It does not add up.

[Fleegle]

So I have posted some posts in other threads, but not really getting a satisfactory response as in fairness it is a little off topic. Therefore thought I would create its own thread.

A bit of history and context. Bad BG at diagnosis - did LCHF - brilliant - figures down in 8 weeks.Through my own testing I found a few things happened, I had really good FBG figures IMHO - around 5 but they shot up 2mmol with a liver dump which just hung around till midday. At this time I was trying to eat less than 10g carbs a day. My BG started to go up a bit and the liver dumps worse. So I decided to try the Newcastle diet and am currently in week 4. What the heck - it is only 8 weeks.

So my questions after that context.
The ND works by removing pancreatic fat and making you produce more normal levels of Insulin. How does that work? Type 2's are most commonly Insulin resistant and are producing too much insulin. How then can producing more insulin put them into normal BG range? Also - the ND diet works best up to 10years after being diabetic. After that it has less positive outcomes. In fairness the success rate in the worse case is about 40% so not a given. Surely if your insulin resistant and you produce more insulin you will become even more resistant not less.

Then I am confused over a post I have read about low carb causing Insulin resistance and some Type 1's having to use more insulin as a result (and they know exactly how much they are producing). Why is that - that sounds counter cultural.

And then finally - why do some people, a few, report that after a time on LC they have to eat more carbs as their BG starts to go up.

Am I the only one who cannot join these dots?

 

[serenity648]

The ND works by removing pancreatic fat and making you produce more normal levels of Insulin.


more normal levels of insulin may not mean more insulin, it may mean less insulin.

 

[Fleegle]

The ND works by removing pancreatic fat and making you produce more normal levels of Insulin.


more normal levels of insulin may not mean more insulin, it may mean less insulin.

Thanks @serenity648 that is an interesting idea but I don't think it is right. Happy to be evidenced that I have got that wrong.
My evidence:-
Firstly there are a set of graphs showing increased insulin production at first phase and overall. Then there are his comments stating that they were producing a pathetic amount of Insulin. Thirdly it says it wakes up insulin producing cells - I doubt you need to wake them up to produce less insulin.

So I would accept that there are other things happening - but not that they are producing less insulin unless you can find a clip where he says that.

 

[oldsle]

I know I've heard that going too low carb can sometimes have the opposite effect than you'd like. I was at less than 20g per day for a bit and it didn't work very well for me, and I didn't feel quite right. I found that about 30-50g worked the best for me. I know that different things work for different people, but 10g per day seems much too low to me.

 

[badcat]

Im another one who cant quite figure out the assosciation between v low carb and increased blood sugars - If I go below about 20g my sugars inexorably rise as do ketones, to the point (highest was 6.5ish for ketones) where I feel v unwell and have to increase carbs again - it then takes about 2 weeks of eating higher (40-50g carbs) to get things back on an even keel
Although I can share the experiece of the effect, sadly I cant help interms of any possible answer to the conundrum tho

 

[Fleegle]

Im another one who cant quite figure out the assosciation between v low carb and increased blood sugars - If I go below about 20g my sugars inexorably rise as do ketones, to the point (highest was 6.5ish for ketones) where I feel v unwell and have to increase carbs again - it then takes about 2 weeks of eating higher (40-50g carbs) to get things back on an even keel
Although I can share the experiece of the effect, sadly I cant help interms of any possible answer to the conundrum tho

Really interesting - good to hear from someone with similar experience. Maybe I just went too low too soon.

 

[CoastGirl]

Hi @Fleegle, ditto your situation.

FBG immediately upon waking maybe a little higher than yours but I then rise up to mid to high 6s and stay there until late morning. I will then begin to regulate and maybe get to mid to high 5s just before lunch. Lunch post prandial can take me up by 1-1.5 mmol depending on what I've eaten and then I will will drop slowly to mid to low 5s before supper at approx 19.30. Sometimes my evening meal can take me just over 7 and I probably go to bed in the high 5s or 6s. My evening meal contains the largest dose of my daily protein so I am going to experiment with this over the next few weeks. I very rarely see a 4.

I am experimenting with intermittent fasting of 18/6 at the moment from end of evening meal through to lunch the next day. I can halt the morning rise with coffee and cream but still stubbornly stays put for most of the morning.

I lost a lot of weight in the first 3 months, 77kg down to 60kg, and I don't really want to lose anymore. I had assumed I had lost any fat in my liver, if I had any to start with, however still appear to have IR. It is either that or, more worryingly, I am not producing enough insulin. I have just had a fasting insulin test and am waiting for the results. Depending on this result I may do a home OGTT.

My carbs are generally between 20g-30g per day but do not accurately measure, just an educated guesstimate

Right now I am not able to join the dots either but am sure the problem revolves around a dysfunctional liver from medication taken in my 20s.

I know none of the above gives you any answers but just wanted you to know I am puzzling about the same things

 

[Fleegle]

Hi @Fleegle, ditto your situation.

