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Tuesday, May 22, 2012

Excess protein turned to glucose?

It seems that part of the more recent trend of defining a "proper" low carb diet as being one that is moderate in protein and high (very) in fat is this notion that excess protein will just be turned to glucose.  Quite often I've seen Dr. Richard Bernstein cautions against eating too much protein because it just gets turned to glucose.  (I did look for a link but was unsuccessful, so if I'm misstating Bernstein here, please do correct me in comments.)   I had looked into this long ago, but never really said much about it, but there are two reasons why this never made sense to me.

First, a little biochemistry.  There are exceedingly few reactions that occur in our bodies without the involvement of an enzyme.   This includes not only anabolic (synthesis, building, energy storing/requiring) reactions, but also catabolic (break down, energy releasing reactions) reactions.  Glucose and fatty acids no more "spontaneously combust" in our bodies than does propane in my grill.  Enzymes are the catalysts of reactions, and reactions that require energy (all of those "genesis" reactions for example) are coupled with energy producing reactions that "drive" them.   Enzyme action is regulated by the amount of the enzyme produced and/or some mechanism of activating/deactivating the enzyme.  While enzyme mediated reactions can be related to substrate (reactant) availability and/or influenced by product availability/build-up, this isn't always the case.  I'd even go so far as to say that unless the reaction occurs in a highly compartmentalized fashion (e.g. within mitochondria), substrate/product concentrations generally have little effect on the reaction rates directly. 


Thus appears to be the case for proteins and the gluconeogenesis reaction.  The mere availability of gluconeogenic substrates does not appear to drive the reaction.  I'll try and dig up the cites I had long ago come across to this effect.  But a pretty well known hormonal response to protein makes for a more common sense based argument against this.  Carbohydrates stimulate insulin to assist in glucose clearance.  Proteins also stimulate insulin, but they also stimulate glucagon.  Why?  Because if you consume protein without any carbohydrate, the insulin secreted doesn't really "know" whether it's supposed to facilitate amino acid transport or glucose transport into cells.  Therefore, protein consumption would result in hypoglycemia without concurrent glucose production in the liver.  Glucagon stimulates glucose output.  If just the protein substrate stimulated glucose production, there would be no need for glucagon, right?  Of course this still leaves us with a potential hypothesis that excessive protein leads to excessive glucagon leads to excessive gluconeogenesis (and glycogenolysis).

Well, continuing on my LoBAG revisit kick, I was actually quite shocked at the protein content of the diets!  Here's the link to the study again.
FIG. 5.The mean fasting glucagon concentrations were similar before and after both the control and the LoBAG diets (95 ± 11, 91 ± 8, 91 ± 7, and 94 ± 7 pg/ml, respectively; Fig. 5). After 5 weeks on the LoBAG diet, the glucagon response was similar to the control for the first hour after breakfast. Subsequently, the glucagon concentration was higher at every time point until 0700 the next morning, except for one time point after dinner. Both the net and the total glucagon area responses were significantly increased after the LoBAG diet (P < 0.05).  ...  The glucagon area response increased 2.5-fold after the LoBAG diet.  (Fig. 5 -->)

FIG. 2.
And let us look back on the glucose profiles.  I'll not clutter this post with the insulin profiles again, but there was no difference in fasting insulin.   In the fasted state is when we expect the gluconeogenesis to be kicked up a notch or two, and if excess amino acids are lying around causing glucose production, we simply would not see the roughly 35-40 point drop in fasting glucose levels.  LC advocates will attribute it to the reduction in carbs, but, again, insulin in the fasted state did not change, and carb intake was just under 150 g/day.   So, well maybe this protein wasn't "excess" in the context of the relatively low carb diet?   For that we can look at a follow-up paper from these researchers.  Now this is for the LoBAG-30 diet, but the protein intake is the same for all LoBAG diets (30% energy) .
http://ajpendo.physiology.org/content/291/4/E786/F3.large.jpg
At right are the ingested and metabolized amounts of protein.  From the paper:
At the beginning of the study, during the first 24 h while subjects were ingesting the control (15% protein) meals, 105 g of protein were calculated to have been ingested, and 88 g were calculated to have been metabolized (84%; Fig. 3). During the last 24 h at the end of the LoBAG30 diet, 214 g of protein were calculated to have been ingested, and 144 g were calculated to have been metabolized (68%). The difference in percent metabolized approached statistical significance (P = 0.064).
The metabolized protein is determined by nitrogen balance.  It's the nitrogen containing group that makes an amino acid what it is, and unless incorporated into proteins, the amino acids are metabolized with removal of the amine group.  This would include amino acids that serve as substrates for gluconeogenesis.  I'm not  sure what to make for the remainder of the protein -- incorporated into lean mass?  In any case, though clearly more protein is metabolized for energy, if there were a direct effect on gluconeogenesis rates, one would expect that would be part of the increased metabolized protein and be reflected in fasting glucose levels.  It seems far more reasonable to conclude that "excess" protein feeds into the Krebs Cycle at various places as shown in the graphic below.   Note that AA's in green are called gluconeogenic, those in white are ketogenic, and some AA's feed in at multiple possible points.  Also, to date this figure remains for the life of me recall where I took the screenshot from.  If anyone recognizes it, please let me know!

