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The High Blood Glucose Dilemma on Low Carb (LC) Diets

by (147)
Updated about 14 hours ago
Created March 29, 2012 at 10:48 AM

If you are on a ketogenic or very low carb (VLC) diet (e.g. with 50-100gr carb/day and/or eating ketone producing MCT oils such as coconut oil), you may have a dilemma of having high Blood Glucose (BG) despite eating LC: If you are keto adapted, that is, your body is using ketones and even though you have sufficient insulin (say >5 microU/ml) your body tries to keep your BG higher than necessary, e.g. above 100-110 mg/dl. That is your BG set-point is always high. If you try to lower the set-point to say 80s, by water Intermittent Fasting (IF), then your body starts to convert your muscles into glucose to keep its high BG set-point. So, you may have a slightly lower BG, but you lose some muscle mass. Having a high set-point has many other problems, e.g. if you eat something with a little bit more carb, say a small fruit, your BG shoots up to 130s and stays there for hours.

This may be due to something called "Physiological Insulin Resistance (PhIR) by Petro Dobromylskyj. He wrote many good articles about it -???thanks Petro--in his blog Hyperlipid. Apparently, PhIR is a normal reaction of the body and quite different from Pathological Insulin Resistance (PaIR). It seems that the main difference between PhIR and PaIR is that insulin is at a normal level in the former and abnormally high in the latter. (PaIR is obviously type2 diabetes.) If I understand correctly, PhIR is kind of IR only in the muscle tissue, that is only the muscles do not react to insulin and NOT use glucose even though it is available. However, if you are eating too much protein, the liver may also be considered IR, because it tries to keep the BG high by converting proteins to glucose, even though BG is already too high, that is, it also may not be responding to insulin. (I think working muscles can use glucose with or without insulin. Would that mean that PhIR does not affect working muscles? If not, then one can reduce his high BG [due to PhIR] by exercising.)

The purpose of this Paleohack question is to understand how this happens to whom and how it can be avoided?

Several things seem to cause PhIR:

  1. ?????? LC eating rapidly induces [Physiological] insulin resistance. This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids (NEFA). These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles. ??????palmitic acid is the primary NEFA released from human adipose tissue during fasting. Think of palmitic as a signal molecule to tell the muscles that inhibition of glucose uptake is needed and to tell the liver that increased gluconeogenesis is required because there is no food coming in. Chris Kresser also supports this view.

  2. Ketone bodies e.g. ???Beta hydroxy butyrate. ??? ketone bodies, one of the hall marks of carbohydrate or total calorie restriction, channel glucose away from muscles, toward brain and add a modest supplementary energy supply to brain tissue too. It's exactly what you expect on an adaptive basis, exactly the same function as palmitic acid performs and clearly the two metabolic pathways are closely linked, though ketones seem to work downstream of the action of palmitic acid.???

  3. Methylglyoxal: ???Methylglyoxal is elevated in ketosis, but the bulk is produced by glycolysis??? Methylglyoxal is an inhibitor of glycolysis.???

According to Paul Jaminet, the high BG problem is caused by too low carbs in VLC diets and can be avoided by eating some more ???safe starches???. According to Dr Ron Rosedale, it is caused by too much protein in the diet. This discussion was taken up also by one Paleohack question, which lists many good links about it. But, I think the best and the most up-to-date link on this discussion is this one, where Dr Rosedale uses color coding to distinguish who said what. It is a good scientific discussion and definitely worth reading to understand many background issues. The amount of protein Dr Rosedale recommends is:

Dr. Rosedale defines his protein recommendation as: ???So what???s high [protein]. Certainly above 1 gram [of protein] per kilogram of lean mass is probably high. Most people, I???ll put on 0.7 or 0.75 grams per kilogram of lean body mass. But if I???ve got a diabetic, and I really want to reverse their aging, which means reverse their diabetes, because diabetics is a model of aging, I???ll put them down to 0.5 or 0.6 grams per kilogram of lean body mass per day.??? For downloading the full PDF version of this article see: "Protein: The Good, The Bad and The Ugly" http://drrosedale.com/Protein_The_Good_The_Bad_and_The_Ugly.htm

