Protocol For Curing Type 2 Diabetes, Anyone?

[Wilfrid]

@yerrag , I think that if your friend can read the following article, it might be a helpful tool as to really understand what's going on with the " insulin " thing.
Please make him read this, I'm sure that it will give him/her the strenght to fight against his disease.
I have shown it to 2 medical doctors, they were absolutely unable to contradict Sonksen's points.
https://watermark.silverchair.com/8...cOKGiWNgsmuKkZbqj_im0NXjdnB5GNeV49vJbB1SZ19i8

 

[yerrag]

My point is that what Peat or Kempner found was interesting, but what your friend needs is what works for him personally. Some people seem to do really well on mostly fruit (I guess you've read Jennifer's thread). Some people don't seem to cope with that much fructose, and do better with more starch. There are examples of people improving their diabetes with both approaches. I don't know where your friend would be on that spectrum. Personally, I have not done detailed blood glucose tests, but in terms of stable energy and well-being, I seem to feel better if I have some of each. Actually, I include potatoes and other roots too, and wouldn't want to live primarily on fruit and rice at this time if I can help it.

There's also the curious case of starch. Some people with higher amounts of salivary amylase may have a better insulin response than someone with less salivary amylase, but eating something sweet first may be a workaround, leading to lower postprandial glucose levels. I get better results (in terms of both glucose levels and overall well-being) by eating a combination of starch and fruit rather than mostly one or the other. Everyone needs to find what's best for them. Sometimes Sugar Is Better Than Starch

Very useful. Thanks. I haven't yet read what @ecstatichamster 's links in his last post on this thread, and together with @paymanz 's thoughts on glucose, it's coming together now. It's all very nuanced. Nothing is cookie-cutter here. It's hard enough knowing these things and applying on oneself these. Plenty of fine-tuning. But it's a minefield if you were the second party helping a friend, who can easily be overwhelmed by a lot of gotcha's.

Unnatural in that most people aren't going to consume 75 grams of dextrose that will be in the bloodstream within 15-minutes. That places a huge burden on first phase insulin response.

Insulin sensitivity is how efficiently insulin shuttles glucose into the cells. Glucose tolerance is simply looking at the glucose levels. I think both should be looked at, but you also need a point of reference, which would be OGTT results from other people, preferably a variety of people. I looked at some results in the past, and was surprised to see some people had a healthy looking glucose curve, but their insulin was 3x the level of what it should have been (probably a good recipe to overshoot and end up hypoglycemic). There's also people with very high insulin sensitivity, but due to limited first phase insulin response, or very little insulin in general, their glucose still spiked higher than desired. It is nice to know what's happening, because in the latter instance, the person would simply need to place less initial burden on the pancreas. Slowing the influx of glucose would allow the pancreas to keep up with insulin production.

How low was your glucose falling after the OGTT?

As to how low my blood glucose went, it started at 105, then 110, 91, 65, 83 ,88 each hour concluding at the 5th hour.

I can see how I fit into that category you described. My hypoglycemia could have been worse. It reached 65 on the 3rd hour, but it came back up to normal. Still, I was a sick person because of it. Flu every year, even if I tried to hide from it during February. I did many things to improve it (chiropractor, mercury amalgam removal, chelation), and I also changed to eating brown rice from white rice, just to let the glucose trickle in slowly than to indulge in a deluge of glucose from eating white rice. Yes, the OGTT may be unnatural, but it exposed my weakness. I haven't had a fever nor flu since I made the change since then.

How is your friend's health? Are they heavy? What is their current diet like? I doubt they're willing to overhaul their lives, but maybe there's simple changes they could make.

Last time I saw him, he had lost weight and looking better. His paunch was visibly reduced. That was at a high school reunion, in which he fainted. I asked him later if it was a diabetic medication that did it, and he nodded. It was his first diabetic medicine, and he just wasn't aware of what it could do. He's interested in a different solution than that of his doctor, but I haven't elaborated on anything to him. I find I'm threading a fine line between something simple and useless and something complicated but helpful. Just like rice and fruit, I have to find the right blend.

 

[Wilfrid]

Sorry, for the link above, here is the right one:
Insulin: understanding its action in health and disease | BJA: British Journal of Anaesthesia | Oxford Academic

 

[Braveheart]

Sorry, for the link above, here is the right one:
Insulin: understanding its action in health and disease | BJA: British Journal of Anaesthesia | Oxford Academic

Excellent...

