carbohydrate-reduced high-protein diet

[Deleted member 21371]

Moderator Note: Reply copied from https://forum.diabetes.org.uk/boards/threads/strategies-after-weight-loss.103842/#post-1223684

Did you miss the 'possibly' and the question mark at the end of @travellor's statement? It was a question, not a statement of fact.

I found this:

Low-carb Improves Pancreatic Function and Type 2 Diabetes – Diet Doctor

A new study shows that independent of weight loss, a low-carb diet improves glucose control and even pancreas function in those with type 2 diabetes.

www.dietdoctor.com

It seems that low-carb has been seen to improve pancreatic function in T2 diabetics. This study did not include weight loss, though.

@harbottle


This is very interesting.

It leads back to

https://journals.physiology.org/doi/full/10.1152/ajpendo.00165.2020?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org

energy-percentage carbohydrate/protein/fat: 30/30/40

So we are looking at a carb percentage of 30%

(as opposed to 50%)

So the dietdoctor is saying low carb is 240g of carbs now?
2000 calories average, (4 calories in a gram of carb, 2000x30%x4)
And a "normal" diet is 400g of carbs?

But the changes happen at the 240g, not the 120g "low carb", or the keto diet?

(Edit, should be150 and 250g, - post #13)

It is definitely an interesting turnaround, especially as the study seems to be for a carbohydrate-reduced high-protein diet, and not the high fat he usually recommends.

I've pulled it out of the original thread, as its irrelevant to the op on there.

I think I have seen reference to this on here before, as saying most people simply have a carb limit they can cope with, and cutting beyond that has no more benefit, this seems to agree?

If he is right, it seems a good way forward without massive carb restrictions.

I always said, if I go south, I'd go low carb, but it seems all that's needed is a small reduction, so that is certainly good news!

(He also quotes it to nail saturated fats, which is a swing for him but that's another thread)

 

[AndBreathe]

@harbottle


This is very interesting.

It leads back to

https://journals.physiology.org/doi/full/10.1152/ajpendo.00165.2020?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org

energy-percentage carbohydrate/protein/fat: 30/30/40

So we are looking at a carb percentage of 30%

(as opposed to 50%)

So the dietdoctor is saying low carb is 240g of carbs now?
2000 calories average, (4 calories in a gram of carb, 2000x30%x4)
And a "normal" diet is 400g of carbs?

But the changes happen at the 240g, not the 120g "low carb", or the keto diet?


It is definitely an interesting turnaround, especially as the study seems to be for a carbohydrate-reduced high-protein diet, and not the high fat he usually recommends.

I've pulled it out of the original thread, as its irrelevant to the op on there.

I think I have seen reference to this on here before, as saying most people simply have a carb limit they can cope with, and cutting beyond that has no more benefit, this seems to agree?

If he is right, it seems a good way forward without massive carb restrictions.

I always said, if I go south, I'd go low carb, but it seems all that's needed is a small reduction, so that is certainly good news!

(He also quotes it to nail saturated fats, which is a swing for him but that's another thread)

Whom are you associating with dietdoctor? I think I must have missed something somewhere.

 

[Deleted member 21371]

Whom are you associating with dietdoctor? I think I must have missed something somewhere.

It seems you have.
I'm not associating anyone.
I'm just following his link.
I suggest you contact him.

 

[AndBreathe]

It seems you have.
I'm not associating anyone.
I'm just following his link.
I suggest you contact him.

Ah, apologies, I guess you are taking a post from elsewhere to start a conversation with another member.

I'll pass on contacting dietdoctor for now. I don't have any itching need.

 

[Deleted member 21371]

Ah, apologies, I guess you are taking a post from elsewhere to start a conversation with another member.

I'll pass on contacting dietdoctor for now. I don't have any itching need.

It's a spin off thread.
I would encourage everyone to do these, start a new thread, rather than bombard an existing thread off track.
Hopefully that way we can have serious discussions about these subjects?

 

[harbottle]

Maybe that explains why I don't see any rises if I go out and have a small portion of chips or potato with a meal - highest I've seen post-meal (1 hour and 2 hours) over the last few months is a 6.6. I do low carb, probably less than 50g most days.

 

[bulkbiker]

Maybe that explains why I don't see any rises if I go out and have a small portion of chips or potato with a meal - highest I've seen post-meal (1 hour and 2 hours) over the last few months is a 6.6. I do low carb, probably less than 50g most days.

Then again you are still taking metformin if your signature is correct?
Also I would suspect your low carbing has allowed insulin sensitivity to return so your body is now capable of processing the carbs in the spuds.