FBG immediately upon waking maybe a little higher than yours but I then rise up to mid to high 6s and stay there until late morning. I will then begin to regulate and maybe get to mid to high 5s just before lunch. Lunch post prandial can take me up by 1-1.5 mmol depending on what I've eaten and then I will will drop slowly to mid to low 5s before supper at approx 19.30. Sometimes my evening meal can take me just over 7 and I probably go to bed in the high 5s or 6s. My evening meal contains the largest dose of my daily protein so I am going to experiment with this over the next few weeks. I very rarely see a 4.

I am experimenting with intermittent fasting of 18/6 at the moment from end of evening meal through to lunch the next day. I can halt the morning rise with coffee and cream but still stubbornly stays put for most of the morning.

I lost a lot of weight in the first 3 months, 77kg down to 60kg, and I don't really want to lose anymore. I had assumed I had lost any fat in my liver, if I had any to start with, however still appear to have IR. It is either that or, more worryingly, I am not producing enough insulin. I have just had a fasting insulin test and am waiting for the results. Depending on this result I may do a home OGTT.

My carbs are generally between 20g-30g per day but do not accurately measure, just an educated guesstimate

Right now I am not able to join the dots either but am sure the problem revolves around a dysfunctional liver from medication taken in my 20s.

I know none of the above gives you any answers but just wanted you to know I am puzzling about the same things

That is a very good match to my own situation @CoastGirl . BTW liver dump has gone completely since ND but I suspect temporary.
Sometimes knowing someone else has a similar situation is as good as an answer - at least I am not alone

 

[Bluetit1802]

Physiological insulin resistance. (PIR)

This is not the same as diabetic insulin resistance.

In the absence of carbs and therefore low glucose in the blood stream, the body reacts to preserve what glucose there is for the brain and the red blood cells (because they need it to function) Cells then reject this low glucose and it gets sent to the brain and RBC. To compensate, the liver dumps some glucose or we might hypo and die. This has the effect of increasing our FBG and also at other times between meals (pre-meals) when there is again too little glucose for our needs. It doesn't affect post meal levels other than they may appear higher due to starting higher, but the actual rise from before to after remains the same..

This is a lot more noticeable in people that are diabetic insulin resistant, because when the liver dumps this extra glucose, the pancreas reacts by secreting insulin to keep the glucose at a stable steady level, but then diabetic insulin resistance stops this insulin from working properly. Hence the increased FBG and pre-meal levels.

It happened to me, and that is why I started doing some research and discovered PIR. It is a temporary thing and a small increase in carbs is all that is needed. The brain and RBC don't need much in the grand scheme of things.

 

[ringi]

Before the pancreatic fat is lost, the liver fat is lost, this greatly decreases insulin resistance. (This is also why people who have been doing low carb for some time, often find they can eat more carbs then they could at the start.)

Intermittent fasting will also remove the pancreatic fat, maybe long term very low carb will as well.

I have also seen it claimed that fat in muscle cells makes them more insulin resistance and this fat takes even longer to remove than the pancreatic fat.

-------------

As I am starting to think that high level of blood insulin is as harmful if not more harmful then BG a little over normal levels, I question if we are focusing too much on BG just because we don't have blood insulin meters.....

 

[bulkbiker]

Before the pancreatic fat is lost, the liver fat is lost, this greatly decreases insulin resistance. (This is also why people who have been doing low carb for some time, often find they can eat more carbs then they could at the start.)

Intermittent fasting will also remove the pancreatic fat, maybe long term very low carb will as well.

I have also seen it claimed that fat in muscle cells makes them more insulin resistance and this fat takes even longer to remove than the pancreatic fat.

-------------

As I am starting to think that high level of blood insulin is as harmful if not more harmful then BG a little over normal levels, I question if we are focusing too much on BG just because we don't have blood insulin meters.....

As its the only thing we can measure at the moment I think you are right.. there were rumours of a home insulin meter on the horizon.. I would join the queue for one right now if were available. Although I do wonder how much the strips will be if a private test costs £40 a pop..

 

[Daibell]

I think the posts on this topic show how complex the subject is and how easy it is to draw possibly unreliable conclusions. I remain sceptical about some of Prof Taylor's ND research as it hasn't so far been broad enough or in enough depth to always draw reliable conclusions. He appears to be obsessed with pancreatic fat when in practice the obese will have fat deposited all over the internal organs. @Bluetit1802 has highlighted that a post I saw yesterday saying low carb increases IR is very misleading and usefully indicates it's PIR and temporary.

 

[Alison Campbell]

I was looking at the graph in the ND researchy ou posted in another thread and I think we are are talking about slighly different things.