 

[yerrag]

Ray's Quote:
Diabetes, scleroderma, oils and hormones

Brewer's Yeast:
Brewer's Yeast Improves Glycemic Indices in Type 2 Diabetes Mellitus
Effects of chromium and yeast supplements on carbohydrate and lipid metabolism in diabetic men. - PubMed - NCBI (Chromium can be helpful too)

Magnesium and taurine don't need an introduction. They are well known and must be used whatsoever.

Thanks for the references, especially the 2nd one. It showed modest improvement in FBS, HbA1c, and insulin sensitivity taking 1800 mg of brewer's yeast daily for 12 weeks. Now would be a good time for me to ask Ray Peat what he meant by saying his father lived off brewer's yeast to cure his diabetes.

Macdougall - see his youtube videos, look up rice diet kempner. He's pretty sharp for a doctor. He believes in some stupid things, but he is on the right track of a high carb, low fat diet reversing type 2 diabetes.

How I Treat Diabetes

Drug therapy has consistently failed patients with type-2 diabetes, and their well-intended doctors, making the search for an alternative treatment imperative. Since the rich Western diet is agreed to be the cause of this epidemic, should diet not be the first place to look for the prevention and the cure?24 Written reports on the benefits of a low-fat, high-carbohydrate, plant-food-based diet on type-2 diabetes date back to at least 1930.25Several published studies demonstrate how type-2 diabetics can stop insulin and get off diabetic oral medications with a change in diet.26-31 One goalpost is weight loss to the point of normal body weight, at this time the blood sugars of most patients diagnosed with type-2 diabetes will normal, and then everyone will agree that no further treatment with medications is needed.

By great good fortune, this same low-fat, no-cholesterol diet successfully used for diet-therapy for diabetes has been shown to prevent and treat heart and kidney disease, and prevent many common forms of cancer. Heart disease accounts for 70% of the deaths in diabetics, diabetes is the number one cause of kidney failure, and cancer is more common in diabetics.​

Here is a convolutedly-written study that demonstrates in terms of Hb A1C, that replacing fat with carbs LOWERS Hb A1C, and improves glycemic control. I think the results were so stunningly un-PC that the writer couched the abstract and conclusion in language that indicates the OPPOSITE of what the study actually says.

Association of high carbohydrate versus high fat diet with glycated hemoglobin in high calorie consuming type 2 diabetics

In contrast to the commonly held view, this study showed that type 2 diabetic patients on high carbohydrate and low saturated fat diet have a better blood glucose control.​

A low-fat vegan diet improves glycemic control and cardiovascular risk factors in a randomized clinical trial in individuals with type 2 diabetes. - PubMed - NCBI

RESEARCH DESIGN AND METHODS:
Individuals with type 2 diabetes (n = 99) were randomly assigned to a low-fat vegan diet (n = 49) or a diet following the American Diabetes Association (ADA) guidelines (n = 50). Participants were evaluated at baseline and 22 weeks.

RESULTS:
Forty-three percent (21 of 49) of the vegan group and 26% (13 of 50) of the ADA group participants reduced diabetes medications. Including all participants, HbA(1c) (A1C) decreased 0.96 percentage points in the vegan group and 0.56 points in the ADA group (P = 0.089). Excluding those who changed medications, A1C fell 1.23 points in the vegan group compared with 0.38 points in the ADA group (P = 0.01). Body weight decreased 6.5 kg in the vegan group and 3.1 kg in the ADA group (P < 0.001). Body weight change correlated with A1C change (r = 0.51, n = 57, P < 0.0001). Among those who did not change lipid-lowering medications, LDL cholesterol fell 21.2% in the vegan group and 10.7% in the ADA group (P = 0.02). After adjustment for baseline values, urinary albumin reductions were greater in the vegan group (15.9 mg/24 h) than in the ADA group (10.9 mg/24 h) (P = 0.013).
CONCLUSIONS:
Both a low-fat vegan diet and a diet based on ADA guidelines improved glycemic and lipid control in type 2 diabetic patients. These improvements were greater with a low-fat vegan diet.
​

I think it was not the VEGAN part, but the HIGH CARB part that helped these diabetics improve on the vegan diet.

Thanks for these. The takeaway here is high carbohydrate and low fat will help type 2 diabetic patients greatly. And low fat is not to be taken lightly.

 

[yerrag]

Excellent...

