What's your morning fasting BG? On average?

Well I've been tracking my BG's for about a month now, since going from a "lenient" low carb diet, to strict low carb. Eating nothing but meat, eggs, and veggies. Occasional small apple or dairy. I even use liquid splenda to avoid the small amount of dextrose/glucose in the packets.

It's rather depressing, but FOR ME at least, my morning fasting BG's seem to have gotten WORSE.

Had one of my highest readings this morning in fact, of 123.

It's seldom under 100.

- BG's one hour after LC breakfast average 94.
- One after lunch = 98 average BG
- Bedtime = 91 Average
- Average of all BG's taken past month = 95

Admittedly, the high morning BG's are skewing my composite average rather high. But still...I'm not happy with high morning BG's.

I will be applying for health insurance soon, and am afraid this will go on my record in a very bad way.

What's really messing with my mind, is that I've lost 3 to 4 pounds of fat during this time. I would expect fat loss ALONE to improve my numbers, but no such luck.

I will continue with the fat loss regardless, because I need to lose another 10 pounds to be truly lean...but man oh man.

Perhaps I'm just genetically screwed, and would do much worse on high carb diet. LC may not be a panacea for all.

Nonetheless, I am determined to get 100% healthy blood sugars AT ALL TIMES....without drugs. So constant tweaking and refining will be part of my lifestyle.

Hey, welcome back. Just yesterday I was wondering what had become of you and your blood sugar woes. On the high morning readings, I hear ya. I've been there. It doesn't make sense, does it? I believe you are being compliant, just as I have been.

First take a deep breath, and look at the long view. You are no longer getting those very high readings that can damage tissues. 123 is hardly stellar for morning readings, but at least you are not damaging tissues.

Second, the high morning readings do not *make sense* when coupled with good post prandials. This is what I am getting at when I describe "physiological insulin resistance". I think it is easy to blame it on non-compliance till you actually experience it. I think high morning readings simply reflect the fact that blood sugar is going down at night, there is no glycogen to keep it up, the body is relying on glucagon. Perhaps there is something amiss with the glucagon mechanism, I don't know, but for some reason our bodies overcompensate with a bit too much glucagon.

There was a youtube video circulating this week on insulin/glucagon. You might find it interesting. I did. http://youtu.be/VjQkqFSdDOc

Now, have you tried IF as prescribed by Dr Jason Fung? It seems to be the most effective solution to those unexplicably high FBSs. Give it a try, it works remarkably well for me. Give it a week or so (fasting every other day) and see if there is improvement.

Have you tried lowering your protein some?

Also, I'd get an HBA1c done before despairing too much. You can buy them at Walmart for $12.

I wish we had a way of lowering glucagon, other than by drugs.

Cortisol also rises in morning, and maybe some of us make more cortisol than normal. Which would raise BG in morning.

Yeah the HBA1c test is next for me. I suspect it's probably decent.

My post prandials are decent, so I guess I should not be so freaked out about the high mornings BG's.

Protein...I probably need to try that out. Lowering it that is.

Although I did test 30 minutes after a scoop of Jay Robb's whey protein, and it did very little to my BG's.

Then again, I have had "hypo" like reactions from whey before, so I may also be sensitive to excess protein.

Also just had my worst post breakfast reading. My post breakfast readings average 97. Today it went up to 113 after 4/5 of an Atkins bar and 18 grams of JIF natural peanut butter.

To put that into perspective, my second highest post breakfast reading was after a METrx meal replacement shake (with 1/2 ounce mixed nuts) that contains 20 grams of maltodextrin. But that only went up to 103.

So the "low carb" atkins bar spiked BG 10 points higher than a shake containing 20 grams of dextrose!

Not sure if it's the sugar alcohols or something else.

BTW...I do NOT make a habit of eating Atkins bars, shakes, or other fake foods. But I do like to test how I react to them on occasion.

Yes, but that would happen whether you are eating LC or not - I think. I am trying to identify why FBG would get worse while eating LC when intuitively we think it should improve.

