Insulin load index / most ketogenic foods

[Spiker]

Great links @Indy51!

Having just read Cooksey I think he is completely wrong. What I mean by that is I think there's barely an inch of difference between his views and Fung's. In fact a lot of his criticism is not disagreeing, but saying "this isn't news to anyone". I think Cooksey can only form that impression because he lives locked down in a Paleo bunker. Outside of the Paleo compound, what Fung is saying is very much news, conflicting with mainstream medicine and public health. I get the impression that he resents Fung as a newcomer who's getting lots of attention. I can see where he's coming from. Fung has come from nowhere, publicised well, is slightly irritating, and not so good at giving credit to the people whose ideas he is promoting. You could almost be forgiven for thinking Fung came up with all this stuff himself. ;-)

Cooksey is also annoyed that Fung cites a study that Cooksey hates for other reasons. But Fung does not rely only on ACCORD. Yes Fung's argument from ACCORD and the other studies that show a negative effect of "overly" tight control is fairly weak. But guess what, Fung and Cooksey prescribe the same action: don't increase insulin, reduce carbs.

I think this is the typical animosity between a trail blazing wild zealot who spent years in the wilderness, and some more polished and TV-friendly guy who comes along and popularises it.

But guess which one has the best chance to influence public health policy and orthodox medicine? Hint: It's not the guy wearing the mammoth skins. ;-)

 

[Indy51]

LOL @Spiker. Tend to agree - there was a lot of nitpicking going on and whenever I read someone say they're opposed to someone else's view because it's "fear mongering" and "can harm people", then I know I'm dealing with the viewpoint of someone who thinks they're smarter than the average bear and that the poor maroons out in internet land need somebody as smart as them to interpret/filter the truth for them. It's always a dead giveaway.

Still, the ACCORD study is pretty shaky ground to use as evidence for anything.

 

[martykendall]

This Jason Fung video is AWESOME.
+100 Likes for this post. Every diabetic and every HCP should watch this video. I will be taking the references to my next consultant appointment. Maybe he will finally give me some d**m metformin.

Jason is a bit of a legend! All of his videos are worth the time. His blog post is extensive and thought provoking.

Obviously Jason's thinking has been a major eye opener for me and I've tried to apply my engineering skill to develop a system that we can use in my family and possibly more widely.

I appreciate your feedback and thoughts Spiker!

"Jason Fung is the new Richard Bernstein." I like that.

 

[martykendall]

Great links @Indy51!

Having just read Cooksey I think he is completely wrong. What I mean by that is I think there's barely an inch of difference between his views and Fung's. In fact a lot of his criticism is not disagreeing, but saying "this isn't news to anyone". I think Cooksey can only form that impression because he lives locked down in a Paleo bunker. Outside of the Paleo compound, what Fung is saying is very much news, conflicting with mainstream medicine and public health. I get the impression that he resents Fung as a newcomer who's getting lots of attention. I can see where he's coming from. Fung has come from nowhere, publicised well, is slightly irritating, and not so good at giving credit to the people whose ideas he is promoting. You could almost be forgiven for thinking Fung came up with all this stuff himself. ;-)

Cooksey is also annoyed that Fung cites a study that Cooksey hates for other reasons. But Fung does not rely only on ACCORD. Yes Fung's argument from ACCORD and the other studies that show a negative effect of "overly" tight control is fairly weak. But guess what, Fung and Cooksey prescribe the same action: don't increase insulin, reduce carbs.

I think this is the typical animosity between a trail blazing wild zealot who spent years in the wilderness, and some more polished and TV-friendly guy who comes along and popularises it.

But guess which one has the best chance to influence public health policy and orthodox medicine? Hint: It's not the guy wearing the mammoth skins. ;-)

Well said Spiker.

 

[tim2000s]

The question this raises for me is which is more right?

Should all T2s have a treatment regime that comprises both views, whereby at initial onset where insulin resistance is high, both a low carb diet and exogenous insulin are introduced to reduce beta cell pressure and insulin resistance (using both Bersteinian and Fungian techniques) with a view to saving beta cells and drastically improving insulin efficiency?