This is good material. I'm still reading it. It turns upside down the dominant medical understanding on blood sugar regulation, starting with the role of insulin in glucose uptake, that it merely helps in glucose uptake into cells, but is not required for glucose uptake. I'm still reading, but I'm taking it slow in order to retain what it's saying. Thanks @Wilfrid !

 

[Rafe]

I was already convinced that RP is right about "sugar for diabetes." But what to do and how to do it in a way that isn't risky? And, we are talking mainly about T2D and not type 1 here.

So, recently I got vain when I looked in the mirror and got frustrated with my stable +30 lbs weight. Experiment: I decided to drop my calories a lot just to see what would happen, would I lose or gain? Surely I would lose. Har. I went down to around 1400 - 1700 cal/day and around 70g/day of that fat with about 4g/day PUFA.

Within 10 days I was getting miserable food comas. All those troubling stress symptoms started to return that we all know. After 14 days I was so miserable I quit the experiment and went to figuring out what to do.

I figured what had happened was I had switched to more fatty acid oxidation, cells had become more sugar resistant, more insulin had given me miserable hypoglycemia. After every meal. I had made myself "a little bit diabetic." [I don't know how I ever lived on beta oxidation mostly.] I confirmed for myself that Peat is right about the sugar for diabetes.

This is what I did that worked nearly immediately since I am now in good health and much less unsaturated:

I stopped eating meals and [at least temporarily] started eating very slowly and continually [just a bite or two at a time if solid food] to keep blood sugar stable-high-ish. But I didn't use a meter.

I read the Minger post around the same time you did on Kempner and others below-20g fat/day plans. So I reduced my daily fat to 20g/day, increased my calories to around 2000 - 2300, which meant I was getting around 120g protein [mostly protein-enriched fat free milk, shellfish, bit of liver, lamb] and 300g carbs [mostly fruit juice, some coke]. Some T3.

I think the continual eating, eating very slowly, keeping blood sugar highish and steady was key. But the very low-fat has been much better and easier than I thought and made the recovery nearly immediate. But then, I was ready for it. I think that how impaired your friend is matters, I mean how long they have been T2D might mean that remission can only be partial, even though I think RP is right to say that we should be hopeful for regeneration, I want to be also a little realistic about what to reasonably expect. Also, yeah, your friend might not be as hopeful or open as you.

There is so much on this thread that is good. @ecstatichamster on PUFA depletion and @cellboy on bear diabetes. Yes.

 

[ecstatichamster]

@Wilfrid thanks, this is a fantastic paper, much appreciated.

 

[Peater Piper]

I can see how I fit into that category you described. My hypoglycemia could have been worse. It reached 65 on the 3rd hour, but it came back up to normal. Still, I was a sick person because of it. Flu every year, even if I tried to hide from it during February. I did many things to improve it (chiropractor, mercury amalgam removal, chelation), and I also changed to eating brown rice from white rice, just to let the glucose trickle in slowly than to indulge in a deluge of glucose from eating white rice. Yes, the OGTT may be unnatural, but it exposed my weakness. I haven't had a fever nor flu since I made the change since then.

It's good to hear you've had such drastic improvements. Your OGTT results really are wild, I wish we knew what your insulin was doing, because you hardly spiked at all (although with how fast the solution can enter the bloodstream, you may have had an earlier spike, but to barely be above baseline at 1-hour is surprising).

It sounds like your friend is open to options, which is good. I've seen a lot of people bottom-out, it's not a pretty picture.

Sorry, for the link above, here is the right one:
Insulin: understanding its action in health and disease | BJA: British Journal of Anaesthesia | Oxford Academic

Interesting. The major point seems to be the overproduction of endogenous glucose. Chris Masterjohn has stated he thinks NAFLD plays a part. The triglycerides accumulate in the same area where glycogen would/should be stored. With nowhere to store the extra glucose, the liver upregulates glucose production.

I'm having trouble reconciling the idea that glucose uptake is actually higher in hyperglycemia even without insulin, though. They then state the ketosis shuts this down, but the entire reason diabetics enter ketoacidosis is due to glucose starvation in the cells causing fatty acid metabolism to run rampant. Ketoacidosis can occur even with hyperinsulinemia so long as it's still not sufficient to overcome the insulin resistance.

 

[Rafe]

@Wilfred @ecstatichamster That is a great article. I can see how there is no real hypoglycemia in reality, but only textbook teaching makes it so.

