. Roy Taylor fat in the liver is the root cause of the beginnings of elevated FBG. According to him, genetics determine how susceptible a person is to insulin resistance in the liver due to excess ectopic fat in that organ. Too much liver fat relative to genetic susceptibility and the liver doesn't 'switch off' glucose output quickly in response to rising insulin levels.

According to Taylor and his 'personal fat threshold' theory if you get below a certain weight, stay there, and avoid drinking too much alcohol, fat won't reaccumulate to excess levels in the liver. I don't trust that theory and so I've set my target weight at a BMI of 25 for the time being - plenty to get below my 'personal fat threshold' if such a thing exists, but leaving enough body fat that I can lose more weight again in future to get fat out of my liver a second time if need be. The warning sign I settled on was rising FBG as an early warning, with rising triglycerides as a kind of 'final warning' that my liver has gotten much too fatty.

There is actually no good scientific reason why carbs would affect FBG in your case. By the time a person wakes up in the morning the carbs eaten the day before have been almost entirely digested and metabolised - in the words of Dr. David Cavan yesterdays meals are a 'distant metabolic memory' come morning. In the fasted state blood glucose is pretty much entirely determined by the liver and the hormones that govern it's function - the primary hormones involved, insulin and glucagon, coming from the pancreas. At very high BG levels there is the possibility of glucose toxicity in pancreatic beta cells leading to elevated FBG - basically BG levels rise so high that the glucose 'poisons' the pancreas and disables (dedifferentiates) the cells that produce insulin. In that instance reducing carbs would lower BG and might allow living but disabled beta cells to start 'waking up', which may in turn affect FBG. At your HbA1c levels though this would seem very unlikely to be a factor.

I would suggest that another round of weight loss might be worth considering, and stopping the weight loss again a few kilos after your FBG levels drop back down to your baseline, assuming that happens. Again I'm no expert in anything, but if Roy Taylor is right about the liver fat thing, and I think he's proved that theory quite well with his various studies and clinical trials, then dropping a few kilos might solve your FBG problem.

 

[AndBreathe]

As ADA has made clear, there is no such thing as reversing Type 2 Diabetes. In the present state of knowledge, once securely diagnosed there is no going back. Gaining Good Control doesn't mean the fundamentals - genes, Metabolic Syndrome, Insulin Resistance have been changed or removed. The words 'reversing' and 'reversal' shouldn't be allowed on this Support Group, they're Fake News that confuses newbies.

The NHS has made it clear for ages that the Eat Well Guide is the way to eat for those living with T2. Unfortunately, many of us actually living with T2 found this to be flawed guidance, so my view on things such as remission/reversal is that they are a work in progress, in terms of understanding.

Secondly that insulin resistance has changed is a bad thing on the way the an A1c of 48+, but an excellent thing on the way to less than 48, or my personal viewpoint, less than 42.

Little in medicine (of the living) is absolute, and even at the extremes there will be n1 or "Black Swan" events - unusual, but actual.

Where does this holy grail of 6 years come from in terms of a metric for reversing/getting T2 into remission? Whilst less usual, there are folks whose understanding of their condition improves after a period longer than 6 years, and who do satisfy the commonly applied remmision criteria.

 

[JITR]

Just a thought.

The best plan, if you can entertain it, is to get down to a 'healthy weight'. A rule of thumb is waist measurement is less than half your height. The most promising documented way I know to do that is to follow the principles of the Harcombe Diet. See 'Weight loss' in what should we eat? https://www.zoeharcombe.com/2021/08/what-should-we-eat/.

You healthy weight sets weight you have to lose. You are less likely to go into remission the longer you have had T2D but some succeed after 25 years and you too will be much less likely to succumb to all the nasty events linked to fatty liver, T2D and Metabolic Syndrome.

Nothing venture, nothing gain!

 

[Austin Mini]

I became diabetic in 1988 was sent to hospital, admitted and given one insulin injection felt great about half hour later. I was seen by a Dietitian who went thro my entire eating habits and a diet plan for myself, then type 2, and on returning home the whole family changed its eating to the plan.
Six weeks later I was diagnosed as type 1 and started my insulin regimen. The change in the whole family’s diet as composed by the Dietitian was a resounding success we are all fitter and healthier thirty-six years after our eating habits changed.