 

[bulkbiker]

But the changes happen at the 240g, not the 120g "low carb", or the keto diet?

If the changes can still happen at 30% carbs just imagine how great the results would have been at 5% carbs!

 

[harbottle]

Then again you are still taking metformin if your signature is correct?
Also I would suspect your low carbing has allowed insulin sensitivity to return so your body is now capable of processing the carbs in the spuds.

My GP wanted me to stop the 500mg of Metformin.

I have no idea goes much insulin I am producing. It might be that it is enough to process a small portion of potato. T2 diabetes is actually more about beta cell deficiency than insulin resistance - that, by itself, is not enough to cause chronically high blood sugar levels.

 

[bulkbiker]

T2 diabetes is actually more about beta cell deficiency than insulin resistance

I have to disagree there.

I think it's more likely to be hyprinsulinemia.

Beta cells are fine and producing more insulin than the body can cope with due to insulin resistance.

Guess we'll have to agree to differ.

 

[rebrascora]

My GP wanted me to stop the 500mg of Metformin.

I have no idea goes much insulin I am producing. It might be that it is enough to process a small portion of potato. T2 diabetes is actually more about beta cell deficiency than insulin resistance - that, by itself, is not enough to cause chronically high blood sugar levels.

I have seen you make this statement quite a few times but if that is the case then why do many insulin dependent Type 2s need such significantly larger doses of insulin than your average Type 1, if insulin resistance is not the problem?

 

[everydayupsanddowns]

I think this is one of those things where the spectrum nature of T2 as a condition. I saw a conference presentation some years ago that discussed multiple sub-types of T2, which was suggested to be more of an umbrella term for multiple related conditions.

This seems to make sense to me, based on the widely varying experiences of members here.

It also may explain the previous ’inevitably progressive‘ mindset of many HCPs. Where for many T2 involved beta-cell loss through a number of routes and ultimately insulin was required.

But Prof Taylor’s breakthrough work, and recent discoveries on the mechanisms behind T2 relating to visceral fat around organs impairing their function, and weight-loss driven remission ‘resetting the metabolism, restarting the pancreas’ once you cross the personal fat threshold (even if you are not clinically overweight or obese to start with).

It may also offer an explanation for the ‘non responders’ to the Newcastle Diet. They simply don’t have that sort of diabetes!

So for me, looking for a one-size fits all approach to T2 management and/or remission is unhelpful. Because different people may have profoundly different types of T2, and are also working with different gut biomes, metabolisms and genetic make-up.

And the observations you make about your own diabetes, may not apply to another member. Because they may have a form of T2 that behaves quite differently.

Your Diabetes May Vary, as the age old adage goes 🙂

 

[Deleted member 21371]

To be fair, after I woke up at quarter to five somehow realising the maths was wrong.....

30/30/40 is 150g of carbs/150g of protein, and 100g of fat,
compared to 50/17/33, 250g of carbs/85g of protein, and 82.5g of fat.

So still not too bad, just ust need to drop the equivalent of 5 to 8 slices of bread, and double the protein, and maybe add a spoonful of olive oil.

 

[Deleted member 21371]

I think this is one of those things where the spectrum nature of T2 as a condition. I saw a conference presentation some years ago that discussed multiple sub-types of T2, which was suggested to be more of an umbrella term for multiple related conditions.

This seems to make sense to me, based on the widely varying experiences of members here.

It also may explain the previous ’inevitably progressive‘ mindset of many HCPs. Where for many T2 involved beta-cell loss through a number of routes and ultimately insulin was required.

But Prof Taylor’s breakthrough work, and recent discoveries on the mechanisms behind T2 relating to visceral fat around organs impairing their function, and weight-loss driven remission ‘resetting the metabolism, restarting the pancreas’ once you cross the personal fat threshold (even if you are not clinically overweight or obese to start with).

It may also offer an explanation for the ‘non responders’ to the Newcastle Diet. They simply don’t have that sort of diabetes!

So for me, looking for a one-size fits all approach to T2 management and/or remission is unhelpful. Because different people may have profoundly different types of T2, and are also working with different gut biomes, metabolisms and genetic make-up.

And the observations you make about your own diabetes, may not apply to another member. Because they may have a form of T2 that behaves quite differently.

Your Diabetes May Vary, as the age old adage goes 🙂

The discussion at the end of the linked article has a very good piece on the pancreas, and the comparison with the effects of a reduced carb high protein diet and a very low calorie diet.
It seems not all insulin is equal either.

 

[harbottle]

I have seen you make this statement quite a few times but if that is the case then why do many insulin dependent Type 2s need such significantly larger doses of insulin than your average Type 1, if insulin resistance is not the problem?