A few other points need to be noted in the above Jaminet-Rosedale (JR) debate in view of several excellent articles recently written by Chris Masterjohn on glycation, glucose synthesis and oxaloacetate :

  1. They generally agree that glycation is important, but ignore methylgloxal, which is higher in VLC and ketogenic diets and 20000 times more glycating than glucose (existence of methylgloxal supports Jaminet???s position) Methylglyoxal is a reactive aldehyde that is very toxic to cells, it can inhibit growth in E. coli at milimolar concentrations. The excessive intake of glucose by a cell is the most important process for the activation of the methylglyoxal pathway. (It is strange that ???methylglyoxal is produced by glycolysis??? and yet also an inhibitor of glycolysis.??? What does it mean?) But, there is also some evidence that methylglyoxal kills some types of cancer cells.

  2. They talk about post prandial blood glucose (PPBG), but ignore PhIR effect on PPBG, which often causes longer PPBG spikes than high glycemic foods (existence of PhIR supports Jaminet???s position).

  3. They do not discuss oxaloacetate (supports Jaminet???s position)

  4. They do not discuss TCA cycle (supports Rosedale???s position)

  5. Although not directly related to the JR debate, apparently, conversion of glucose to fat is not significant in humans.

It should be noted that Dr Rosedale always emphasizes deleterious effects of hormonal changes e.g. of insulin, leptin caused by PPBG spikes, (rather than glycation caused by glucose,) such as mTOR, autophagy etc. He notes that: ???However a main point of my argument is that BG levels are only a small part of the story; What higher carb intake does to insulin and leptin is even more important; it raises them promoting insulin and leptin [pathologic] resistance.??? " ???only measuring blood glucose without knowing what insulin and leptin are doing gives very incomplete and often misleading information when it comes to effects of any intervention such as diet.???

So my question is how can we avoid the high BG caused by PhIR, do we have to keep exercising to reduce BG? Or is high protein the real issue, if yes, then what exactly should be the protein amount. Or should we try to avoid ketosis, but, if you eat MCT oils (e.g. coconut oil) the body produces ketones even at higher carb levels. Also does this happen in other LC diets, such as Atkins and the Optimal Diet of Jan Kwasniewski.

13: http://drrosedale.com/resources/pdf/Insulin and Its Metabolic Effects.pdf

15: http://drrosedale.com/resources/pdf/Insulin and Its Metabolic Effects.pdf

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15 · October 26, 2013 at 4:02 PM

Yes, I did not want to suggest that low carb leads to diabetes per se. You can say low carbing doesn't cause diabetes, despite high FFA, suggesting that another triggering factor is missing. That may be the carbohydrates. I think things only turn out of whack once you reintroduce carbohydrates (which require proper insulin signalling to be metabolized efficiently). I occasionally read here and there, that people who come from low-carb and up their carbs develop things like postpandrial hypoglycemia, a sign of excessive insulin release.

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2401 · October 26, 2013 at 3:49 PM

It was my understanding that when a body becomes fat-adapted, the muscles use FFA as a source of energy, sparing ketones for use in the brain, heart, and diaphragm. I thought that this is adaptive physiologic insulin resistance.

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0 · October 26, 2013 at 1:21 AM

@jake3_14

Both IFG and poor PPBG are bad. The research shows that poor PPBG is worse because it is more likely to lead to diabetes, the cardiovascular risks are more similar to diabetes.

As far as my IFG, I'm actually not sure if its bad because my a1c is 5.2, which correlates to an average blood glucose of 105 which does agree with my meter. My numbers are high 100-125 from 4am - 10am but stay between 90 - 110 for the rest of the 24 hour cycle including post prandials.

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147 · May 06, 2012 at 2:37 PM

So I wonder if this settles the matter. I was on low carb to reduce small/dense LDL. I assume it must have gone too high now.

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147 · May 06, 2012 at 2:36 PM

I have been travelling for more than a month and it was difficult keep my diet LC, in fact many days I ate high carb. When I returned home, I checked my BG again and found out that my PPBG now goes down 30+ points/hour without doing any exercise. This never happened when I was eating low carb before. I assume this implies that I did not have IR and high PPBG was due to LC. I should note that there were two other changes in my diet during my travels: I ate more calories, about 2000+/d and never ate coconut oil as it was not available in restaurants.