So, I don't see any evidence for claims that too much protein leads to increased glucose and glucose burning.  It might lead to less "fat burning" as protein feeds into Krebs or is directly converted to Acetyl CoA -- the intermediary product of both glycolysis and fatty acid oxidation.  There may be reasons to limit protein, but it does not appear that glucose production is one of them.




41 comments:

Beth@WeightMaven said...

The whole "deaminated amino acids == glucose" concept has been something I have accepted as gospel, so this post is a bit of a wow for me.

I have furiously started googling and came across this from your former school which is gonna be my read over lunch!

LeonRover said...

Nice analysis Evelyn.

Back to Gannon & Nuttall again. Like.

You may remember that it was as a result of your posts "way back when" on LoBAG (& Hunter Gatherer studies)that I became an occasional commenter.

I have read most of their studies and note they have produced little recently.

Wonder if funding has stopped?

Slainte

OnePointFive said...

This is a subject that resulted in some quite heated discussion on one of the diabetes forums recently. T2 diabetics said that they had no increase in glucose levels after a no carb meal,type 1 (including myself) said that we had to take some insulin for the protein in a no carb meal or glucose levels would rise at 3 or 4 hours.
One small study in 1996 confirms this later rise in T1s http://okicent.org/docs/anyas_cr_diet_2007_1114_434s.pdf,

Marion Franz reviewed the evidence in a paper back in 2000.
" Perhaps 50–60% of protein goes through the process of gluconeogenesis in the liver, but virtually none of this glucose enters into the general circulation"
However
"In people with type 1 diabetes, the effect of protein on glycemia will be dependent on the state of insulinization and the degree of glycemic control. Protein requires insulin for metabolism, as do carbohydrate and fat, but has minimal effects on blood glucose levels. In well-controlled diabetes, large amounts of protein have the potential to contribute to glucose production, minimally increase blood glucose levels, and require additional small amounts of insulin."
http://journal.diabetes.org/diabetesspectrum/00v13n3/pg132.htm
(she also cites Gannon and Nuttall and for T1 the Peters and Davidson study cited above )
Dr Bernstein is a T1 so I suppose a rise in glucose levels would be supported by his personal experience.

Nigel Kinbrum said...

Google Reverse Image Search produced:- A little more on Protein.

TinEye Reverse Image Search produced:- Amino Acids and Proteins.

Evelyn aka CarbSane said...

Thanks! Oh, I don't know, PubMed is quite active for them. This from last September on LoBAG-30 http://www.ncbi.nlm.nih.gov/pubmed/21406307

Evelyn aka CarbSane said...

Thanks Nige -- definitely not the first, good chance for the second. SparkNotes doesn't reference its content. Hmmm.

Evelyn aka CarbSane said...

I will look into this further OPF, but what came to my mind first was that T1's lack insulin and protein normally elicits an insulin response, therefore apart from BG levels, it should be appropriate to inject insulin for protein. So the rise later on may be due to the missing suppression of GNG (and glycogenolysis?) by insulin and not the presence of the protein per se. IOW the hyperglycemia in T1's is highly attributable to unchecked GNG (I'm sure you've read that insulin paper I refer to here often) whereas a T2 is likely hyperinsulinemic and protein sensitizes the liver to suppress GNG. Just my first thoughts. More later.

Paul Jaminet said...

Possibly from here: http://perfecthealthdiet.com/2011/02/ketogenic-diets-i-ways-to-make-a-diet-ketogenic/

Paul Jaminet said...
This comment has been removed by the author.
Sanjeev said...

one thing I'm curious about is insulinogenic amino acids and all these diabetics not injecting insulin when they go low carb.