But am I getting this: in the authors' view insulin really targets & slows the liver's production of glucose, which brings down the massive loss of sugar in urine in diabetes, and there is no real cellular glucose resistance. But wouldn't this [just] shift the hyperglycemia problem away from the plasma and into the cells? If diabetics are "utilizing glucose" even more than non-diabetics then why is the respiratory quotient lower? See, I'm just starting to understand the ATP and beta oxidation cycles so I'm probably missing something obvious. They make it sound like diabetics have super-mito-respiration if that were possible. They go straight to ketoacidosis after that.

I wonder if their view is not forced by the requirement of seeing a cell membrane, an imperative osmotic equilibrium, & that glucose can't resist the gradient? I see that they are looking at labeled glucose as the evidence but they seem to stop the analysis once they've said glucose is produced by the liver, which is inhibited by insulin, and in the cells "utilized at a greater rate." I can hardly say that the article isn't doing enough. You have to stop somewhere.

 

[ecstatichamster]

(Dr. Peat has stated that insulin is a relatively minor element to the utilization of glucose and this paper shows he is right. He has said, for instance, potassium may have far more to do with it.)

To your point @Rafe maybe the glucose enters the cell but is not energizing it...? The mitochondria are burning fat instead and through the Randle "cycle" they can't metabolize the glucose...maybe the transport into the cell is just transport.

 

[Rafe]

Oh, that Peat point about potassium and glucose uptake does ring a bell.

I'm forgetting that it's a process. That any of the enzymes/cofactors could be unavailable even if glucose is. And since it's a self-intensifying system [the "whirlwind of atoms" thing] then if anything is missing then CO2 gets low, making O2 less available. I guess I got so caught up in the view that "sugar = oxphos!" that I got stuck. I think you're right, transport is just transport. Nice way of putting that.

 

[tara]

But it's a minefield if you were the second party helping a friend, who can easily be overwhelmed by a lot of gotcha's.

Peat's approach seems to always have been very strong on having people learn about physiology themselves, so that they can think about what might be worth trying, and on paying attention to the effects of foods and other things on oneself, so one can see what's working. This is one of the things I really like about Peat. It also encourages us to keep learning new ...
Much harder to choose appropriate foods by proxy.
If you are able to make some guesses about which articles would be worth sending your friend's way, perhaps that would help spark his interest and ability to guide his own choices?

Last time I saw him, he had lost weight and looking better. His paunch was visibly reduced.

This may be good, depending on how it's happening.
But not certain. Diabetes, before supplemental insulin and other medications, was a wasting disease.

 

[tankasnowgod]

Has anyone here ever attempted to cure type 2 diabetes successfully?

A friend just started diabetes medication, and in a party we were in, he passed out because the medication made his blood sugar go way low. I told him I'll see if I can provide a method where he can get his condition cured. I've been thinking about it for a week, and I can write down what I think will work. But I'd like to hear from our collective what you have that has already worked.

Thanks.

Never has Type 2 Diabetes, but, I did improve my blood sugar regulation and carb tolerance by lowering iron.

Get a full iron panel with TSAT and Ferritin, and look into blood donation.

 

[Wilfrid]

@Wilfred @ecstatichamster That is a great article. I can see how there is no real hypoglycemia in reality, but only textbook teaching makes it so.

But am I getting this: in the authors' view insulin really targets & slows the liver's production of glucose, which brings down the massive loss of sugar in urine in diabetes, and there is no real cellular glucose resistance. But wouldn't this [just] shift the hyperglycemia problem away from the plasma and into the cells? If diabetics are "utilizing glucose" even more than non-diabetics then why is the respiratory quotient lower? .

Hi, you may find a starting answer with this:

Glucose and free fatty acid turnover in normal subjects and in diabetic patients before and after insulin treatment

Glucose and free fatty acid turnover in normal subjects and in diabetic patients before and after insulin treatment.

« The tracer calculated rates of glucose utilisation correlated well over a wide range with the respiratory quotient in untreated diabetics, while respiratory quotient was inversely related to free fatty acid turnover rates. In untreated diabetics plasma cortisol and 3,3′, 5′-triiodothyronine (rT3) were increased whereas thyroxine and 3,5,3′-triiodothyronine (T3) were decreased. 3,5,3′-Triiodothyronine concentration was closely related to the metabolic clearance rate of glucose (p<0.05), while cortisol concentrations correlated with glucose production (p<0.02) and blood ketone body concentration (p<0.02).

It is concluded that glucose overproduction is the major contributor to the hyperglycaemia of untreated diabetes. »

 

[yerrag]

Never has Type 2 Diabetes, but, I did improve my blood sugar regulation and carb tolerance by lowering iron.