Whey is quite insulinogenic, right? By increasing insulin, it is actually going to lower blood sugar. The problem is that high insulin is just as dangerous (more so?) than high blood sugar. Ideally you want to keep both low.

I read an interesting article by Jenny Ruhl last night which includes some info on sugar alcohols: http://www.phlaunt.com/lowcarb/19059967.php BTW since you posted the video on Quest Bars raising blood sugar so significantly, I have read that Quest is being sued for inaccurate labeling. It's not been settled yet, but based on the fact that my blood sugar went up by 50 pts when I ate one, I'm staying away.

I was eating those Quest Bars for while, but kept getting hypo shortly after. Which prompted me to investigate them. I also stay away from those now. Hard to beat real food really. Real LC food that is. Though I retain my Splenda habit for now. Coffee sucks without it.

I didn't have anything to fix really, but there's still a clear difference in my blood glucose between protein intake of say 120 grams a day and 80 grams. Something else that went down--my biggest blood glucose reading on the higher protein intake was always when I did deadlifts--the most stressful lift, biggest increase in blood glucose. When I went ketogenic, that changed, where at higher protein blood glucose might go up 20 or 30 points, at the lower level it was more like ten or less.


One experiment I've been wanting to try, next time I buy some glucose strips is a carb-up. First a few meals with 50 grams of carb or so, to see what happens to my blood glucose--expecting awful numbers--and then two or three days of higher carbohydrate intake--250 grams+, like they say to do before trying to pass a glucose tolerance test, and see how my carb tolerance/morning blood glucose progresses.

Ugh... I just ordered a bunch of Quest bars. Okay! No more after these are gone.

I just posted this in another thread, and it made me think of this thread, because of the blue letters below;



http://www.wheatbellyblog.com/2012/...sterol-went-up/



Another thing I'd throw in--as omnivores, humans store mostly the fats they eat. So a previous long-term diet high in corn oil = fat stores relatively high in polyunsaturated fat, a diet high in olive oil=fat stores relatively high in monounsaturated fat, a diet high in butter, coconut=fat stores higher in saturated fat. There is some back and forth synthesis between saturated and mono, but there'll be a trend. I think this probably means that that variable change in LDL cholesterol during a low carb/ketogenic diet might come down to the fatty acid profile of our fat stores, not just degree of saturation, but particular sub-types of fatty acid, as much as diet.

I wrote the last paragraph thinking of the possible effects of different stored free fatty acids on cholesterol metabolism--if these fats, in the diet, change ldl cholesterol/hdl cholesterol, it seems logical that they might also have an effect when released from storage in adipose tissue.

Oleic acid, palmitic acid, etc. also have differing effects on blood glucose. The "physiological insulin resistance" Peter at Hyperlipid writes about depends on palmitic acid specifically. And the effects of free fatty acids on insulin secretion in beta cells differs from free fatty acid to free fatty acid. Free fatty acid profile in our fat tissue is something with a longish half-life--something that could take years to change, sort of creep up on a person, if fat tissue fatty acid profile were an issue in long-term changes in glucose tolerance.

Wow, that is so interesting, Teaser, about the insulin being blocked and blood sugar rising - something I've never seen mentioned before. Hmmmm.....makes me wonder.

Can you summarize how the different sorts of stored fat might affect glucose levels - or cite some research? How can we anticipate how the fat we eat will be stored?

This explains a lot about how new low carbers have blood lipid profiles that go all over the place while they are losing weight?

I was gone for the weekend, my oldest nephew got baptized. No time to answer until now.

Last question first--I'm not sure. Generally, the fat storage will reflect the dietary fat, on a high-fat diet. On a diet that's low in fat, and high enough in carbohydrate that there's lots of fat being synthesized de novo, you'd end up with high levels of the sorts of fats that we synthesize. Mammals synthesize fatty acids in a certain order. First palmitic acid. Palmitic acid can be elongated to form other saturated fatty acids, the next in line after palmitic acid is stearic acid. Palmitic acid can also be desaturated to produce the monounsaturate palmitoleic acid, and stearic acid can be desaturated to oleic acid. This position of palmitic acid, as the first in line of the synthesized fatty acids in humans, might make sense of a special role of palmitic acid as a sort of molecular signal for a cell to switch between glucose and fatty acid metabolism. A cell might not start synthesizing fatty acids until it has taken in a certain amount of glucose.

