He's been low-carb for the past year and his weight hasn't changed. He also keeps his calories in check. Actually, I think he could eat more fat.

He's had a gut on him the past 20 years (skinny arms, skinny legs though), so maybe it could be lipid-induced hypertrophy. Once he gets onto medicare, he'll be able to get a bunch of tests done in hopes of better figuring out what's going on inside. I think the older you get, the more challenging it can be to take off even a couple pounds of weight. My family certainly is no exception.

As for the other benefits, he has seen positive changes such as being able to eat every 8 hours instead of every 4, not constantly snacking, no hypoglycemia, improved bike rides.

Sorry for the third post, but I found this interesting. Probably nothing new to the veterans out there:

From 'The Art and Science of Low Carbohydrate Performance':
Pg. 45

Well, if we go with Eric Westman's explanation about why blood glucose is in the blood, then we can come up with a pretty good explanation for why athletes remain insulin resistant after a marathon.

First, blood glucose is not intended to be used by anything else but red blood cells, with few exceptions. Therefore, all other cells must remain insulin resistant to protect the now-limited supply of blood glucose to red blood cells. Second, recovery post-marathon requires tons of energy, therefore tons of oxygen, therefore tons of energy specifically for red blood cells that transport this ton of oxygen, which supports the idea of the protection mechanism through insulin resistance of all other cells. Third, muscles don't store glycogen for themselves, but for red blood cells as needed when they do their thing with oxygen and carbon dioxide, therefore it makes little sense for muscle cells to prioritize glycogen storage post-marathon to the detriment of red blood cells, which need glucose more than ever right now, which is ultimately why muscle cells store glycogen in the first place. Think of it as water towers used to extend the range of the centralized water pump, storing water in off-hours, then releasing it locally according to demand. Fourth, the paradox exists only because marathon athletes do not typically eat low-carb, which is to say the high-carb diet they eat interferes with normal glucose and lipid metabolism through its action on insulin, thereby resulting in this apparent paradox. Were they to eat a low-carb diet instead, the paradox wouldn't exist since the liver would more than suffice for all glucose needs post-marathon. Fifth, we believe glycogen stores should always be full (at least more full than they would be on a low-carb diet), therefore we believe glycogen replenishment should be prioritized post-marathon. Lastly, the paradox exists only because we believe blood glucose is the preferred fuel, therefore should do some good from a dietary standpoint post-marathon, but we see that it doesn't.

I cite Steve Cooksey's website again to point out that blood glucose level is driven by demand in the absence of dietary carbohydrate, especially during exercise, most probably by post-exercise recovery as well. If red blood cells demand more glucose post-marathon for recovery, it makes little sense that storage would be prioritized post-marathon.

However, a while ago I read an article (forget which one, there was a post here about it though) about some experiment with isotope-marked glucose to see if it would be used immediately or first converted to glycogen before use. They found that glucose must be converted to glycogen before it can be used. So, while it appears that glycogen storage is not prioritized post-marathon, dietary glucose must still be first converted to glycogen before it can be used. In a way, this makes perfect sense. After all, the fat we eat isn't directly used as fuel from the gut, it must first be put inside lipoproteins called chylomicrons, then shuttled to fat cells, then released by fat cells according to demand. It follows that dietary glucose metabolism would go along similar lines. It makes sense because otherwise we'd have to eat constantly to provide a constant supply of glucose, or of fat and ketones for that matter. Think of it like a car, we don't supply the engine with fuel directly from the gas station's very large hose. That's what we do when we eat. We take in literally hundreds of times our immediate needs in just a short time.

One last thing I just thought of. Fat inside fat cells is in constant flux between esterification and de-esterification, i.e. the back and forth conversion of triglycerides and its constituents, fatty acids and glycerol. This process requires glucose, which is converted into glycerol, which then allows conversion into triglycerides. So while we believe glycogen replenishment should be prioritized post-marathon, fat cells need to be replenished as well, and this also requires glucose, which suggests one more reason for post-marathon insulin resistance, as it would favor an increased response from fat cells to insulin, just like it does for the rest of us who grow fat the same way.

Anyway, that's my take on that.

That was very interesting. I admit, I had to re-read that second paragraph a couple of times to take all of it in.

I'm going to sound really stupid here, but it's all a learning process for me.

This is something I found off wikipedia:

http://en.wikipedia.org/wiki/Glycogen


So in low-carb, I'm assuming the muscle cells are repleted with glycogen? Or maybe the glycogen stores aren't utilized in the highly keto-adapted athlete. Meanwhile, the liver is pumping out glucose to be used by the red blood cells.