Get a full iron panel with TSAT and Ferritin, and look into blood donation.

How does iron affect blood sugar regulation? I know I had hemachromatosis and donated blood, but not sure if it had helped with improving my blood sugar regulation. Perhaps it did.

 

[tara]

here is the right one:
Insulin: understanding its action in health and disease | BJA: British Journal of Anaesthesia | Oxford Academic

Thanks. That broadened my view of insulin, and some of how its lack can cause acute trouble (ketoacidosis or electrolyte loss).
A couple of bits:
"When fasting hyperglycaemia develops, as in diabetes mellitus, it could result from either over‐production of glucose, through excess glycogenolysis and gluconeogenesis, or a failure of adequate glucose uptake in the peripheral tissues (including the brain). Most people think that hyperglycaemia reflects a reduction in glucose uptake as a result of insulin deficiency. This is not true."
"... the fasting hyperglycaemia of diabetes results from hepatic over‐production of glucose alone, since peripheral glucose utilization is increased despite the lack of insulin. Insulin treatment reduces glucose concentration through inhibiting hepatic glucose production. Under these conditions glucose utilization decreases, thus insulin administration reduces glucose utilization. This indicates that the plasma glucose concentration, rather than plasma insulin, is the prime determinant of glucose uptake. "

 

[ecstatichamster]

the authors of the first paper talk about "futile cycling" -- too much glucose enters the cell, and then leaves the cell, transported in and then out, without resulting in any energy production.

Basically these papers point to the liver producing too much glucose overwhelming the cells. The cells apparently pick up glucose without insulin even being present. Insulin's role is more of suppression of fat burning than anything else.

I have to absorb this more. This totally transforms my views of insulin and glucagon and cortisol. I think this is yet another case of Dr. Peat being right.

 

[tankasnowgod]

How does iron affect blood sugar regulation? I know I had hemachromatosis and donated blood, but not sure if it had helped with improving my blood sugar regulation. Perhaps it did.

Quite a few studies have shown that iron markers are elevated in diabetes, such as this one- Body Iron Stores in Relation to Risk of Type 2 Diabetes in Apparently Healthy Women

In fact, hemochromatosis initially was referred to as "bronze diabetes."

Even more important than the association, iron lowering measures (in those with high iron, and even "high-normal" iron), such as phlebotomy, have shown improvements in glucose tolerance and insulin resistance- Iron Depletion by Phlebotomy Improves Insulin Resistance in Patients With Nonalcoholic Fatty Liver Disease and Hyperferritinemia: Evidence from a Case-Control Study

I'm sure you can find more on pubmed. Chris Kresser mentioned quite a few studies in his Iron Presentation. If you jump to the 9:20 mark, he talks about quite a few studies as related to diabetes-

 

[yerrag]

the authors of the first paper talk about "futile cycling" -- too much glucose enters the cell, and then leaves the cell, transported in and then out, without resulting in any energy production.

Basically these papers point to the liver producing too much glucose overwhelming the cells. The cells apparently pick up glucose without insulin even being present. Insulin's role is more of suppression of fat burning than anything else.

I have to absorb this more. This totally transforms my views of insulin and glucagon and cortisol. I think this is yet another case of Dr. Peat being right.

I think this paper meshes very well with Peat's ideas. After reading this, I get to understand more what Peat was saying in Glucose and sucrose for diabetes. The one thing this paper diverges from Peat is its ascribing the variance of glucose uptake (as well as liver glucose production) among different people to genetics. Ray Peat ascribes this to PUFAs blocking glucose uptake.

Given insulin's role in inhibiting lipolysis and ketogenesis, as gleaned from the paper,it would be reasonable to infer that insulin promotes sugar metabolism. The consumption of fat enables fat oxidation, thus competing against glucose metabolism, and invariably lessens glucose uptake, contributing to higher blood sugar levels. And if the fat is PUFA, it also blocks glucose metabolism. Does this make a case for a low-fat dietary approach to counter diabetes?

And in the case of type II diabetes, where apart from PUFA inhibiting glucose uptake, an inability to produce sufficient insulin would make it hard to fully inhibit endogenous glucose production (by the liver), thus causing high blood sugar. Does this make a case for a high-carbohydrate approach, since both glucose and fructose would help restore the beta cells in the pancreas, thus increasing insulin production?

Kempner's approach looks to be validated. With the incorporation of Peat's ideas on PUFA elimination, even better.