 

[Drummer]

The problem might well be that a 'normal diet' is what is causing us all the problems in the first place.

 

[JITR]

The problem might well be that a 'normal diet' is what is causing us all the problems in the first place.

It is.

- Proof: something like half the world's population is now overweight.
- Reason: mass produced processed foods combine sugar and simple carbs with fat. Our bodies have no defence against them. They create cravings so we eat more.
- Answer: eat to satiety on a diet based on proteins, healthy fats and complex carbs such as veg and some fruit; keep other carbs within your personal tolerance limits.

 

[s'nic]

On the subject of fat build up in the liver, I have an appointment towards end april for an ultrasound to check mine out. I could not sleep last night, so ended up looking for info on weight loss and liver fat.
I found an interesting paper written in 2021, which looks at fatty livers in both lean and overweight people. I found this section particularly useful ...

"The impact of weight loss on liver improvement depends on the degree of weight reduction. A weight reduction of >5% is usually necessary to reduce liver fat, 7–10% to improve liver inflammation and >10% to improve fibrosis/scarring, although even lower reductions can be helpful.
Therefore, the guideline, jointly written by three scientific societies (the European Association for the Study of the Liver (EASL), the European Association for the Study of Diabetes (EASD), the European Association for the Study of Obesity (EASO)) recommends a weight loss target of 7–10% if you are overweight or have obesity with NAFLD.
The favourable effects of moderate weight loss also extend to lean patients who do not have obesity-associated NAFLD. In this case, a 3% weight loss is likely to drive NAFLD remission. Lifestyle changes that produce even modest results, such as a sustained weight loss of 5%, can induce clinically meaningful reductions in triglycerides and blood glucose."

"a low-carbohydrate diet appears to be similarly effective as a low-fat diet in reducing liver fat and the liver enzyme alanine aminotransferase longer term, as long as a 7% weight loss is achieved."

Non-alcoholic fatty liver disease: A patient guideline

This patient guideline is intended for all patients at risk of or living with non-alcoholic fatty liver disease (NAFLD). NAFLD is the most frequent chronic liver disease worldwide and comes with a high disease burden. Yet, there is a lot of unawareness. ...

www.ncbi.nlm.nih.gov

 

[frustrated]

On the subject of fat build up in the liver, I have an appointment towards end april for an ultrasound to check mine out. I could not sleep last night, so ended up looking for info on weight loss and liver fat.
I found an interesting paper written in 2021, which looks at fatty livers in both lean and overweight people. I found this section particularly useful ...

"The impact of weight loss on liver improvement depends on the degree of weight reduction. A weight reduction of >5% is usually necessary to reduce liver fat, 7–10% to improve liver inflammation and >10% to improve fibrosis/scarring, although even lower reductions can be helpful.
Therefore, the guideline, jointly written by three scientific societies (the European Association for the Study of the Liver (EASL), the European Association for the Study of Diabetes (EASD), the European Association for the Study of Obesity (EASO)) recommends a weight loss target of 7–10% if you are overweight or have obesity with NAFLD.
The favourable effects of moderate weight loss also extend to lean patients who do not have obesity-associated NAFLD. In this case, a 3% weight loss is likely to drive NAFLD remission. Lifestyle changes that produce even modest results, such as a sustained weight loss of 5%, can induce clinically meaningful reductions in triglycerides and blood glucose."

"a low-carbohydrate diet appears to be similarly effective as a low-fat diet in reducing liver fat and the liver enzyme alanine aminotransferase longer term, as long as a 7% weight loss is achieved."

Non-alcoholic fatty liver disease: A patient guideline

This patient guideline is intended for all patients at risk of or living with non-alcoholic fatty liver disease (NAFLD). NAFLD is the most frequent chronic liver disease worldwide and comes with a high disease burden. Yet, there is a lot of unawareness. ...

www.ncbi.nlm.nih.gov

Thank you