I will answer this tomorrow, but just want to say that my protein levels were always low on the low carb diet and on the plant based diet they are mid range. I am very pleased.
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Hi again Marilyn, back from 11-mile run now. Can write a bit more. I am not surprised that you had low protein intake while you were not feeling so well. That would fully explain lethargy and other symptoms you mentioned.
I will try to summarize key mechanisms of diabetes that are relevant.
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Within endrocrine pancreas (aka islets), islet (local) insulin (secreted by beta cells) is the primary regulator of alpha cell hormone secretion including glucagon.
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Alpha cell hormone secretion is secondarily regulated by blood glucose levels, much less potently than by insulin. Both regulators have inverse relationship to alpha cell hormone secretion.
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In all forms of diabetes (except MODY-2) there is an insulin secretion deficiency.
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Hence, in diabetes there is portal hyperglucagonemia driving excessive hepatic glucose output/production (aka HGO or HGP).
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Both portal glucose and amino acids (with varying potency for each AA) stimulate the beta cells. AAs also stimulate alpha cells directly â glucose does not. Glucose is a more potent stimulator of the beta cells than are any of the AAs, by a factor of three or four or more.
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The deficient islet blood levels of insulin, relative to portal nutrient stimulation, result in deficient restraint of glucagon secretion â i.e. hyperglucagonemia.
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Because of this the daily HGO of the liver is larger in a diabetic than in a non-diabetic. This has been confirmed by measurements in the research lab.
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Without a direct supply from dietary carbohydrates hepatic glycogen is supplied only by gluconeogenesis from certain AAs. The daily requirement for protein is therefore higher in a diabetic than for a non-diabetic on a ketogenic diet.
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It is important to understand that the hyperglycemia of diabetes is caused by local islet blood insulin deficiency in response to AAs and glucose. It is not significantly contributed to by hepatic uptake of portal glucose (i.e. dietary carbâs) directly.
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Dietary protein CAN be compensated for with peripheral (injected) insulin. Dietary carbâs CANNOT. In diabetics the islet glucagon response to portal glucose is INVERTED â in a non-diabetic it is reduced (usually to zero) but in a diabetic it INCREASES (often by a factor of 3 or 4). This results in positive feedback rather than negative feedback, and is the fundamental reason why it is impossible to compensate for carbâs with peripheral insulin.
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Portal AAs stimulate both beta cells and alpha in a different way. Feedback remains negative for AAs (i.e. dietary protein), and a certain flux of peripheral insulin will predictably compensate a certain flux of portal AAs in the peripheral blood. The flux is a rate of flow from subcutaneous adipose into blood (for peripheral insulin) and from small intestine into portal vein (for AAs from dietary protein).
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Peripheral insulin CANNOT compensate for AAs in islets, portal vein or liver. It can only compensate in peripheral blood by driving excess HGO in peripheral tissues (e.g. muscle which stores it as local glycogen). The diabetic will always (at least with current technology) produce excess HGO.
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With inadequate gluconeogenic substrate and dietary glucose (combined), the liver will take AAs from the lean tissues of the body as required. This is almost certainly part of what was occurring with the low-protein, low-carb diet, and is catabolic and very unhealthy over the long term.
The above summary is minimal for protein and carbohydrate metabolism and diabetes â there is a lot more. But few understand just the above and it is vital.
Suffice it to say that one should get no less than the 1.5g (of complete or animal-sourced protein) per kg of lean body mass that I recommended, based upon the protein metabolism science for non-diabetics. One could argue a diabetic might need more, at least of the gluconeogenic AAs.
You can, alternatively, supply hepatic glycogen directly from dietary carbâs. That is essentially what you are now doing, from the sounds of it. But one cost will be complications of diabetes accumulating over time (i.e. death of neural and microvascular tissues). If you use a glucose meter to monitor the prandial (meal-absorptive) period every half hour (and there is a typical half-hour delay from serum to capillary blood glucose level) after a meal you will observe the problem. It does not matter how you choose to apply peripheral insulin â with a large bolus of carbâs it is essentially impossible to maintain normal BG due to the positive-feedback phenomenon discussed above. If you are aggressive you will likely observe first hyperglycemia followed by hypoglycemia. If you are less aggressive you can avoid the hypoglycemia with even larger peak blood glucose. One can try various fast-acting insulin mimetics, but compensation for carbâs cannot be made reliable. Dietary protein must dominate the portal islet stimulation during a prandial period for reliable and predictable compensation of peripheral BG.