On one level it may make sense - if there are no cheap, easy tests to determine blood levels of those amino acids those patients can't titrate the insulin dose.

On another[0] level they've set themselves up for some big unpleasant surprises in 5, 10 or 20 years when research uncovers all the ways insulin influences disposal of those aminos.

Another way in which low carb sets up later metabolic disaster.

[0] more important

Galina L. said...

Here is the link where Dr.Bernstein writes in his book about how to limit protein for a weight loss

http://www.diabetes-book.com/book/chapter12_3.shtml

I am not sure that it is exactly what you are looking for, but at least it is about weight loss and the amount of protein.

julianne said...

Interesting. I went back to my Sipanuck textbook and the only cite for glucose from protein in the liver is this one
Quantitative analysis of amino acid oxidation and related gluconeogenesis in humans
http://www.ncbi.nlm.nih.gov/pubmed/1557428

Cant get immediate access to full text though. And this review looks interesting Protein turnover, ureagenesis and gluconeogenesis.
http://www.ncbi.nlm.nih.gov/pubmed/22139560

ItsTheWooo said...

Sorry this info is wrong.
Protein does absolutely increase blood glucose. Insulin deficient types of diabetes develop hyperglycemia from protein as they cannot cover the glucose load.

Type 2 diabetics are not insulin deficient, quite the opposite, and easily handle the glucose output of protein.

This is similar to how type 2 diabetics rarely develop diabetic ketoacidosis, but type 1 diabetics easily do. It's about the severity of insulin deficit. Type 2s almost never become so insulin deficient they go into DKA, the closest they get is a related syndrome called non-ketotic hyperosmolar hyperglycemia. This syndrome is the type 2 equivalent of DKA, and it is marked by severe, severe hyperglycemia (like, 900s!) and hypertonic dehydration (so many solutes in the blood from glucose). The emergent nature of this condition is related to the hypertonic dehydration which can cause cardiovascular emergency and mental status impairment/coma.

Since type II diabetes is a liver disorder, and type I diabetes is a pancreas disorder, this is entirely expected. The primary organ dysfunction in type II diabetes is the liver. It makes ridiculous amounts of glucose, all the time, due to genetic enhanced output (fact, type II diabetic prone individuals make 3 times the glucose generating output of non-diabetic individuals, not even considering the additional issue of resistance to insulin). It would be like having a bulldog with a short snout; its genetics make it prone to respiratory issues.

The type 1, in contrast, is in some serious shit if his or her sugar is running 300 or 400. That's severe insulin deficiency for a type 1 who has a normal liver, so sugar levels that high are only possible if they have like no insulin at all, and ketoacidosis is imminent. If this continues more than briefly it's a short way to the ER for an insulin drip/rehydration!

On the other hand, the type II will be sitting at 300 after dinner being like "and what?" So not even close to imminent medical decompensation; many type IIs live this way for years. They have plenty of insulin the problem is their liver is like HAHA I AM A SUGAR FACTORY.



So, when we observe that type 1s need to bolus insulin or else suffer hyperglycemia from protein, but type 2s do not, that's because your average type 2 has a TON of blood insulin and the amount of sugar from exogenous protein is very trivial compared to the amount of sugar their diseased liver is spewing out uncontrolled 24/7, which is barely being kept under wraps by their basal insulin of "omg your kidding". It would be like comparing an ant hill (a few grams of glucose from increasing protein intake) to a mountain (a liver constantly abnormally generating extreme amounts of blood glucose).


@Sanjeev, I assure you the diabetics who adopt low carb diets to manage their diseases are going to be much more concerned with the fact they get to keep their toes, legs, eyesight, and kidneys due to avoiding the absolute WRECKING BALL to anatomy and physiology known as diabetic hyperglycemia. The "unpleasant surprise" they will see is that they get to live healthy complication free lives meanwhile their diabetic relatives are invalids in wheelchairs with no legs on a 3 day a week dialysis schedule in assisted living/nursing homes.

Evelyn aka CarbSane said...

Possibly you got it from me? carbsanity.blogspot.com/2010/06/protein-for-energy.html ;)

I'm leaning towards it coming from SparkNotes ... in which case I'd love to know their original source as that looks like a text book graphic to me!

Evelyn aka CarbSane said...

Thanks Galina, Not exactly what I was looking for, but helpful nonetheless. Also, I now know where one low carber with high triglycerides picked up the myth that trigs generally rise during weight loss (haven't seen this in context of weight loss).

Evelyn aka CarbSane said...