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280 · May 03, 2012 at 10:21 PM

Sunny Beaches wins the thread! How many places can you go on the 'net and find "Paleo" people chowing down on 2-3 pounds of meat a day? You all know the sites. . . "just don't eat a cow for dinner." Yes.

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5132 · March 31, 2012 at 3:01 PM

Well, u can't be sure. That's just one possiblity I mentioned along the line of recent research breakthrough. My guess is it probably isn't that, since the BCAA relationship develops over a longer period, years, not over 2-3 months. Plus, it is pretty hard to consume lots of protein unless it's been "appetizied", that is, from Paleo sources. If I had to guess, you were IR before turning low carb or Paleo and what you did wasn't enought to counter it. I'd get tested after eating some carbs.

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147 · March 31, 2012 at 6:00 AM

I reduced it only recently after I found about Rosedale’s new recommendations, but the protein binge I had before then probably caused IR as you guessed. My A1c did not change much after I started low carb. It was usually between 5.4-5.8. I never had OGTT test, had fasting C-peptide twice and they were about 1.8. I am aware of inaccuracy of the BG meters ( I sometimes repeat a test and find +- 8 point difference and check immediately before a lab test to compare the results). Maybe I try low protein/BCAA for a few months and then do OGTT. Thanks for your insight.

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147 · March 31, 2012 at 5:59 AM

Thanks for the BCAA articles. They are interesting and you are probably right that high BCAAs was/is my problem. I am/was not taking any BCAA (or whey) supplements, but until about 1-2 months ago, I was eating much higher protein as I was losing muscle mass and everyone seemed to be recommending higher protein intake as a remedy for it. I am using a diet software to estimate the nutrient totals and I checked what I was eating then and my total protein intake was about 110 g/d with 20% from BCAA and 10% from tyrosine + phenylalanine.

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5132 · March 31, 2012 at 3:12 AM

Liek Peter says, I would go on a 150g carb diet for 3 days before taking my OGTT. They'll only check up to pp2 but also check pp3 and pp4, if still elevated. That should tell u what the story is.

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5132 · March 31, 2012 at 3:10 AM

There're many possibilities. (1) You may be IR and moving toward diabetes in the continuum. How were your A1cs before? (2) Ru sure ur only doing 85g protien? How about doing >20% at 70g?

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5132 · March 31, 2012 at 3:05 AM

Why eat only 1500 calories. Unless ur tiny, that's not a lot. 80-85g protein shouldn't elevate your BG much. I"m familiar with Peter's post regarding PHIR. He saved the day because his A1c is 4.5 while ur 5.6, which may be considered prediabetic by some but normal by many. What's unsual is the 3-4 hour BG elevation. Have you had your OGTT test w/insulin or C-Peptide at intervals? And ru sure it's that elevated after 3-4h? Many meters can be wrong / unreliable and testing a few times can be faulty. It's tricky because the PP elevation cannot be reliably checked by either FBG or A1c.

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147 · March 30, 2012 at 8:51 PM

Namby Pamby, please see my reply below in the answers section. It was too long to fit here. Thanks. Marc.

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147 · March 30, 2012 at 8:36 PM

Rose, thanks for your comment. Your case is exactly opposite of mine, you seem to go to BG hypo and I never do. It seems my liver is crazy about keeping BG high by converting proteins to glucose..Apparently we are all different. Marc.

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1399 · March 30, 2012 at 9:13 AM

Rose's point is exactly what I do not understand: why did my FBG (and A1C) rise and hers didn't????

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5132 · March 29, 2012 at 3:17 PM

So, yes, with proper protein restriction, your BG should improve while VLCing, than under VLC diets with no protein upper limit.

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5132 · March 29, 2012 at 3:12 PM

Actually I agree with Rosedale's observation regarding protein's effect on BG: longer PP BG rises. But unless you're eating 200g+ protein, the effect should be small. But then we have people posting here at least once a month that their BUN is above 20 and some people here think that has nothing to do with gorging on protein-rich meals. Even Jaminet agrees with protein restriction. And that's not taking into account the hormonal impact of high BG, temporary or sustained, as mentioned by Rosedale.

