This is a cheat "copy-paste" entry trying to clarify the difference between a fasting blood glucose of 5.5mmol/l in an insulin resistant SAD eater and a FBG of 5.5mmol/l in a LC very high fat eater running their metabolism on free fatty acids. The original exchange is in the comments section of this post. Here we go:
Peter,
I've read again you post "Helicobacter and glucose" and yes, the Hisayama study suggested an increase in Fasting Plasma Glucose (FPG) to be a risk factor for gastric cancer (Helicobacter Pylori positive).
A modest increase in the FPG, but not a "modest increase" in the incidence of gastric cancer.
7.2 gastric cancers per 1000 person/years in the high FPG (> 5.8 mmol/l) vs. 2.2 per 1000 person/years in the low FPG (< 5.3 nmol/l) in men.
In women 2.5 per 1000 person/year in the high FPG vs. 0.8 per 1000 person/years in the low FPG.
More than three times higher incidence?!?
Good if you have a low FPG. Ok, but do you have a low FBG if you're on a LC diet?
I don't want to spoil the party to many LCers here, but I read on this Blog that "LC eating rapidly induces insulin resistance" and that "elevated non esterified fatty acids induce physiological insulin resistance and a higher than expected FBG level.".
Uhmm... Bad news for LCers who carry their "beast"?
p.s. - Peter, you said: "This carbohydrate derivative may be more important than sugar for H pylori gastritis, though perhaps NOT IN THE GASTRIC CARCINOGENESIS ASPECT".
I don't understand. Why "not in the carcinogenesis aspect"? Could you explain?
Thanks again.
Marco
Reply
OK, here we go.
A LC eater has a FBG of 5.5mmol/l, technically pre diabetic, but blood insulin is 3.5 IU/ml. This is VERY low. Glucose is in very short supply but blood glucose is maintained by physiological insulin resistance, ie the muscles are full of triglycerides assembled from free fatty acids (NEFA) from lipolysis. The LC eater has breakfast, with enough protein from his eggs or particularly casein from his yoghurt to raise insulin from 3.5 IU/ml to 5.0IU/ml. This inhibits lipolysis enough to reduce NEFA in the bloodstream, intramuscular triglycerides fall and muscle insulin sensitivity returns. There's minimal glucose coming from the gut and so plasma glucose drops to between 4.0 and 5.0mmol/l, probably nearer 4.0mmol/l. It fluctuates between 4.0 and 5.0 after and between each LC meal. In the early hours of the morning there is a growth hormone surge and NEFA from lipolysis peak early morning to give insulin resistant muscles and an elevated FBG.
MEAN glucose over 24h will be in 4 point somethingish, HbA1c will be between 4 and 5%. INSULIN will probably average out around 5-10 IU/ml, averaged out over 24h.
A SAD eater has a FBG of 5.5, prediabetic, because he is prediabetic. His muscles and liver are permanently and pathologically insulin resistant. His pancreas is cranking out 50 IU/ml of insulin to just keep that FBG in the 5.5mmol/l range. He eats bagels, jam and a large mocha for breakfast and his blood glucose hits 15mmol/l. His pancreas ups the insulin output as high as it can get it, perhaps to 150 IU/ml and just manages to to get blood glucose back down to 5.5mmol/l before lunch. Lunch is pasta and the cycle repeats.
Mean glucose over 24 hours will be between 7 and 12mmol/l. HbA1c might just hover around 7%. INSULIN will average 100 IU/ml over the 24 hours.
Helicobacter lives on the hydrogen from flatus, so is present in far too high a number for health in our flatulent carb eater and chronically irritates the gastric lining. Insulin-like Growth Factor-1 (IGF-1) receptor is over expressed and converts disorderly proliferation of gastric mucosa in to gastric cancer. See here.
Insulin acts on IGF-1 receptor to achieve this transformation.
A high carb eater with FBG of 5.5mmol/l implies chronic hyperinsulinaemia, 24/7 and is looking for something to die from.