I recognize your stated preference for plant foods. I wish I could say that it is possible for a diabetic to be optimally healthy on a predominantly plant diet. But it simply is not. While some non-diabetics can do so (much more practically, at least), it is really a harsh compromise for any diabetic (excepting MODY-2). The plant foods richest in AAs, and none of which offer complete protein with all essential AAs in the optimal proportions of animal protein, are all heavy with both carbâs and dangerous phytochemicals that cause a lot of problems in many people. Optimal proportions of AAs are what is required for substrate to generate (and regenerate) tissues in animals, including humans. Out-of-proportion AAs will result in unusable excesses of most and protein metabolism will be limited by those in the lowest supply proportions. Even a very carefully planned plant diet will supply out-of-proportion (aka incomplete) AAs. The proteins in plant tissues simply perform a vastly different role to those in animals. There is little relationship of function and no relationship of ratios of AAs.
And inadequate dietary protein results in increasing health problems as we age (independent of diabetes) â this is the second âcostâ or tradeoff. Sarcopenia is one of the most common examples, and bone health is another, and there are many more. There is both a deficiency of mTOR stimulation and AA substrates that increases with age with inadequate dietary protein.
I suspect that what I am advising will not be terribly palatable (forgive my pun), but if you adequately investigate on your own you will see that it is all very fundamental and well established (even if not broadly recognized). I think that if you take it to heart you will achieve a greater longevity and quality of life. It is offered in that spirit, for you in particular but also for others on the forum.
I will add one more phenomenon that mostly applies to T1DM (or any diabetic producing well under 5% â close to zero â islet insulin). This is named the âdecrement in intraislet insulinâ in the research literature. The phenomenon generally begins three to five years after a diagnosis of type 1 diabetes. It takes a few years for beta-cell function to decline from 20% (at time of diagnosis) to nearly zero. After this the alpha cells adapt epigenetically to the lack of insulin signal (degrading direct response to BG), and maybe more crucially the âdecrementâ disappears because islet insulin is always at zero. This causes a degradation in responsiveness to hypoglycemia, and there is added lag and a lower BG threshold before glucagon secretion raises peripheral (including brain) blood glucose. A drop just a bit below normal fed-state BG levels in a non-diabetic (and in myself or anyone still producing significant endogenous/islet insulin) will generate a prompt decrement in islet blood insulin, and this is what generates the prompt and sensitive normal âprimaryâ response in alpha cells to raise portal glucagon and hepatic glucose output (derived directly from hepatic glycogenolysis, very quickly).
On the other hand, in long-term T1DM and very advanced T2DM (i.e. all ketoacidosis-susceptible diabetes), the glucagon response will be sloppy and tardy. The secondary response (adrenal epinephrine) will kick in first, and the energy crisis in brain generates an unpleasant sensation (jitters, nausea, etc.) and is a much weaker stimulant of increased hepatic glucose output. The brain may induce unconsciousness or coma (to protect itself by eliminating energy consumption by other tissues) in more severe sustained hypoglycemia.
This phenomenon of course complicates insulin therapy, mainly for bolus injections to cover meals. It is something to be aware of for anyone producing nearly zero endogenous insulin. It is well recognized and documented in the research literature, but little recognized by clinicians and patients.
Best of wishes.
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P.S. For those who might ask the very good question of why peripheral insulin cannot have any effect portally (i.e. upon liver) or within the islets (i.e. upon beta and alpha cells), I should explain. There are two reasons.
- Because injected insulin starts in peripheral-tissue blood, and the peripheral tissues make up most of the mass of the body and are mostly insulin-regulated (i.e. consume insulin), nothing reaches the portal vein and liver before insulin exhaustion by peripheral tissues. This has been verified by measurements.
- More fundamentally, portal blood hormone levels are up to 40 times higher than in peripheral blood, and up to 400 times higher in islet blood (where they are first secreted by alpha, beta and delta cells). They reach the highest levels during the prandial period (stimulated by nutrients, glucose and AAs, from a meal), which is also the most important period for insulin therapy in a diabetic.