@Sanjeev, I share that concern. I think it messes up insulin signaling, or at least has the potential to. Certain AA's are more insulinogenic than others, especially the BCAA's. Interestingly the obese (IR?) tend to have elevated circulating BCAA levels.

Evelyn aka CarbSane said...

Hi Julianne,

That first one looks interesting, efforting the full text on that ... will let you know. That second one led me to another paper and I've tracked down a few more. Follow-up post in the works!

Evelyn aka CarbSane said...

@Wooo: Do you have any citation for the fact, as you say, that T2's genetically have 3X the EGP of non-diabetics?

ProudDaddy said...

@Wooo: I know nothing about protein's effect on serum glucose, but as a pre-diabetic I have looked into T2. My research indicates you are spot on in labeling it a liver disease, at least in it's early stages. It's amazing how many supposed experts think it's a beta cell problem.

Evelyn aka CarbSane said...

@Wooo & PDaddy: I think it's a bit incorrect to say that T2 is pretty much only the liver while T1 is only the pancreas. Tis true about T1, but with inappropriate diet, T1's can actually become IR as well. More importantly, however, while T2's are hyperinsulinemic, there is clear beta cell dysfunction. This is actually the "event" that converts a severely IR pre-diabetic to a frank diabetic. T2's produce basal insulin but cannot mount the appropriate post-prandial acute insulin response.

@PDaddy: On what basis have you been diagnosed pre-diabetic? FBG and/or OGTT? The reason I ask, and I will be blogging on this hopefully sometime this summer, is that part of the problem with T2 is that it's a "disease" with more than one, possibly several etiologies. I'm not a big fan of all of her work, but Jenny Ruhl does say it best when she says diabetes is no more a disease than cough. Whacked glycemic control is a symptom. There is a fair overlap between those who have both elevated FBG and IGT, but there are clearly subgroups exhibiting only elevated FBG with normal oral glucose tolerance, and vice versa.

ProudDaddy said...

FBG between 100 & 125. I practically fainted from hyPOglycemia during my only OGTT. Fasting insulin is high-normal, so all these things lead me to conclude that my beta cells are AOK. I look forward to your upcoming article and agree on "several etiologies". I would particularly be interested in whether you think T2s who are normalized with metformin alone have pancreatic problems.

I suspect my problem is solely mild hepatic steatosis, but my doc says he can't palpate it because my abs are too developed. (I'm guessing that last part was just a nice person giving an old man a moment of joy.)

Evelyn aka CarbSane said...

Sounds about right to me if I were to venture to guess. Do you eat a lot of butter and beef for fat sources? The reason I ask is that even many of the young'uns over on PaleoHacks will report symptoms associated with hepatic IR from those (and strangely CO in some cases) fats (and we're not talking JM half sticks on a sweet potato amounts either).

ProudDaddy said...

No beef at all, a pat of butter on a veggie once a day and another pat sometimes to fry eggs. Fasting glucose has stayed pretty consistantly in the borderline area regardless of diet for over a decade of quite extreme differences in fat consumption.

I suspect the fat causing the problem is hepatic, which is further evidenced by a small hard paunch (assuming visceral and intraorgan fat usually accompany one another).

Got to run - daughter needs this computer for homework. Thanks for your interest.

Galina L. said...

Not sure 100%, but I think I recollect reading about trigs rising during weight loss on Dr.Davis blog some time ago, not recently.

Jason Sandeman said...

I can't cite any studies, but from personal experience as a T1D, a high Protien meal will convert to a post prandial rise after 3-4 hours. I
Suggest this is supported by the science as well, because even the exchange program for diabetics accounts for the Protien/glucose exchange as part of the calculations of total carbs for day. 1 exchange or protein is the equivalent of 1 carb exchange as such.

Also, despite the LC dogma, even fat will raise a T1D blood glucose levels, albeit at a very slow rate. It is or this reason a T1D requires insulin in order to survive.

The diet prior to the discovery of insulin was a HFLC diet, but the morbidity rate prior to 1920 was max 2 years for a T1D.

Finally, T2 is generally linke with liver problems. That is why metformin is given to T2s, AFAIK, it stops the liver from dumping excess glucose into the system, an also drives down IR.

I'm speaking as a t1 with IR. lucky me.

Evelyn aka CarbSane said...

Jason, do you take Metformin? I came across an article a while back that also used Byetta (GLP-1 analog) with T1's and it improved insulin therapy. I'll try and see if I can dig that up. It might be in my library if you want to search there. The incretins label perhaps.