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11986 · March 29, 2012 at 1:29 PM

Nice first question, Marc! I don't mean to detract from your main point, but I just want to make sure it's noted that not everyone on a LC or VLC plan has high fasting BG. I've been VLC/ZC for over 2-1/2 years, and my BG is in the 85-90 range consistently (except after a very high-protein meal, when it will drop into the 60s after an hour or so). And I know other VLC/ZCers with in-range BG.

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5132 · March 29, 2012 at 2:51 PM

The overall issue is insulin sensitivity and the effect is somewhat exaggerated. The prior studies cited by Jaminet and others had rather large A1c ranges: 0.5 intervals. I doubt a VLC diet will push your FBG too much above 110. If you do, you may have failing BG control. You're less sensitive to insulin, for sure. And it is true that on a high carb (i.e., safe starch) diet, your FBG could be 70-80, as your body is just primed for you to ingest carbs. It's like always having your gun loaded, lest you ingest a large glucose heaping.

But I fail to understand the underlying issue. VLCing should not deteriorate your BG control. In other words, VLCing will flatten out your BG volatility, while a high-carb / safe starch diet will have much higher peaks (esp. at 1h pp) but lower overall FBG. And when measuring your A1c, the postprandial peaks seem to be averaged out and you end up with lower overall A1c when doing safe-starch / high carb diets, especially when combined with HIT. But you WILL have peaks above 140 at 1h pp even with normal BG control. Whether that's harmful is another matter, as some premise their entire VLC effort on "preserving" remaining pancreatic beta cells; supposedly, even breaches above 110 will render some of your beta cells non-functional. But I think the recent breakthrough in diabetic reserach has shown that it's the incretins, BCAAs and gut hormones which really control insulin secretion, not the beta cells, whose functionality could be restored.

If you see your FBG go up above 110 consistently and closer to 150, then you may be losing BG control for reasons other than the lack of insulin sensitivity caused by the VLC diet. If you're more closer to 110-120, I would think it is the VLC diet. People on VLC diets still progress on their paths to diabetes. Many T2 diabetics become insulin dependent or "double diabetics." Many LADAs or MODYs not previously diagnosed have to be on insulin and will graudually or abruptly lose BG control. But for the healthy, the difference in FBG should be within the normal ranges mentioned above, not at the diabetic range (129+).

And as mentioned above, the lower A1c with higher carb diets are achieved via higher volatility but the regress toward the mean phenomemon. It's not clear which one is superior: the lower volatility but higher A1c and higher FBG vs. the higher volatility but lower A1c and lower FBG.

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5132 · March 29, 2012 at 3:12 PM

Actually I agree with Rosedale's observation regarding protein's effect on BG: longer PP BG rises. But unless you're eating 200g+ protein, the effect should be small. But then we have people posting here at least once a month that their BUN is above 20 and some people here think that has nothing to do with gorging on protein-rich meals. Even Jaminet agrees with protein restriction. And that's not taking into account the hormonal impact of high BG, temporary or sustained, as mentioned by Rosedale.

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5132 · March 29, 2012 at 3:17 PM

So, yes, with proper protein restriction, your BG should improve while VLCing, than under VLC diets with no protein upper limit.

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147 · March 30, 2012 at 8:51 PM

Namby Pamby, please see my reply below in the answers section. It was too long to fit here. Thanks. Marc.

best answer

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5132 · March 31, 2012 at 3:35 AM

Other possibilities are that you've developed IR. You may have been over the hump before you started low-carbing. Or it may have developed even while low-carbing. These are all plausible but it's all guesswork. Get tested first.