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P.S. Marilyn, I guess I should suspect that you might use an insulin pump and probably have a CGM. Despite my old-fashioned terminology (I use vials, syringes and finger sticks), the same principles apply. Pumps inject into subcutaneous adipose, with significant potential complications from scarring, etc. And CGMs sample capillary blood (mostly still, I think), also with potential complications of both scarring, drift (out of calibration), etc. Both are subject to the same limitations, plus additional ones, as with syringes or pens and discrete testing by meter and reagent strips.
@Mac2, do you have a concise set of peer reviewed references to support your assertions? Most of what you say is uncontroversial in isolation, but not commonly combined to make such definitive recommendations, let alone quantitative ones. I must admit that some statements like âdangerous phytochemicals that cause a lot of problemsâ also raise my âcrank alertâ hacklesâŚ
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Lol CGMs measure glucose in the interstitial fluid not capillary blood
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Thanks Peep. Would be similar in lag vs. serum, to capillary, I think. Maybe even a bit more.
Mac, I switched to pens about 2 yrs ago. I used vials for about 58 yrs. I must admit that pens are easier.
I purchased my first CGM 2 weeks ago. I like it when it is working well for me. It is easy to wear.
I have never used a pump and donât plan to. My A1câs have ranged from 4.6 to 5.8 the last almost 20 yrs. I see no reason to wear a pump since my diabetes is so easy to control with food and exercise. I may eventually though.
The diet I follow lowers insulin resistance because it is very low fat. I use close to the same amount of insulin for 30 carbs of low carb food as I do for 275 carbs of plant food.
I do more exercise on the organic whole food plant based diet.
This diet was designed by a type 1 who has degrees and a doctorate from Berkeley and Stanford in nutrition. He is super smart and extremely healthy.
If you want to understand the way this diet works go to Mastering Diabetes. He and his partner are vegans and are extremely healthy.
There are all kinds of opinions out there with many brilliant people who are convinced their science is correct.
If my protein levels were low, which they arenât, they are finally in the middle range after being in the low range for 11 yrs low carbing, or if I had felt good while low carbing I would certainly be in the low carbers camp.
I have been around for along time now and have discovered that a fat/meat diet is the last thing my body needs at this time.
I appreciate all the effort you have put in sharing what works for you. I hope that it helps someone else.
Mac, I reread what you wrote and understand a bit more of it this time. I do not have a scientific background, and can only go by medical books written for the layman. I will look up the professionals you mentioned.
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Hi Marilyn, wow â you are a 60-year survivor of T1DM. That is impressive.
CGMs are pretty nice â I would use if I could afford to. More beneficial for T1DM I think, in any case. Easy to move sites around often enough to get reliable performance.
Good practice to avoid pumps I think, too. These are very problem-fraught, and I think inferior to discrete injections for that reason. They are not so easy to move around, and constant supraphysiological insulin develops scar tissue and this is a big problem for reliable performance.
5.8 is an interesting number for HbA1c. I can offer the comparison of my own case as food for thought. Once I first self-diagnosed diabetes and started monitoring blood glucose with a meter, between eight and nine years ago (mid 2010), I had had HbA1c in the range of 5.3 to 5.7. The HbA1c was my tipoff, because I was already eating a ketogenic diet. I did not get a full physical exam from a diabetologist until mid 2014. Shortly after this I recognized that I was HNF1-alpha, by phenotype, and I also have more recently discovered a biomarker for diabetes-causing mutations in this particular homeobox that are otherwise unobserved in the population as far as I know (i.e. as rare as HNF1-alpha diabetes). This biomarker had already caused me endless problems with screening tests for kidney function and generates a large discordance between the eGFR (extrapolation of GFR from the single parameter of serum creatinine) vs. legitimate or explicit GFR tests such as C-cystatin and 24-hour creatinine clearance. I have had many of both full GFR tests over the years, and actually measure top-of-range and out-of-range on the high end with these tests. Because of my most serious genetic condition (CVID) I have had more problems even in 2019 with immunologists who do not understand the discordance and had screened initially with serum creatinine alone.