The idea behind the ND is that it clears out liver and pacreatic fat improving the amount and speed of insulin response to a glucose challenge. Job done in one hour and insulin back down to background levels

When I think about insulin resistance I think about high levels of poor quality insulin that arrives late and does not work and requires more and more for upto many hours after the glucose challenge. As longs as your levels are high the pancreas keeps trying until it can't get the job done.

 

[Tannith]

If someone decides to try the ND what would be measurements before and after to verify beyond doubt it worked? I'm thinking if I try it and it works there's bound to be doubters. Home OGTT, A1c, FBG, fasting insulin????
Sorry, a little off topic. Maybe it should have it's own thread?

If you try it and it works you won't care if there are doubters. You don't do it to convince other people but to help yourself.

 

[Tannith]

So I have posted some posts in other threads, but not really getting a satisfactory response as in fairness it is a little off topic. Therefore thought I would create its own thread.

A bit of history and context. Bad BG at diagnosis - did LCHF - brilliant - figures down in 8 weeks.Through my own testing I found a few things happened, I had really good FBG figures IMHO - around 5 but they shot up 2mmol with a liver dump which just hung around till midday. At this time I was trying to eat less than 10g carbs a day. My BG started to go up a bit and the liver dumps worse. So I decided to try the Newcastle diet and am currently in week 4. What the heck - it is only 8 weeks.

So my questions after that context.
The ND works by removing pancreatic fat and making you produce more normal levels of Insulin. How does that work? Type 2's are most commonly Insulin resistant and are producing too much insulin. How then can producing more insulin put them into normal BG range? Also - the ND diet works best up to 10years after being diabetic. After that it has less positive outcomes. In fairness the success rate in the worse case is about 40% so not a given. Surely if your insulin resistant and you produce more insulin you will become even more resistant not less.

Then I am confused over a post I have read about low carb causing Insulin resistance and some Type 1's having to use more insulin as a result (and they know exactly how much they are producing). Why is that - that sounds counter cultural.

And then finally - why do some people, a few, report that after a time on LC they have to eat more carbs as their BG starts to go up.

Am I the only one who cannot join these dots?

Fleegle the answer to the ND diet enigma is to be found in the Prof Taylor video with the picture of the bridge at the front. It is in the sequence at the end about the bicycle and reversing IR in the liver. Losing liver fat does 2 things, it reverses IR in the liver which is the most important IR (somewhere else - in an article -he explains that IR in the muscles is of little importance). Secondly it stops the liver continuing to dump fat everywhere which it does when its own IR makes it unable to take any more of the fat/calories ingested. This also enables the pancreatic fat to be lost and not replenished. This allows the beta cells to wake up and start producing insulin if needed.

 

[Kristin251]

And where does the enzyme amalyse play in? If we do t have the enzyme that breaks down carbs properly where does that leave us ? Could thing sin our child hood changed us? Antibiotics? Or present? Food intolerances like gluten, grains, dairy , eggs nuts? I never believe in one smoking gun. Estrogen, progesterone, testosterone, thyroid hormones. They all fluctuate daily, hourly. Is that why we can eat the same meal at the same time and get different results every day?

The NCD wouldn't work for me for years with the shakes. Way too many carbs and not enough fat.

As always, just MY opinion

 

[tim2000s]

And where does the enzyme amalyse play in? If we do t have the enzyme that breaks down carbs properly where does that leave us ? Could thing sin our child hood changed us? Antibiotics? Or present? Food intolerances like gluten, grains, dairy , eggs nuts? I never believe in one smoking gun. Estrogen, progesterone, testosterone, thyroid hormones. They all fluctuate daily, hourly. Is that why we can eat the same meal at the same time and get different results every day?

The NCD wouldn't work for me for years with the shakes. Way too many carbs and not enough fat.

As always, just MY opinion

@Kristin251 The main reason the ND wouldn't work for you is that you're not type 2 and from what you've mentioned, don't seem to suffer fatty liver, which is what it is aimed at reducing.

Losing liver fat does 2 things, it reverses IR in the liver which is the most important IR (somewhere else - in an article -he explains that IR in the muscles is of little importance).

This is important to note. For non-insulin dependent diabetes, the majority of insulin acts on the Liver. It is dumped by the pancreas into the hepatic portal vein and something like 75%-80% of insulin use is the liver removing glucose. In non-insulin producing diabetes, the majority of the insulin is administered subcutaneously and only around 5% reaches the liver, with the majority being used by muscles to remove glucose, so physiologically, insulin resistance is rather different between those producing insulin and those not producing it.

 

[Tannith]

Do you happen to have a link? Much appreciated, thanks.

I THINK, but I have to say I'm not sure, that I saw it in the long article by Prof Taylor about the second study he did. You can get all his articles by googling Newcastle University site.

 

[ringi]

Some people with T1 do have fatty liver due to eating LOTS of carbs and increasing their insulin due to the carbs. But in the UK it is not common.

 

[Fleegle]

Can I just say a big thank you to all of the posters on here. I have learnt a lot - a lot to think about.