A LC, very high fat eater with a FBG of 5.5mmol/l implies they haven't had breakfast yet. They are not going to be hyperinsulinaemic at any stage. Unless they eat a bagel instead of their normal bacon and eggs that is. If they do this their blood glucose will hit 10mmol/l before insulin can shut down lipolysis and get the muscle accepting glucose.
It's NOT the FBG of 5.5mmol/l that matters. It's what that means about insulinaemia if you are eating a rice based diet. It's bad. The Kitavans eat a sweet potato based diet, are not insulin resistant and have FBG of 3 point something.
Does that clarify matters? Did I screw up in terms of clarity in the posts on physiological insulin resistance and H. pylori? If so, I'd better get a new post up!
Thinking in terms of FBG = 5.5mmol/l = huge cancer risk is thinking like a cardiologist. Don't go there. Think why, think holistically.
Peter
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20 comments:
Wow! Thanks for this explanation. I have been really worried about my highish morning glucose. It seems to return to the 80's after I eat, which is generally around noon, but in the mornings it has been getting up to 100 or more and I've been a little worried.
Hi zute,
Your physiology works like mine. Not everyone is the same. My wife's FBG at the end of a 12h night shift used to be around 2.9mmol/l, she'd be ketotic and fully functional. But then she would have been working hard all night as an intern, so that may well have affected intramuscular triglyceride levels.
Peter
Nice explanation Peter
I'm just curious what you think of people like myself who are chronically hypoglycemic even when eating rather LC (50-60% fats and <60 average carb).
When I eat more calories on average my FBS increases somewhat, but my FBS is never above 65, often it is in 50s.
My a1c is always at least 5. Couldn't imagine having an a1c of <5. I find this strange considering how low my blood sugar is when fasting. I never cheat and eat high carbs so that can't explain things. Maybe I just have long lived RBCs? Some people do and always have high a1c even if sugar is good.
Hi ItsTheWoo,
The cross check is fructosamine...
Go for it
Peter
Oh, and I guess you've checked your post prandials and they're fine...
Peter
My fructosamine seems to follow my A1C.
When I was underweight it was 255 (which is rather high, I know). My A1C at this time was 5.4. I was eating low calorie and about 70 carbs/average.
Next year I had an A1C repeated, with my weight and eating a little more normal. A1C at this time was 5.1, did not have fructosamine done.
I haven't had a test done in 3 years, due to lack of insurance. Intuitively I know my sugar control must be better - I never experience hypoglycemia and horrible reactions to food (severe lethargy after eating). When I was underweight, that was constant.
It's interesting to note that when I was overweight, but on a very low carb diet, my fructosamine was 204. Perfect evidence body fat doesn't cause diabetes and in fact my blood sugar went to hell from being underweight and restricting too much.
If I take a random sugar, in between my normal meals, it is likely to be 80s or so. Only my fasting sugar is ridiculously low... I think my body doesn't release fats well so I actually have low everything after an extensive fast (which means I experience metabolic conservation, which is why I am so intolerant of fasting).
After 50g of glucose, one hour later my blood sugar was 140, and 2 hours later it was 45... but that was after 50 g of glucose.
ItsTheWoo,
I can readily understand the hypoglycaemia when you essentially had no fat in your fat cells to release as NEFA, so couldn't develop adequate physiological insulin resistance. Like anorexics who have excellent insulin sensitivity despite extreme fasting. If there's no fat available, muscle will take anything it can get.
But why you should glycate Hb and albumin excessively when you are hypoglycaemic is a bit of a mystery.
Perhaps you are the living proof that HbA1c has nothing to do with glucose!
Peter
"Perhaps you are the living proof that HbA1c has nothing to do with glucose!"
I never said that HbA1c has nothing to with glucose, if that is what is being implied. I said that there is not a 1:1 correlation between HbA1c and blood glucose. Some have a high HbA1c with low average blood sugar. Others have the reverse. It is more complex than just carbs. PUFAs also cause glycation, as do cooked meats and proteins. Refined foods are the worst of all probably, so I require studies using fresh whole foods and not cooked, processed, or refined.