With insulin therapy I maintain around 5.0 for HgA1c. Because I generally require a 2nd injection of Novolin R four hours after my meal (I eat once daily when not fasting) due to a prandial period of more than four hours, but usually have not applied the 2nd dose, I believe that I could probably get down into the 4âs with more rigorous covering of meals.
I have extensive complications of diabetes from over 5 decades of mild hyperglycemia (I have ~40% beta cell function by extrapolation from three clinically tested parameters) and undiagnosed diabetes. I ate a conventional diet until 2009. I have higher than average insulin sensitivity which is a trait of my type of diabetes. In an OGTT applied in 2010 my serum BG dropped from the 0-hour baseline to the 2-hour lab result. I measured myself with a personal meter every 1/2 hour in between. My meter at the time was not the one I use now, which is the most accurate on the market. But I am pretty confident that I peaked at 135 to 140 mg/dL before dropping, at around the 2-hour mark. Figuring for a half-hour lag of serum-to-capillary blood glucose this would correspond actually to the 1-1/2-hour mark. At 2 1/2 hours I showed about the same BG on my meter as the 2-hour lab result. I plateaued for about an hour or more before dropping fast. With the high insulin sensitivity (and quite low basal blood insulin at the time also) I am much more similar in phenotype to a T1D and very dissimilar to a T2D.
I have experimented, before starting insulin, a few times with mixed meals of the type I used to eat and I reach BG levels of 150 to 170 mg/dL at the most and can stay up there for hours before dropping. Such meals would have contained protein and something like legumes (i.e. beans). My peaks were still a bit below the typical 180 mg/dL threshold for polyuria. I have never experienced polyuria in my lifetime, nor polydipsia. This occurs at about 20% beta-cell function. My beta-cell function and basal glucose has been rock-stable ever since I have started testing for glycemic parameters. That is consistent with the monogenic condition. The conventional treatment is sulfonylurea (although a 20% dose compared to that for T2DM) and this is the sole cause of the progression observed, to varying degrees, in other HNF1-alpha diabetics. The HNF (Hepatic Nuclear transcription Factor) monogenic forms of diabetes are intrinsically non-progressive â Stefan Fajans, one of the earliest of all researchers of monogenic diabetes, wrote late in his life that he also believed this specifically for HNF1-alpha I found recently. The HNF beta cells are considerably smaller in size than normal due to the underexpression of many insulin-related proteins and this can be observed with a microscope.
All of my BG testing prior to 2009 was not at all indicative of diabetes by any conventional measure. Even once I self-diagnosed with my mild form of diabetes, two successive PCPs refused to believe that I was diabetic. This was a mild annoyance, but since all therapy was self-administered with over-the-counter (human) insulins it really did not matter.
Nevertheless, when I was finally examined by Dr. Richard K. Bernstein (with more than a full day of just physical exams) for complications I had almost all of them. The vagus nerve damage was one of the most advanced cases he had seen, based upon his comments. He uses an old-fashioned R-R interval ratio test. My result was 1.1. 1.0 is as low as possible, and he only mentioned one long-term uncontrolled T1D that registered this low with extensive physiological symptoms including gastroparesis that sounded much more severe than mine.
It is a difficult comparison to your case as a T1D, but still worth considering I think. After about 51 years of conventional diet before starting low-carb, and almost five more years before beginning to administer bolus (and basal) insulin to cover meals, I had quite advanced complications despite the mild diabetes/hyperglycemia. My basal/non-prandial intrinsic (i.e. without any peripheral insulin) BG is 95mg/dL which is also typical of HNF monogenic forms of diabetes. This would have been not a factor at all in development of my complications in my estimation.
Michael Brownleeâs research indicates, in agreement, that the vast majority of diabetic complications result from the rapid hyperglycemic transients from meals. Indeed, MODY-2 (or glucokinase MODY) requires no treatment and in this form of diabetes there are never any complications, despite typical basal BG of 150mg/dL due to the islet BG sensing defect. The cells easily compensate in the long term to a higher BG baseline. But not for transients that occur within a several-hour timespan.