This then leads on to a similar question in relation to T1 diabetics. At diagnosis should Metformin and Low Carb be prescribed to keep insulin low and potentially try and protect what is left of beta cells whilst introducing exogenous insulin. Can exogenous insulin reduce the level of damage caused by the autoimmune system by reducing the load on the beta cells and therefore reducing the proinsulin production that seems to be key in the trigger for the killer T cells that attack the beta cells?

Would this be even more beneficial to LADA or MODY type diabetics who typically have a slow descent into full insulin dependence that appears to the outsider to look like T2?

Between them, Drs B and F raise as many questions as the solutions they provide!

 

[martykendall]

The question this raises for me is which is more right?

Should all T2s have a treatment regime that comprises both views, whereby at initial onset where insulin resistance is high, both a low carb diet and exogenous insulin are introduced to reduce beta cell pressure and insulin resistance (using both Bersteinian and Fungian techniques) with a view to saving beta cells and drastically improving insulin efficiency?

This then leads on to a similar question in relation to T1 diabetics. At diagnosis should Metformin and Low Carb be prescribed to keep insulin low and potentially try and protect what is left of beta cells whilst introducing exogenous insulin. Can exogenous insulin reduce the level of damage caused by the autoimmune system by reducing the load on the beta cells and therefore reducing the proinsulin production that seems to be key in the trigger for the killer T cells that attack the beta cells?

Would this be even more beneficial to LADA or MODY type diabetics who typically have a slow descent into full insulin dependence that appears to the outsider to look like T2?

Between them, Drs B and F raise as many questions as the solutions they provide!

@tim2000s my understanding is that both of them would promote a low carb dietary approach for both T1 and T2.

Low carb / low insulin can extend the honeymoon period for T1s significantly meaning that the exogenous insulin doses are small leading to better control. I see lots of T1s on the GRIT group that likely fit this category (e.g. Dr Troy Stapleton and Lisa Schergers son) who are doing fabulously because they started a Dr B style approach soon after diagnosis.

I think Fung would go with the low cab / low insulin load approach for T2 and then titrate back the exogenous insulin. I think Berberine / Metformin to increase insulin sensitivity would be preferable to excessive exogenous insulin for T2s. If you start out with high doses of insulin then there's a higher chance that they'll not do the work to get off the insulin because they can't see the effect of the diet on their blood sugars because the insulin is covering the symptoms. I think Fung would go more intensive with the fasting protocol rather than ramping up the insulin.

Just my 2c as a non-diabetes drug expert.

 

[tim2000s]

@tim2000s my understanding is that both of them would promote a low carb dietary approach for both T1 and T2.

Low carb / low insulin can extend the honeymoon period for T1s significantly meaning that the exogenous insulin doses are small leading to better control. I see lots of T1s on the GRIT group that likely fit this category (e.g. Dr Troy Stapleton and Lisa Schergers son) who are doing fabulously because they started a Dr B style approach soon after diagnosis.

I think Fung would go with the low cab / low insulin load approach for T2 and then titrate back the exogenous insulin. I think Berberine / Metformin to increase insulin sensitivity would be preferable to excessive exogenous insulin for T2s. If you start out with high doses of insulin then there's a higher chance that they'll not do the work to get off the insulin because they can't see the effect of the diet on their blood sugars because the insulin is covering the symptoms. I think Fung would go more intensive with the fasting protocol rather than ramping up the insulin.

Just my 2c as a non-diabetes drug expert.

I agree that's the approach that apostles of each Diabetes messiah would take. I guess my hypothetical question was is this correct, or would it be better to combine treatments for all diabetics in order to achieve a better outcome?

One thing that's very clear about the "diabetes community" is that there are those who care about treating their condition and those who don't.

If someone falls into the latter category, it doesn't really matter what approach you advocate. Personally I would go with the one that reduced overall healthcare costs in the long run for this group. Even then, they may not last long enough for that to matter.

If someone falls into the first category, and therefore cares, they will also listen to the reasoning relating to T2 and the use of insulin. I suspect that (based on the stories that we see in the forum), they would prefer not to have to use insulin, so use as a short term medication while bringing the body back on line would be considered reasonable.