Ha, now I have even more questions. Now I need to find out how the muscles use ketones. It's all very interesting to me.

In a keto-adapted individual, muscle glycogen doesn't get used unless it's for those short bursty actions (sprints, heavy weights, etc.). I can only tell you where I've been reading recently: Attia's blog, MDA, A&SofLCL, A&SofLCP, and PubMed. One or more of those has a lot more information about this.

In those marathoners mentioned, first priorities for survival would be to replenish liver glycogen if needed, and replenish fat stores---the latter to keep leptin in range and thus allow overall metabolism to be restored to homeostatic levels. Muscle glycogen would be a low priority.

(On the other hand, if those marathoners had been keto-adapted, they wouldn't have such problems with having depleted muscle glycogen to that degree.)

IR in myocytes in those marathoners is a survival mechanism---shunt what glucose is available to the tissues that require it for use (RBCs, retina, peripheral nerves, etc.), which does not include muscle tissue, and also get some lipogenesis going to make sure the fat stores have adequate supply to produce leptin.

IR in adipocytes in those marathoners would be a survival mechanism, too, but would also suggest a much more severe situation of having depleted hepatic glycogen stores to such a degree that the body would sacrifice (at this time) lipogenesis (and leptin) in favor of making sure those glucose-dependent tissues "get their's".

IR in hepatocytes would suggest that hepatic glycogen is adequate, and glucose can go to myocytes and/or adipocytes.

NOTE: all of these examples of IR presume a non-diabetic. Someone who has diabetes, of course, can be insulin resistant for totally different, pathological reasons than those mentioned above.

Also, just for more to think about, IR in myocytes doesn't necessarily mean amino acids won't get into muscles. In physiological insulin resistance, which happens on a LC diet when we're keto-adapted, muscle cells are insulin resistant to glucose, but not to fatty acids. Lipoprotein lipase acts on muscle cells to get FAs into them for energy, just as it acts on adipocytes to get FAs into them for storage. Insulin increases the action of lipoprotein lipase something like 150x more. So "insulin resistance" is a pretty broad term. My suspicion is that even in an insulin resistant post-marathoner, amino acids would be able to repair muscle after a marathon, provided that survival and health maintenance mechanisms (e.g., hepatic glycogen stores and restoration of leptin homeostasis via fat storage) were returned to homeostatic levels. (If not, AAs could be converted to glucose and/or ketone bodies as needed.)

I stand corrected on the muscle-glycogen thing. But then I can come up with another reason why muscle cells remain insulin resistant post-marathon. Blood glucose rises during exercise, this causes more glycation, which is then taken care of by ketones, which are preferentially taken in as cells are insulin resistant, therefore glucose resistant.

Come to think of it, this could also explain pathological insulin resistance in diabetes, where blood glucose is chronically high by chronic ingestion of carbohydrates. Cells protect themselves from all that glycation by becoming insulin resistant, therefore glucose resistant, in an attempt to take in more ketones, which would fix the glycation.

It's all conjecture but it makes sense to me.

That alone is an awesome benefit! I'd love to see that. I love all the questions above. I wish there was a transcript of the show I hate listening to podcasts.

Yeah, I know what you mean. I also hate podcasts, generally.

My BG is still low and I stopped the 2 day semi-fasting.

What do you suppose is lowering it then? Lower protein?

Maybe it's the ketosis. The SIRT-1 stays active for awhile, but if my numbers stay this low over the next week or two, I'll assume it is because of the ketosis.

I haven't been this deep in ketosis in quite some time. Last time I did this low carb it was also very high in protein. So could have been the protein.

Atkins replaced a several day total fast induction, suggested by an earlier low carb doctor (Donaldson) with his very low carb. That's maybe one more thing that needs a good, double blind test. Does it take less time to keto-adapt if you kick things off with a total fast, than with Atkins-style induction? would be a nice question to have an answer to.

I would never tell anyone to start with a several day total fast. 99% would bail under those circumstances, and rightly so. Throwing a metabolically challenged body into this, especially while carrying out the busy day most people would still need to accomplish, is asking for trouble.

However, some people do have trouble with Induction; a variation which allows more carbs, from vegetable sources, would offer plenty to chomp on and still be a drastic slashing of carb content.

That would be the purist version of the Protein Power plan: 40g of carbs from veggies daily; no more than 10g at a sitting/snack.

I wouldn't tell anyone to start with a two-day total fast, either. Not unless I liked the results of that study I'd like to see.


If Phinney and Volek are right about salt being the main culprit behind Atkin's flu, the number of people who could tolerate a two day fast might be higher than we'd think. And of course, there would be particularly busy, stressful times when it wouldn't make sense to go into a fast.