My conclusion is that diabetic complications will accumulate at a significant annual rate with a HbA1c in the upper 5âs that is dominantly generated by inadequate suppression of peripheral blood hyperglycemia during prandial excursions. BG peaks always below 180mg/dL are likely what I had on a higher-carb diet for 51 years â I never experienced polyuria and other experiments are also consistent with this assumption of lifelong mild hyperglycemia while absorbing nutrients from meals portally.
With BG peaking above 200mg diabetic complications would develop more rapidly, and above 300mg even more rapidly, and so on. I suspect that you are able to keep BG below 200mg with your present diet, but you will know your numbers by experiment and measurement.
With insulin I stay well below 100mg/dL, usually near 80mg/dL or lower, with the only exceptions being occasional morning hyperglycemia a bit over 100 (due to gastroparesis and eating too late quite infrequently) and mild hyperglycemia of up to 100 and occasionally a bit higher towards the end of a prandial period for which I do not apply a 2nd injection.
Some of my diabetic complications are pretty painful and debilitating, episodically. Some of them are admittedly amplified by my primary immunodeficiency, I think. But their origin is the diabetic hyperglycemia. Dr. Bernstein concurred (during the less than a year period during which I consulted with him) and has much experience with many other patients with simlar complications.
I assume you were diagnosed as a juvenile. If you live for another few decades (Bernstein, also a juvenile T2D, is 85 now I think and still seems as active as when I saw him in 2014) with higher HgA1c it is a risk for increased complications. Prandial peaks between 100mg/dL and 200mg/dL are pretty dangerous IMO. My own case is rare, even for HNF type diabetes, because I never approached 20% beta-cell function, where insulin granulation is lost and polydisia and polyuria develop all of a sudden, only then leading to the diagnosis of virtually diabetics. The vast majority of HNF type diabetics are misdiagnosed as either T1Ds or T2Ds â it is about half and half. The specific combination of SNPs within the HNF homeobox vary amongst individuals, and hence the severity of hyperglycemia also varies. The milder diabetics like myself are misdiagnosed with T2DM and those with more severe hyperglycemia with T1DM.
Hence, I think my history is a good reference for rate of accumulation of complications with mild hyperglycemia. My own goal, since I had no idea what was going on for over five decades, is to regenerate lost tissue with tight control of BG. The most important one is to recover vagus nerve tissue and function, and based upon my observation of degree of gastroparesis I think I have made some progress but have by no means normalized.
I wish you the best of luck, and have enjoyed our discussion. I hope some of my info might be useful for you and others.
-Ken
Sorry, but unless and until you use a pump, your assumptions and conclusions are misleading to those who may be considering using them. First off, they are not âproblem fraughtâ as long as you know what youâre doing. The same can be said about MDI. Having been on injected insulin for 18 years and on a pump the following 28 (including one or two âpump holidaysâ on MDI in that period), I can tell you first hand both
technique have their unique challenges and unique benefits. As far as scar tissue, with proper site rotation and site change intervals, that can largely be avoided by most.
Iâm not preaching that anyone choose one technique over the other. Itâs a personal choice. Iâm just pointing out some incorrect generalizations about pumps in your post.
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Point taken â fair enough. My comment only echoes what I have heard from some diabetologists about patients. Your experience seems to have been much better.
October 9
Mac2:
Good practice to avoid pumps I think, too. These are very problem-fraught, and I think inferior to discrete injections for that reason. They are not so easy to move around, and constant supraphysiological insulin develops scar tissue and this is a big problem for reliable performance
Sorry, but unless and until you use a pump, your assumptions and conclusions are misleading to those who may be considering using them. First off, they are not âproblem fraughtâ as long as you know what youâre doing. The same can be said about MDI. Having been on injected insulin for 18 years and on a pump the following 28 (including one or two âpump holidaysâ on MDI in that period), I can tell you first hand both
technique have their unique challenges and unique benefits. As far as scar tissue, with proper site rotation and site change intervals, that can largely be avoided by most.
Iâm not preaching that anyone choose one technique over the other. Itâs a personal choice. Iâm just pointing out some incorrect generalizations about pumps in your post.
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But itâs the Canadians. Not surprising, eh. 
Sorry @Jimi63 - lol
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Ken,
I have great admiration for Dr. Bernstein and I started following his low carb way of eating 15 yrs ago. I read his books and was impressed with his knowledge. He was almost a decade older than I was when diagnosed, but he is also older and I think had had diabetes about 10 yrs longer than I had when I read his books.