 

[Indy51]

Was just listening to the latest Bernstein webinar and he got pretty hot under the collar about repeated use of the LCHF acronym in people's questions. Made it plain he supports LCH(igh)P(rotein) and only as much fat as naturally comes with the protein. He seemed to be under the impression that LCHF is a low/minimal protein diet.

He also got pretty heated about people testing for blood ketones if they don't have high BG - says it's a waste of money. I kind of got the impression he's missed the whole point which was pretty disappointing. However, he fielded one question about someone being told by an HCP that long term ketosis causes kidney damage and said it was nonsense and that ketosis is a perfectly normal physiological state - yet also said he doesn't advocate people living their whole lives in ketosis - which seemed kind of odd to me as I would think his level of carbs (30g) would naturally cause you to be in permanent ketosis unless you were eating massive amounts of protein? He seems to believe that ketones are only produced by fasting/weight loss.

 

[Baruney]

Was just listening to the latest Bernstein webinar and he got pretty hot under the collar about repeated use of the LCHF acronym in people's questions. Made it plain he supports LCH(igh)P(rotein) and only as much fat as naturally comes with the protein. He seemed to be under the impression that LCHF is a low/minimal protein diet.

He also got pretty heated about people testing for blood ketones if they don't have high BG - says it's a waste of money. I kind of got the impression he's missed the whole point which was pretty disappointing. However, he fielded one question about someone being told by an HCP that long term ketosis causes kidney damage and said it was nonsense and that ketosis is a perfectly normal physiological state - yet also said he doesn't advocate people living their whole lives in ketosis - which seemed kind of odd to me as I would think his level of carbs (30g) would naturally cause you to be in permanent ketosis unless you were eating massive amounts of protein? He seems to believe that ketones are only produced by fasting/weight loss.

Testing for blood ketones isn't cheap but I'd rather spend my money on that than a pint and a packet of crisps.

Mind you if I spent my money on beer and crisps I wouldn't have to test my blood ketones! !

 

[phoenix]

Gave up on the video, my internet is too slow for it. So just from the first part (given the length probably just as well!)

Fung appears to have derived much of his early argument from this paper from 2008. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse http://care.diabetesjournals.org/content/31/Supplement_2/S262.long
Many researchers however postulate that it is energy excess that leads to ectopic lipid deposition , inflamation and consequent insulin resistance . Here's a simple explanation. (it is taken from the Coursera Global diabetes course; it is a bit strange to read since it is automated. This course is being shown again and if you sign up the lecture this is taken from is lecture 3:4)

When the cells become full of as much fat they can hold, and there is obviously an upper limit for the cells, they become dysfunctional. When fatty acids cannot be easily used as fuel in the body and in the metabolism, or be deposited as reserve energy and triglyceride in the fat cells and the accumulation of free fatty acids and also, mono and diglyceride takes place. These compounds are toxic and the so called state of lipotoxicity develops. This initiates inflammatory signaling from the cells, as if they were foreign bodies and they may die ,so called apoptosis, and they initiate local inflammation and the formation of collagen networks around the cells, like the fibrosis occurring in other inflamed tissues.
The state of lipotoxicity and inflammatory process and signals make the cells insulin resistant, which in this context may be seen as a defence mechanism since insulin blocks the release of fat from the cells, so-called lypoloysis and stimulates the formation of fat from glucose in the cells so-called lipogenesis. If the process continues, the insulin resistance leads to impaired glucose tolerance and eventually diabetes.

There are lots of complicated papers outlining the various pathways involved .I think that it is this current theory that underlies Prof Taylors thesis of individual fat thresholds.(ie this process happens at different degrees of fatness depending on when the persons cells become overfull.) This theory accounts for why most obese people don't develop T2 diabetes; the fat stays safely in the cell .It also accounts for why some individuals and ethnic groups develop T2 diabetes at far lower weight levels than others. Whether there is overspill .would be dependent on cell size, number and elasticity . This in turn may be determined in utero, in childhood or genetically.