Evelyn aka CarbSane said...

The only context by which fasting trigs would rise in weight loss *might* be if there's a high liquid sugar meal replacement, but that seems doubtful (as calories of meal replacements are generally low so even if sweetened with sugar it won't be the doses needed to raise trigs). They don't always fall significantly, but generally do because in negative energy balance there would be less NEFA for the liver to repackage up to remove from circulation.

Galina L. said...

I never had elevated trigs associated with a weight loss. Wooo recently blogged about her patients getting fat on liquid meal replacements(her May 21 post), especially Ensure.

Jason Sandeman said...

I do take metformin. It was added to my existing regimen of Levemir and NovoRapid because of my weight, and IR issues.

Byetta has been getting a bad rap lately. I'm not too keen on taking a medicine where the long term effects aren't well known.

My problem is its har for me to know what the heck to do as a protocol, because they all amount to the same thing - I have to take insulin and Metformin.

ItsTheWooo said...

@Carbsane I've been searching for the article where I read that propensity to GNG was elevated not just in type II diabetics and healthy family members, but I have been unable to locate it.

This study shows that gluconeogenesis is three times greater in type II diabetics although it does not support my statement this is genetic:

http://www.ncbi.nlm.nih.gov/pubmed/11118008?dopt=Abstract

Chronically abnormally elevated gluconeogenesis is hallmark of type II diabetes, I may have been mistaken there is an enhanced genetic tendency to GNG but most likely I just can't properly search or locate the article where the genetic contribution of enhanced GNG is part of type II diabetes vulnerability.

Evidence that there is an abnormally increased capacity for GNG is the fact that total insulin deficiency in a person with a normal liver (i.e. type I diabetes) will never produce the kind of hyperglycemia seen in type II diabetes with no insulin deficiency or a milder insulin deficiency. As stated, a type 2 in non-ketotic hyperosmolar hyperglycemia has sugar readings topping 1000... and this occurs without total insulin deficiency.

A normal liver simply cannot do this and a type 1 diabetic with NO insulin is max hyperglycemic at 400 or 500. Type 1 diabetics cannot produce the sugar type II diabetics produce because their liver is otherwise normal. THere is clearly an element of abnormally increased capacity for glucose generation in addition to a lack of normal suppression from IR which is part of the pathogenesis of type II diabetes.

Elevated BCAA in insulin resistance would be similar to elevated triglycerides or FFA - a sign of impaired insulin action.


Certainly there is more involved to type II diabetes than the liver, peripheral IR is part of it, loss of normal beta cell functio occurs in severe type II diabetes that progresses to insulin dependency, and of course there is the 1.5 type of diabetes which combines autoimmunity to insulin production plus metabolic disease similar to type II. My statement meant to suggest the site of origin of type II diabetes is insulin resistance in the liver; the liver is diseased and this is the primary site of dysfunction. Insulin resistance alone poorly predicts type II diabetes conversion. There are lots of insulin resistant people who will never become diabetic. However, liver disease and excessive glucose from the liver without normal suppression is pretty specific for type II diabetes.

I agree beta cell dysfunction is also very important to type II conversion, but this is the more severe type II diabetic who cannot get control of sugars until he or she uses insulin like a type 1 diabetic. It is a later stage problem whereas insulin resistance and abnormal chronic GNG in the liver is the earlier primary abnormality. Most type IIs will never need insulin if they adopt carb controlled diets/take metformin/supplement nutrients.

Type 1 IR may relate to autoimmunity to injected insulin, a phenomenon not widely discussed or identified - the body makes antibodies to exogenous insulin leading to an inability to normally cover meals, huge doses of insulin required for coverage, with unexpected hypoglycemia when antibodies disassociate.

T1s may become insulin resistant similar to T2s but I would venture to guess the insulin resistance of type 1s is more commonly a result of living on insulin that is genetically foreign. The pharmacodynamics of insulin therapy get screwed up and it seems as if they have a metabolic disorder like type II diabetes (because they require huge doses of insulin) but in reality they are just experiencing a normal immune response to foreign insulin, where much of it is biounavailable.

When I took leptin it was commonly observed patients made antibodies to leptin, another protein hormone similar to insulin. This also occurs in patients on insulin therapy and in type 1s who live on insulin it can royally mess up their dosing and capacity to predict their blood sugar responses.

Evelyn aka CarbSane said...