I followed his diet strictly for 11 yrs. my A1câs ran from 4.6 to 5.1. Eventually my body rebelled and I started eating low fat organic plants. My insulin resistance plummeted. I became healthier. Not all ways of eating are good for all bodies.
5.8 was my latest A1c and is the highest A1c I have had in almost 20 yrs. The one 3 months before that was 5.4. I was not happy with 5.8 either but I also was fighting a nasty infection and exercising less.
I am so sorry that you have had so many complications. I thought about having Dr. B check me out, but it would have been a cross country trip and since I donât have any noticeable complications or didnât before heart stents which I received while low carbing, I saw no need to go. I really donât want to know if I have internal complications that I canât do anything about because they would cause me stress.
My eyes had a little retinopathy after 22 yrs of urine testing, but once I got my first huge glucose monitor about 40 yrs ago, I cleaned up my act and the retinopathy disappeared. I was very fortunate. I imagine the need for stents was tied to my first 22 yrs of having diabetes. When I had my first A1c test in about 1980 it read 10. I was very, very fortunate that I didnât have many complications by then.
I am extremely disciplined and I think that is why I do well. I have eaten all kinds of ways since being diagnosed. I certainly wasnât disciplined at all the first few decades. For now I am happy being a low fat plant based vegan. Hopefully I will be able to live another 15-20 yrs, but I will have to see if my early years catch up with me.
I wish you a healthy life Ken.
Thanks for your thoughtful response, Marilyn. It sounds like you have done very well in regenerating tissues, as had Dr. Bernstein also, from early years with type 1. I have it pretty easy in many ways, as I produce still more endogenous insulin than almost any diagnosed/overt diabetic of any type.
I understand the various types of diets you have adopted over the years, and I think your current meal composition is understandably more tolerable. You will be able to see easily, and probably already know, where you peak prandially for your meals. It does take a lot of dietary protein, and a T1D is worst case I would think because of zero insulin (hence, maximum hyperglucagonemia and HGO and hepatic glygenolysis), to supply adequate substrate for gluconeogenesis to keep hepatic glycogen stores replenished.
Dr. Bernstein is a really tiny guy, and eats very small meals (tiny by my standards), and I think that makes things easier for him. Also, he uses a method (having observed him first-hand, this is my own characterization) of essentially always administering a bit more than compensatory subcutaneous insulin, and he checks his BG every single hour and brings it up, if necessary (which it often is), with dextrose solution (i.e. fast-acting liquid). He also justifies this method because he lost consciousness leaving the hospital where he gets his IVIg infusions (he has mild CVID which he detected in his sixties I think) years ago, due to a surge of endogenous insulin that can occur with T1DM, especially in response to an infusion of antibodies. So he is vigilant about keeping his BG up (i.e. avoiding hypoglycemia), and tolerates a higher HbA1c because of this. I think his HbA1c is similar to mine now.
By contrast I donât worry about moderate iatrogenic hypoglycemia, and I never feel it and only detect it if I use a meter. I produce substantial ketones at all times, and if I cover a meal with a bit too much insulin my primary response (i.e. endogenous glucagon) kicks in right away. This does not work with T1DM as I discussed earlier.
If you can keep your rate of portal glucose influx low with slow-digesting plant foods containing more fiber and more amylose vs. amylopectin, which is probably what you are doing, it will be best of course. I think that minimizing the peak BG is really the name of the game, and a lower peak portal blood glucose with equivalent HbA1c (say, between two types of meals, with a longer absorption period for the lower-peak meal) will generate lower aggregate free-radical stress in cells.
Have you read anything about so-called âresistant starchesâ? These might also be helpful. Chilled (cooked) potatoes, unripened plantains, and other specially selected or prepared plant foods are supposed to have a fairly high proportion of starch that is resistant. This can stretch out the prandial interval and lower peak HGO while also providing glucose to the liver, for replenishing glycogen, while dietary fiber stretches the prandial interval but does not contribute any more glucose.
There are many ways to âskin the catâ, and all of us are somewhat different to be sure.
Best âŚ
Ken