Insulin toxicity
The recent reports from Accord don't point to toxicity from insulin;
ACCORD: Insulin Dose Not Responsible for Increased CV Mortality Risk
http://www.medscape.com/viewarticle/806903
also since the video was made the Accord data has been further analysed with1- 2 years of follow up.
Effects of intensive glycaemic control on ischaemic heart disease: analysis of data from the randomised, controlled ACCORD trial
conclusion,
"Raised glucose concentration is a modifiable risk factor for ischaemic heart disease in middle-aged people with type 2 diabetes and other cardiovascular risk factors"
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(14)60611-5/fulltext

The Origin trial is also interesting and doesn't suggest toxicity. This trial, had a very different population to Accord .It was longer, Subjects were people with pre diabetes or early T2 though they did select a large proportion of participants with a high CVD risk. The starting HbA1cs weremuch lower than in Accord and the use of insulin was definitely supplementary .
They were hoping to find that Glargine had a protective effect against CVD. It didn't but it was neutral.
http://professional.diabetes.org/CongressReport_Display.aspx?CID=91304
They have reported since that this continues to be the case . More importantly, they have also reported a reduction in micro vascular complications in those that started with an HbA1c greater than 6.4%.

Type 1

We have to replace insulin.
.How much insulin is released into circulation by the normal non diabetic? Here's my answer from a couple of years ago . It varies according to calorie intake.
http://www.diabetes.co.uk/forum/threads/how-much-insulin-do-healthy-people-produce.34730/
How does that compare with people who have lived for 50+ years using insulin ?
The average insulin dose in the Joslin 50 year study, was 0.46 ± 0.2 u/kg. For a person weighing 75kg that would be about 35 u .That seems to be slap in the middle of the various estimates for non diabetics.

edit spelling

 

[Spiker]

The question this raises for me is which is more right?

Should all T2s have a treatment regime that comprises both views, whereby at initial onset where insulin resistance is high, both a low carb diet and exogenous insulin are introduced to reduce beta cell pressure and insulin resistance (using both Bersteinian and Fungian techniques) with a view to saving beta cells and drastically improving insulin efficiency?

This then leads on to a similar question in relation to T1 diabetics. At diagnosis should Metformin and Low Carb be prescribed to keep insulin low and potentially try and protect what is left of beta cells whilst introducing exogenous insulin. Can exogenous insulin reduce the level of damage caused by the autoimmune system by reducing the load on the beta cells and therefore reducing the proinsulin production that seems to be key in the trigger for the killer T cells that attack the beta cells?

Would this be even more beneficial to LADA or MODY type diabetics who typically have a slow descent into full insulin dependence that appears to the outsider to look like T2?

Tim I think it's YES on all your points.

In summary I think exogenous insulin should be minimised and used as an emergency measure for stabilisation, but then carb reduction should take up as much of the slack as possible - which will vary based on whether the individual is T2, LADA/MODY, or full on T1.

 

[Spiker]

Low carb / low insulin can extend the honeymoon period for T1s significantly meaning that the exogenous insulin doses are small leading to better control. I see lots of T1s on the GRIT group that likely fit this category (e.g. Dr Troy Stapleton and Lisa Schergers son) who are doing fabulously because they started a Dr B style approach soon after diagnosis.

Do you have any links to evidence for this other than anecdotal? I ask not because I don't believe you, but because this question is often asked and there is not much solid evidence on the subject one way or the other. The approach differs from country to country, even within Europe.

 

[Spiker]

Fung appears to have derived much of his early argument from this paper from 2008. Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse http://care.diabetesjournals.org/content/31/Supplement_2/S262.long
Many researchers however postulate that it is energy excess that leads to ectopic lipid deposition , inflamation and consequent insulin resistance

Good link. But I don't think it matters from Fung's point of view what the mechanism is. He's saying high insulin causes insulin resistance, and that is still true even if there is an intermediate mechanism of lipotoxicity, due to high lipid deposition, mediated by - insulin.
With us taking exogenous insulin, we have to increase our energy intake accordingly, in fact specifically we have to increase our carb/protein (glucogenic) energy intake accordingly, otherwise we go hypo. So even [if] he is wrong about the intermediate mechanisms, over which opinions as you say are divergent, isn't he still right about excess exogenous insulin leading to insulin resistance[?]