Wooo, Hyperglycemia in both T1's and T2's is primarily due to unchecked gluconeogenesis. The T1 b/c there's no basal insulin to control it, T2 b/c the liver is IR. So 3X GNG in T2's is not surprising, and as you say doesn't suggest an underlying genetic defect. There is clearly an underlying genetic predisposition to T2 diabetes, but this alone cannot explain the obesity epidemic that seems to have spurned a diabetes epidemic. We are in agreement that the "disease" is primarily in the liver, but a diminished pp insulin response is also a characteristic of T2. Beta cell dysfunction is not just the inability to produce insulin, it's also the inability to produce it in proper amounts to stimuli.

Evelyn aka CarbSane said...

@Jason: I can understand the problems you must face. My thoughts on Byetta are based on the fact that it is a GLP-1 analog, GLP-1 being a peptide normally produced by the body. So I think it's a bit like insulin in that regard. I'm coming upon lots of links to it's use in islet transplants in T1's or in preventing beta cell demise if "pre-T1" is caught soon enough. Interesting stuff, that, but not related to your situation unless you're intending to get an islet transplant. Still, I tend to think the GBP "cure" has some GLP-1 component. GLP-1 has lots of actions for glucose homeostasis it appears. So although Byetta (and Victoza) are relatively "new", personally (as in were I in your shoes) I wouldn't be as concerned about long term detriment as with other compounds that target a specific enzyme and such (where there's no way of knowing that it's not doing something deleterious elsewhere).

ProudDaddy said...

Evelyn, is the production of glucose from glycogen included in the GNG? I've always had a problem figuring out where my blood sugar was coming from in a fasting state, having no way of knowing how fast my liver glycogen was being used up.

bentleyj74 said...

That seems to be a sedentary woman being fed 1800 cals a day though. Why wouldn't she gain fat?

Galina L. said...

She is not sedentary "Please note the patient walks frequently, and compared to our other patients she is extremely active"

Evelyn aka CarbSane said...

No, but it is part of glucose "production" from the liver that maintains blood glucose levels. In Wooo's metformin study, they used different radiolabels to differentiate the source of the glucose.

ProudDaddy said...

I downloaded Wooo's study and, as usual, there's a lot I don't understand. Since there weren't any raw data tables, I couldn't tell if the reduced glucose clearance rate was due to peripheral IR or just the result of a higher serum glucose (denominator). Then I noted a study (mice) referenced in Wikipedia on GNG that claimed renal and intestional GNG makes up for the absence of hepatic glucose production and wonder if metformin also inhibits this GNG. Finally, the authors state that hyperinsulinemia is typically present in T2D. This implies that for at least elevated fasting glucose, beta cells aren't typically the problem?

Finally, finally, I was disappointed that the study couldn't determine the ratios of GNG precursors so I might better understand my protein breakdown.

jpatti said...

I just want to say... this T1/T2 differentiation is not universal.

I was a T2 for two decades before going on insulin. Lots of experimenting with both one-macronutrient meals and mixed meals, I discovered for tight control, I had to dose for both carb and protein.

I need about twice as much insulin for carb as for protein, but cannot maintain < 140 mg/dL postprandials without dosing for protein if a meal has any significant protein at all.

I realize this is unusual, but have a hypothesis as for why this is true for me. I spent the majority of my pre-insulin time as a diabetic on low carb (which not only doesn't make all of us skinny, but also doesn't keep diabetes from progressing). I suspect my body got VERY VERY good at gluceoneogenesis, that I adapted to low carb.

Anyways, whether my hypothesis is true or not, the fact is that SOME T2s do have to dose for protein as well as carb.

ItsTheWooo said...

It sounds like you have the sort of diabetes which involves a progressive loss of insulin function. I wonder if you have type 1.5? Seeing as you were controlling blood sugar and still lost your insulin function, this suggests you have an autoimmune destruction of insulin secretory capacity occuring. Either way, your case is not at all like type II diabetes and suggests a more complicated sort. It is not normal for type II diabetics to lose their insulin secretory capacity to the point where they operate like type I diabetics (needing to bolus for protein, for example).

If you did suffer a progressive loss of insulin secretory capacity, the precipitous increase in fasting glucose and inability to suppress GNG would be expected and would not be a fault of low carb diet, although low carb diet might make an unmedicated type 1 or 1.5 worse by augmenting GNG relative to slightly more carb diet which might ironically control sugar better in an unmedicated insulin deficient person.

I'm just wondering if your doctors have ruled out insulin deficiency?

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