I never said insulin resistance is not a problem? Not sure where you got that idea from. It can lead to T2 diabetes, but once you're diabetic the biggest problem is loss of insulin secretion, and the rise in blood sugar due to this is far greater than the rise insulin resistance causes.

It kind of makes sense that someone who is insulin resistance, and develops T2 diabetes, they'll need more insulin to get their levels down, whether it's from their own pancreas or injecting.

There's a good discussion in this paper about some of the current thinking behind the condition, including some of the paradoxes, such as the reduced beta cell mass doesn't account for the larger loss of insulin secretion and the fact that patients who have bariatric surgery can reverse the condition without losing weight:

Diabetes Mellitus and the β Cell: The Last Ten Years

Diabetes is a major global problem. During the past decade, the genetic basis of various monogenic forms of the disease, and their underlying molecular mechanisms, have been elucidated. Many genes that increase type 2 diabetes (T2DM) risk have also been identified, but how they do so remains...

www.cell.com

Perhaps one of the most radical changes in the field in the past decade has been widespread recognition that reduced β cell function is the key problem in T2DM. Ten years ago, many leading groups still continued to regard T2DM as largely a disease of insulin resistance; today, this is not the case. In part, this paradigm shift has come about because studies of human islets have shown reduced glucose-dependent insulin secretion in T2DM even when allowance is made for the reduction of insulin content (Figure 2). In part, it derives from linkage studies and genome-wide association studies (GWAS), which have identified more than 40 genes associated with increased risk of T2DM over the past 5–6 years. Here we discuss a selection of these genes; for a more comprehensive summary, see
Bonnefond et al., 2010
and
McCarthy, 2010
.

 

[Proud to be erratic]

I think this is one of those things where the spectrum nature of T2 as a condition. I saw a conference presentation some years ago that discussed multiple sub-types of T2, which was suggested to be more of an umbrella term for multiple related conditions.

This seems to make sense to me, based on the widely varying experiences of members here.

It also may explain the previous ’inevitably progressive‘ mindset of many HCPs. Where for many T2 involved beta-cell loss through a number of routes and ultimately insulin was required.

But Prof Taylor’s breakthrough work, and recent discoveries on the mechanisms behind T2 relating to visceral fat around organs impairing their function, and weight-loss driven remission ‘resetting the metabolism, restarting the pancreas’ once you cross the personal fat threshold (even if you are not clinically overweight or obese to start with).

It may also offer an explanation for the ‘non responders’ to the Newcastle Diet. They simply don’t have that sort of diabetes!

So for me, looking for a one-size fits all approach to T2 management and/or remission is unhelpful. Because different people may have profoundly different types of T2, and are also working with different gut biomes, metabolisms and genetic make-up.

And the observations you make about your own diabetes, may not apply to another member. Because they may have a form of T2 that behaves quite differently.

Your Diabetes May Vary, as the age old adage goes 🙂

As so often the can occur, the obvious isn't obvious until its pointed out. Even before my own surgery and consequent T3c, I was vaguely aware that my late brother's T2 didn't seem to "fit" or match other T2s in my close family on my maternal side. I never gave it much thought and my brother didn't talk much about his diabetes, even though he lost both legs to it; he was more open about the amputations, the phantom pains in particular and we were very aware of his clear vulnerability to almost any ailment. So we naturally were alert to and focussed on his needs as someone profoundly disabled.

Once you, Mike, after my first posting had pointed out that I was not T1 (as written on my discharge paperwork in Feb 2020 by the HPB Dept that specialised in Whipples Procedures) but actually T3c, I subsequently came across the list of T3(a-k) that someone had researched, categorised and a symposium had discussed but neither endorsed or refuted (it seems). For the World Health Organisation the jury was out (and never came back?). The variation in T2s became more apparent to me, but again as a passing thought rather than a firm concept.

If alcohol can damage one's pancreas in a certain way, steroids in another, pancreatitis, thyroids et al - resulting in discrete types of T3, that need discrete treatments (in conjunction with possible treatments for the original cause) and not necessarily making someone insulin dependent - then why not the same spectrum for T2s? Also, there are almost certainly some T2s who are actually T3 - their pancreas damaged (naturally or by other causes) and they presented symptoms akin to T2, so attracting the T2 diagnosis; as there are T2s who are probably really T1.

It's an easy step for a GP to take and the wider question of 'why' is too easy to step over, particularly when the GP has a formulaic approach from a NICE Guidance note. The symptoms present the patient as T2, so it must be so. Too little time to do much else, along with inadequate research or Guidance notes. Just a thought triggered by your comments.