To be fair to him, he is cautious and says that excess insulin 'CAN' cause insulin resistance, not that it's the sole cause, and he is careful not to say it's necessarily the initial cause. He's just saying it's ill advised as a treatment for diagnosed T2s because it WILL make their insulin resistance worse, progressively, over time.

 

[martykendall]

Protein effect on bg levels - a graphical response.

But what's actually going on? To put this in context, I had eaten no carbs from about 6pm yesterday evening., as shown in this image.

Basal insulin was taken at 9.30 as usual and the protein shake was ingested at around 9.30pm-9.45pm. After about 10 mins, I see an ifg level climb from 4 to 9 that takes about an hour (ignore the lows showing on the libre scan prior to this, I wasn't in the red according to bg tests). This corresponds to my normal increase due to roughly 18g of carbs and the rate of increase is similar to that seen with brown rice. This continues till roughly 11pm-11.30pm. This shows a rate of increase of ~2.5mmol/l per hour.

The curve then flattens off, in as much as the rate of increase drops to around a quarter, but there is a clear rise from 9 to 13 between roughly 11.30 and 5am that I attribute to gng. The rate of change here is (again approximately) 0.7mmol/l/hour in this period.

For full disclosure, the nutritional information relating to the protein shake, which was made with a mix of coconut milk and water, is as follows:

Shake:
CHO: 1.8g
Protein: 46.6g
Fat: 2.6g

Coconut Milk:
CHO: 3.8g
Protein: 0.2g
Fat: 2g

Total carb content 5.6g.

Protein Content: Whey Protein Concentrate (Milk, Soya), Milk Protein Concentrate,Egg White Powder
Additional Amino Acids: Glutamine in the form Glutamine Peptides

These are just my observations but I think it clearly shows what I regularly see.

@tim2000s, I've used your CGM plot as and example at https://optimisingnutrition.wordpre...e-insulin-reaction-to-protein-dose-dependent/

Let me know if this is OK?

Have you ever done this sort of test with 100% fat like butter or coconut oil? I would be interested to see the result.

 

[martykendall]

Do you have any links to evidence for this other than anecdotal? I ask not because I don't believe you, but because this question is often asked and there is not much solid evidence on the subject one way or the other. The approach differs from country to country, even within Europe.

Spiker, only anecdotal. But it makes sense to me to not burn out your remaining beta cells.

Here are some 'anecdotal' videos from people that I have the privilege of calling friends from a seminar in Brisbane.

I asked Troy and he said that he thought he would still be in the honeymoon phase of his diabetes an that the dietary approach that he's taking would be extending that. I think Lisa's son Daniel would be in the same boat.

At the same time I asked on the TYPEONEGRIT group whether it was possible to get an excellent HbA1c after decades of high carb abuse and was met with heaps of examples of people who had used Bernstein's approach to get HbA1cs in the 5s and 4s after decades of having Type 1.

 

[martykendall]

If someone falls into the first category, and therefore cares, they will also listen to the reasoning relating to T2 and the use of insulin. I suspect that (based on the stories that we see in the forum), they would prefer not to have to use insulin, so use as a short term medication while bringing the body back on line would be considered reasonable.

Yes. Particularly given the recent realisation regarding the risks of insulin toxicity I would think for type 2s insulin should be seen as a short term crutch until they can modify diet and lifestyle to eliminate the need for it and their own pancreas an supply the requirements. I wonder if there's any research on the relative risk of high insulin versus high blood sugars?

For type 1s the dream would be to minimise the insulin load of the diet to a point similar to a normal health person's insulin levels with excellent blood sugars.

The danger of the low carb / high carb debate is that the high carb proponents will run a straw man argument and say that the body needs insulin (which is correct) and it's nuts to try to eliminate it. I just think you need to reduce it so you can achieve optimal blood sugars and minimise the risks of insulin toxicity.