Dr. Michael Eades (a long-time LC proponent) suggests that the high FBG in low-carb eaters has to do with a lack of enzymes:
It’s not really the “physiologic insulin resistance from fat” that causes the problem you describe; it is simply a temporary deficiency of enzymes. Virtually all physiological functions in the body are controlled by the enzymes that catalyze the various reactions required. Our DNA codes for all of these enzymes, all of which are proteins. Our DNA codes for many enzymes that we may never use because we don’t need them given our lifestyle, but the coding and ability to make them are still present. We send signals to the DNA that we need them when we need them, and our RNA/DNA system cranks them out. Such is the case with the enzymes we use to metabolize carbohydrates, which are different than those used to metabolize fats. If we are on a long-term low-carb diet, we don’t need the enzymes to metabolize a lot of carb, so we don’t make them. We do need the enzymes to metabolize fat, so we have plenty of those. If we take in a large load of carbohydrate, we don’t have the enzymes we need to dispose of the carbs quickly, so they remain in the blood as sugar a little longer, giving a glucose tolerance test reading that looks like that of one with glucose intolerance or outright diabetes. If we eat carbs for a few days before, we crank out the enzymes, which are then in place when we take the glucose tolerance test, and we get a normal reading. It has nothing to do with the fat causing insulin resistance; it’s simply a matter of lack of enzymes.
I don't know what he bases this on, but do you have any thoughts? It seems too simplistic to my eye...
Peter,
Excellent recommendation regarding holistic thinking - lots of FUD factors out there.
IMO, "physiological insulin resistance" and pre-diabetic condition of FBG>110 (the other unit) are really applied to and defined for SAD eaters. The esoteric LC dieters need different yardsticks.
For LC, having sufficiently high FBG means no feeling of hunger, clear-headedness and that your brain is primed for any required anaerobic tasks due to the readily available glucose supply. What's not to like?
It took several years for my FBG to settle from 121 to about 106 (last November) after I scaled back endurance activities (running and biking). Your liver will adjust to the decreasing demand of glucose but slowly.
Eades' explanation of unavailable enzymes to digest starch makes sense but lacking evidence. Again, thinking holistically (or from the evolutionary perspective), HGs may be permanent LC eaters but not zero-carb so the enzymes should still be at one's beck and call.
On another subject: I'm questioning whether GH really induces "insulin reistance". Shouldn't it be the opposite effect and whether glucagon surge is responsible for the "dawn phenomenon"? GH production should not be taken for granted unless you sleep well and exercise correctly.
John
Charles and John,
Yes, I think Eades' explanation is a simplified view. I've a lot more time for NEFA as an explanation, they seem to explain a lot of phenomena.
John, is there an early morning glucagon surge? It's there for GH and does produce lipolysis. I've not chased glucagon at this time. I'd fully agree re sleep and the presence of a GH surge. I also think that a 3am carb snack would eliminate its effect. Over on Dr Bernstein's forum there is huge variation in the severity of dawn phenomenon, though individuals tend to be quite consistent.
Peter
Hi Peter,
You are probably right about GH being responsible for the rise in BG at dawn when present in quantity (adolescents, healthy young adults, etc). Otherwise, the epinephrine-glucagon cascade may produce similar outcome (for diabetics or adults without significant GH production).
For the unfortunate SAD dieters, the alpha cells may develop insentivity to insulin produced from their neighbors - the beta cells - overtime. When this occurs, the body's finely tuned feedback control mechanism breaks down and disaster ensues because of the constant and simultaneous presence of both glucagon and insulin. It's like having a futile conversation with your friend in a loud party where both of you have to shout to be heard with high probability of miscommunications.
There are symtomatic treatments to suppress the liver's glucose production (acetic acid, alcohol...) but I'm wondering if any protocol exists that can reverse or dissolve the amyloid plaque built up around the alpha cells to restore the situation.