They study essential fatty acid deficiencies in rats. The main model is a way of inducing the deficiency through a very low-fat diet and fasting. A relatively lean human's fat stores will last a month, or months. A lean rat's stores will last days, a week might be a stretch. If you suppose it's a week--fast the animal a full day, say it's run through 1/7th of its fat stores. The polyunsaturated levels will go down, there even seems to be a tendency for polyunsaturated fat to be oxidized as a percentage that's higher than their percentage in stores. During feeding, the animal makes the fats rats make--pretty much the ones we make, if overfed carbohydrate.

The process is slower in humans, because of a much longer half-life of our stored fats. The half-life can be shortened, through some form of accelerated fat-loss. I think this could probably be sort of hacked to speed up changes in fatty acid profile. If they could ever figure out what a desirable profile looked like. Going back to the rats, instead of fasting them a day, and then making them replace the burned fats with synthesized fats, you could feed them cocoa butter, or some high-oleic acid fat like olive oil, on the fed days, and weight their fatty acid profile more strongly towards stearic acid and oleic acid. Or put in a little fish oil.

For palmitic acid-induced insulin resistance, I got that concept mostly from Peter at Hyperlipid, there are seven posts in his physiological insulin resistance series. And any number of posts that belong in that series, but are filed differently. I've never really dug right into the actual mechanism that Peter's talking about here, so until I've done a little more homework there, all I can do is point at his blog, and trust that Peter knows what he's talking about...

This post is one of those, the effect of butter vs. some other fats on insulin secretion. Peter wrote it when his ox (should that be milk-cow)? got gored when Dr. Davis suggested in a blog post that dairy fat had an insulin-stimulating effect. So by "blocks insulin" I guess Dr. Davis meant blocks its signal, not its secretion.

http://high-fat-nutrition.blogspot....nd%20Dr%20Davis



Any free fatty acid can compete with glucose for oxidation, if the free fatty acids reach a high enough level. Peter has a specific mechanism in mind for palmitic acid. There are two main issues to deal with here. One is the simple insulin resistance, the acute effect that Peter is talking about. The second is lipotoxicity, the damage done to cells, including beta cells, when free fatty acids and glucose are both elevated at the same time. I think oleic acid might have a role to play against both the benign short term glucose intolerance and the lipotoxic, evolving sort of insulin resistance.

It's the free fatty acids that compete with glucose, though--not the triglycerides. There are studies in pancreatic and liver cells, where the cells are exposed to either palmitic acid plus glucose, or palmitic acid plus oleic acid plus glucose. In the first case, various lipid products like ceramides, that are supposed to damage the cell, are produced in high quantities. The oleic acid prevents this--and seems to do this by increasing the synthesis of triglycerides. By lowering the free fatty acid levels in a cell, it makes sense that oleic acid should be capable of reducing not just ceramide formation and potentially long term damage of the cell, but also shorter-term physiological insulin resistance.

http://high-fat-nutrition.blogspot....tance%20%281%29







That's from the first in Peter's physiological insulin series. What Peter says here with the three days of carb feeding is something I meant to say in a more direct way here--



I typed it out a few times as a suggestion, but social anxiety got the better of me, and I retyped it as something I'd wanted to try myself (which is true, but no longer a direct suggestion). The 150 grams of carb a day is above the amount of carbs that coachjeff was eating, when he was on a moderate low-carb diet, as opposed to the more strict ketogenic diet he's eating now. Just because fasting morning blood glucose are elevated at a habitual carb intake of 70 grams a day, and even more-so at lower carbs, that doesn't mean anything is broken, and it doesn't mean that after three or four days of a higher carbohydrate intake, fasting morning blood glucose would go up, it could as easily go down.