The recent breakthrough I'm referring to is the finding that elevated BCAAs are associated with IR. Even years before diabetes diagnosis. This would be like pre-pre-diabetes.

http://www.ama-assn.org/amednews/2011/04/04/hlsa0404.htm http://www.dukehealth.org/health_library/news/too_much_protein_eaten_along_with_fat_may_lead_to_insulin_resistance

There are animal models which implicate BCAA supplementing with IR. Just a few days ago, the NE J of M published findings regarding bariatric surgery patients that reversed their pre-existing diabetes (many of them were insulin-dependent T2 diabetics), whose beta cells were largely thought to be non-functional. After the surgery, these patients showed significantly decreased BCAA levels, got their BG control back, and got off of insulin. Most were "cured" of their diabetes in the sense that they attained normal BG even before losing any weight from the surgery.

Implication: increased BCAAs could promote IR, and a gut restructuring could immediately lower BCAAs and restore normal BG control and reverse IR. We don't know how this works but all we know is that there is association between high serum BCAAs and IR. Paleos might pooh pooh this finding. In fact, there were studies indicating exactly the opposite, how leucine benefits IR, until a few years ago. Howver, there seems to be something else going on. And no one knows for sure.

http://www.cell.com/cell-metabolism/abstract/S1550-4131(09)00040-0

It is possible that IR can develop and even accelerate while doing low-carb, high-fat, and high-protein diets. One thing I wouldn't do is supplement with BCAAs while low-carbing, as weightlifters do.

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147 · March 31, 2012 at 5:59 AM

Thanks for the BCAA articles. They are interesting and you are probably right that high BCAAs was/is my problem. I am/was not taking any BCAA (or whey) supplements, but until about 1-2 months ago, I was eating much higher protein as I was losing muscle mass and everyone seemed to be recommending higher protein intake as a remedy for it. I am using a diet software to estimate the nutrient totals and I checked what I was eating then and my total protein intake was about 110 g/d with 20% from BCAA and 10% from tyrosine + phenylalanine.

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5132 · March 31, 2012 at 3:01 PM

Well, u can't be sure. That's just one possiblity I mentioned along the line of recent research breakthrough. My guess is it probably isn't that, since the BCAA relationship develops over a longer period, years, not over 2-3 months. Plus, it is pretty hard to consume lots of protein unless it's been "appetizied", that is, from Paleo sources. If I had to guess, you were IR before turning low carb or Paleo and what you did wasn't enought to counter it. I'd get tested after eating some carbs.

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147 · March 31, 2012 at 6:00 AM

I reduced it only recently after I found about Rosedale’s new recommendations, but the protein binge I had before then probably caused IR as you guessed. My A1c did not change much after I started low carb. It was usually between 5.4-5.8. I never had OGTT test, had fasting C-peptide twice and they were about 1.8. I am aware of inaccuracy of the BG meters ( I sometimes repeat a test and find +- 8 point difference and check immediately before a lab test to compare the results). Maybe I try low protein/BCAA for a few months and then do OGTT. Thanks for your insight.

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30 · May 03, 2012 at 8:49 PM

Summary

VLC eating raised my fasting BG from 95 to 115 - just adding my data to the discussion.

Details

  • For many years, I ate moderate carb - maybe 35% - with some binging here and there.
  • Around the time I started VLC, my FBG was 95.
  • After two weeks of VLC, my FBG was 115, and my PPBG would skyrocket after consuming a moderate amount of carbs. This makes sense if you consider that the muscles become IR and can't take up much glucose.

Personally, after spending a lot of time reading about this issue, I have decided to side with Dr. Jaminet, and I will be adding safe starches soon.

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30 · March 29, 2012 at 1:55 PM

This issue is kind of scary. This post pushed me to order a glucose monitor from Amazon to make sure I'm still in normal range - it's kind of scary not knowing what this way of eating is doing. Yeah, I've lost a ton of weight and I've got a 6 pack starting to show, but what long term negative health effects are there with high blood glucose?

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11204 · May 03, 2012 at 9:15 PM

Not enough glucokinase? It would seem the liver would want to store the glycogen rather than leave it in the blood stream. I think paleo amounts of fructose are necessary for the release of glucokinase.

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5509 · March 29, 2012 at 2:08 PM

I don't have time to read the whole thing so I'm sorry if I missed something (I'm heading to work) but one thing caught my eye:

"According to Dr Ron Rosedale, it is caused by too much protein in the diet."