Regards,
John
Hi John,
How about Bernstein's chronic blood glucose of 4.3mmol/l 24/7? How many achieve this???? But, yes, I think I've come across this phenomenon of lack of cross talk before. Probably very real.
Peter
Peter,
Regarding Bernstein's approach (*) and his excellent sugar management of 4.3 mmol/l: he clearly adjusts the exogenous insulin to get this number being a type 1 DM, right? I suspect it's also better long-term to use a little of the real thing (rather than Splenda per his recommendation which still causes insulin response) and less and less of it over time when your taste buds develop better sensitivity to sugar.
*: I read his book years ago. He may have modified his approach by now.
My favorite minor complaint is the term "physiological insulin resistance" supposedly developed by LC dieters - the title of your post. How do you know without a dynamic test? I suspect muscle contraction would move GLUT-4 to the surface of the cell membrane to pick up the sugar. Speaking from personal experience, my body will be so grateful for that sugar to kick-start the fat burning process. When it comes to running my legs are like a car struggling to find its fifth gear that it's used to have.
Regards,
John
Yes,
The insulin resistance is there to provide glucose, it can go to muscles as soon as they use their intramuscular triglycerides and at this stage blood glucose will fall and so will insulin. Then more glucose will come from the liver and more NEFA from adipose tissue. How you feel depends I guess on the balance between available glycogen in the liver (not much but some) and muscle ability to perform on NEFA and adipose tissue's ability to provide those NEFA...
Though I have to say there is another post about 80% fat fed mice which suggests that the insulin resistance is an hepatic phenomenon rather than a muscular one. Which turns my ideas on their head and suggest the effect is via liver glucose release...
Still thinking
Peter
"...muscle ability to perform on NEFA..."
Agree. The small amount of glucose is still needed to start the Krebs' cycle in the form of oxaloacetate. Our pets (slaves?) mitochondria are doing the muscle contraction by burning NEFA but the glucose is the one cracking the whip.
One of the things that set me on the LC trail was my wife's obvious blood sugar / insulin problems.
She was getting horrendous reactive hypoglycaemia mid-morning after a bowl of porridge for breakfast. This went away when we subtituted bacon and eggs. As did her acne, back pain and disrupted sleep.
This week she had her FBG and an OGTT done and the results were FBG: 4.7, OGTT (1 hr 50 mins later) 3.7
This OGTT level is low, and she was feeling pretty ropey by that point, but reckoned that it would have got worse had they left it another half hour.
What I'm struggling to work out is whether this is likely to be due to insulin resistance, and subsequent hyper-insulin release, or some sort of problem with glycogen mobilisation at the bottom end. I haven't found any way to tell.
Her Dad was diagnosed as (a skinny) diabetic at age 60, soon after retiring as a farmer (and therefore being very physically active).
As a follow up, the GP commented that he had seen reactive hypoglycamia in thin young women before and mentioned that they must have some problem mobilising glycogen.
When browsing through the light reading that is Good Calories, Bad Calories I came across a paragraph saying that fructose impaired glycogen metabolism in the liver.
So the wife is now off the fruit (2-3 pieces a day, so no bad thing!) and we're going to see how that affects things.
I just wondered whether skinny young women tended to get a lot of fructose either from fruit if they were 'healthy' or otherwise the fizzy stuff, and why it might specifically affect them.
That's as long as the GP wasn't miles off the mark of course.
what about blood glucose readings after a meal?
I've been low carbing for a while, but for the past few months i've been eating 30g carbs in the form of white rice a day (only carbs of the day) and my glucose levels go crazily high. Is this normal, or should my body have adapted to it by now?
would appreciate any thoughts!
I am skinny female and have been low carb for around 2 yrs. fbg varies between 4.6-5.4 but post meal spikes can be v high. After a bowl of butternut soup followed by lamb chop and chickpea/veg mix at 1hr was 10.5! What is going on.....?
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