I hope the discussion shifts from carbs to focus more in managing insulin...

 

[martykendall]

Was just listening to the latest Bernstein webinar and he got pretty hot under the collar about repeated use of the LCHF acronym in people's questions. Made it plain he supports LCH(igh)P(rotein) and only as much fat as naturally comes with the protein. He seemed to be under the impression that LCHF is a low/minimal protein diet.

He also got pretty heated about people testing for blood ketones if they don't have high BG - says it's a waste of money. I kind of got the impression he's missed the whole point which was pretty disappointing. However, he fielded one question about someone being told by an HCP that long term ketosis causes kidney damage and said it was nonsense and that ketosis is a perfectly normal physiological state - yet also said he doesn't advocate people living their whole lives in ketosis - which seemed kind of odd to me as I would think his level of carbs (30g) would naturally cause you to be in permanent ketosis unless you were eating massive amounts of protein? He seems to believe that ketones are only produced by fasting/weight loss.

@Indy51, I will have to check this one out. Sounds like it was a doosie. Seems you can listen to it at http://instantteleseminar.com/?eventid=66550773

My experience aligns with Dr B's comments about testing for ketones. Seems light ketosis aligns with optimal blood sugars. See https://optimisingnutrition.wordpress.com/2015/03/22/ketosis-the-cure-for-diabetes/ I would love to see this dataset explanded past my n=1 experiment.

It makes sense to me that Bernstein would advise to eat protein rather than carbs for T1s as you can get glucose from protein via GNG at a slower rate. But then what about the wider population? I would argue that there's a sweet spot for insulin load (i.e. carbs plus glucose from protein via GNG) that provides adequate glucose but not too much that would lead to obesity or insulin toxicity? Thoughts?

 

[Winnie53]

As a type 2, with a blood glucose level of 282 mg/dL (15.7 mmol/dL) after not testing for 4 or more years, I am so grateful I refused metformin and a statin initially and immediately started the LCHF diet. Also, the idea of using insulin initially on a short term basis would also have been unacceptable, more so actually.

My thinking is this...

It's hard enough adjusting to the LCHF diet, followed by the beginning of ketosis...and the liver dumps...and the electrolyte imbalances that follow. Oh, forgot to mention the initial shock, immediately followed by fear that you permanently damaged your eyes, nerves, vascular system, kidneys and liver, and now you're on this diet that will supposedly "clog your arteries and give you a heart attack".

I can't imagine doing more than I did those first two months. Testing my blood glucose, often 7 or more times a day and charting my progress, kept me plenty busy. If I had to transition to beginning two to three medications on top of all that, I...I don't think I could have done it, perhaps if I was hospitalized... It's just too much change. And frankly, it would have taken away my drive and determination.

Interesting conversation...I'd like to return to this topic and re-read it in a few years when I have a half a chance of understanding it. For now, it's enough to focus on just type 2. Those of you in the type 1 world amaze me.

 

[Pasha]

@ Winnie53

" Those of you in the type 1 world amaze me". Exactly my thoughts. Also their knowledge re insulin puts them streets ahead.

"clog your arteries and give you a heart attack". LOL, I started the LCHF diet about 10 years after quadruple bypass surgery .

I was attracted to the science behind the LCHF and reasoned that "what have I got to lose at my age" because

the conventional low fat diet had not proved itself.

 

[tim2000s]

@tim2000s, I've used your CGM plot as and example at https://optimisingnutrition.wordpre...e-insulin-reaction-to-protein-dose-dependent/

Let me know if this is OK?

Have you ever done this sort of test with 100% fat like butter or coconut oil? I would be interested to see the result.

That's fine @martykendall . I was going to say that I've not tried it with a 100% fat trial, and then I remembered that most mornings I make a bulletproof coffee with Butter and Coconut oil

Unfortunately I can't show you the traces for those, but it's an easy enough experiment to redo. Just as a from memory exercise, I don't recall seeing any real impact on BG levels with that. Certainly not anything that made me stop, take a photo and post it on here. It usually contains 25g of butter and 25g of Coconut oil....