Well, then don't eat a cow for dinner, right? Being Paleo isn't about eating massive quantities of protein or eating it to an excess. I think many people here don't eat a cow for dinner. They just eat LC and replace some of the sugar/starches with fats.

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280 · May 03, 2012 at 10:21 PM

Sunny Beaches wins the thread! How many places can you go on the 'net and find "Paleo" people chowing down on 2-3 pounds of meat a day? You all know the sites. . . "just don't eat a cow for dinner." Yes.

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0 · March 06, 2014 at 7:04 PM

I don't think protein has anything to do with higher fasting glucose on VLCD. Dropping carbs will de-activate pyruvate dehydrogenase enzyme and activate pyruvate carboxylase. What it means that all glucose that is going though glycolysis will either be recycled back to glucose or used as spark to burn ketones and fatty acids. It will not be burned completely, that is, no AcetylCoA will be made out of it (which pyruvate dehydrogenase does). Remember that ketones are basically two AcetylCoA molecules joined together. aCoA cannot enter krebs cycle without oxaloacetate, which is by-product of glycolysis. In other words, you cannot burn fat or ketones without some amount of glucose going through glycolysis to produce oxaloacetate. When carbs are low, any oxaloacetate that is not used to help enter aCoA into citric cycle is recycled back to glucose. Adding starches or any other carbs will slow down burning fatty acids and ketones because glucose from these startches will be burned instead. I don't think this is a problem - this is actually an indication that you are really ketogenic.

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15 · October 28, 2013 at 6:03 PM

"Even in the absence of manifest type 2 diabetes mellitus or impaired glucose tolerance, chronically higher blood glucose levels exert a negative influence on cognition, possibly mediated by structural changes in learning-relevant brain areas."

http://www.neurology.org/content/early/2013/10/23/01.wnl.0000435561.00234.ee.abstract

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15 · October 25, 2013 at 10:40 PM

In addition to the above, free fatty acids are a cause of insulin resistance and diabetes. Low carbohydrate diets elevate free fatty acids.

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2401 · October 26, 2013 at 3:49 PM

It was my understanding that when a body becomes fat-adapted, the muscles use FFA as a source of energy, sparing ketones for use in the brain, heart, and diaphragm. I thought that this is adaptive physiologic insulin resistance.

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2401 · October 25, 2013 at 10:33 PM

So, is IFG dangerous, per se? Is IFG better or worse for you than bad PP BG readings?

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0 · October 26, 2013 at 1:21 AM

@jake3_14

Both IFG and poor PPBG are bad. The research shows that poor PPBG is worse because it is more likely to lead to diabetes, the cardiovascular risks are more similar to diabetes.

As far as my IFG, I'm actually not sure if its bad because my a1c is 5.2, which correlates to an average blood glucose of 105 which does agree with my meter. My numbers are high 100-125 from 4am - 10am but stay between 90 - 110 for the rest of the 24 hour cycle including post prandials.

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0 · October 25, 2013 at 9:27 PM

@marc 6

I'm posting this here because although its an old post it's the first one that comes up when you search for high glucose on a low-carb diet. I have been struggling with the same thing. I read and re-read this post over and over trying to make sense of what was going on. How could I go from regularly getting readings in the mid 70's in the late afternoon to never having a reading below 85, period.

Why were my fasting glucose numbers so high?

I found this information (IFG means impaired fasting glucose):

"As mentioned above, HOMA-IR largely reflects resistance of glucose production by liver and kidney to suppression by insulin, whereas hyperglycemic clamp-determined insulin sensitivity largely reflects the sensitivity of muscle glucose uptake to stimulation by insulin (22). Our finding that in IFG, HOMA-IR was increased but hyperglycemic clamp-determined insulin sensitivity was not decreased lead us therefore to postulate that in IFG individuals, there may be selective or preferential hepatorenal insulin resistance."

Since my fasting readings are in the pre-diabetes stage I researched that and determined that I would be considered to have Impaired Fasting Glucose but normal glucose tolerance (since my post prandials are fine). Apparently they are very different. IFG results when you have a reduced basal insulin secretion and impaired glucose-stimulated first phase insulin secretion. And most importantly:

People with impaired fasting glucose have insulin resistance to glucose that their liver makes.

So if that is part of my problem it would explain it quite well since that is just about the only glucose I'm getting at 5am....the glucose that my liver makes.

Here is the citation:

Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans.

John Gerich, Christian Meyer, Asimina Mitrakou, Walkyria Pimenta, Ervin Szoke, Timon Van Haeften,, et al. Diabetes Care. 29.8 (Aug. 2006) p1909. Word Count: 3730.

Hope this helps somebody out there.

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147 · March 30, 2012 at 8:31 PM

Namby Pamby, thank you for your note. Please see my replies to the points you raise after the >> signs below.

I doubt a VLC diet will push your FBG too much above 110: >>It does not, in fact it is almost always between 100-110.

But I fail to understand the underlying issue. VLCing should not deteriorate your BG control:>>Apparently, muscles do not use glucose, but liver continues to make glucose. Please see the Hyperlipid blog links I gave.

But you WILL have peaks above 140 at 1h pp even with normal BG control.: >>Yes I have, if I eat more than 25g of carbs in one meal. The problem is that it lingers between 130-140 for 3-4 hours, unless I do some exercise. Maybe with little carbs in the meal, protein is converted to glucose as it is digested and its digestion takes 3-4 hours. My A1C is about 5.6.

But I think the recent breakthrough in diabetic research has shown that it's the incretins, BCAAs and gut hormones which really control insulin secretion, not the beta cells, whose functionality could be restored: >>That’s interesting. Could you please give some links/references about this recent research.

Actually I agree with Rosedale's observation regarding protein's effect on BG: longer PP BG rises. But unless you're eating 200g+ protein, the effect should be small. >> I eat 80-95g/d of protein on average, but maybe my calorie intake is too low, about 1500 cal/d, so %protein cal maybe a bit high and as I noted above, it may be converted to glucose to compensate for lack of carbs, although I doubt it as I eat 30-40g/d coconut oil and about 60-100g carbs/d. This is exactly the point I do not understand and that is why I wrote this paleohack question.

So, yes, with proper protein restriction, your BG should improve while VLCing, than under VLC diets with no protein upper limit. >> I agree. Apparently Rosedale has reduced his protein recommendation. So, probably I need to eat about 65-70g/d protein (and more fat to compensate for its calories).

Thanks again for your response..

Marc.

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5132 · March 31, 2012 at 3:10 AM

There're many possibilities. (1) You may be IR and moving toward diabetes in the continuum. How were your A1cs before? (2) Ru sure ur only doing 85g protien? How about doing >20% at 70g?

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5132 · March 31, 2012 at 3:05 AM

Why eat only 1500 calories. Unless ur tiny, that's not a lot. 80-85g protein shouldn't elevate your BG much. I"m familiar with Peter's post regarding PHIR. He saved the day because his A1c is 4.5 while ur 5.6, which may be considered prediabetic by some but normal by many. What's unsual is the 3-4 hour BG elevation. Have you had your OGTT test w/insulin or C-Peptide at intervals? And ru sure it's that elevated after 3-4h? Many meters can be wrong / unreliable and testing a few times can be faulty. It's tricky because the PP elevation cannot be reliably checked by either FBG or A1c.

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5132 · March 31, 2012 at 3:12 AM

Liek Peter says, I would go on a 150g carb diet for 3 days before taking my OGTT. They'll only check up to pp2 but also check pp3 and pp4, if still elevated. That should tell u what the story is.

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147 · May 06, 2012 at 2:36 PM

I have been travelling for more than a month and it was difficult keep my diet LC, in fact many days I ate high carb. When I returned home, I checked my BG again and found out that my PPBG now goes down 30+ points/hour without doing any exercise. This never happened when I was eating low carb before. I assume this implies that I did not have IR and high PPBG was due to LC. I should note that there were two other changes in my diet during my travels: I ate more calories, about 2000+/d and never ate coconut oil as it was not available in restaurants.

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147 · May 06, 2012 at 2:37 PM

So I wonder if this settles the matter. I was on low carb to reduce small/dense LDL. I assume it must have gone too high now.

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