https://proteinpower.com/drmd_blog/...gall-of-it-all/

They were involved in a low fat study, a surprising number of people developed gallstones during it.

Quick weightloss seems to be a factor, lots of cholesterol being released from the fat cells and needing to be disposed of through bile was one thing I read earlier today. So, quick weightloss plus low food/especially fat. Mary Dan Eades says they rarely saw anybody develop gallstones on their low carb plan, although they didn't do MRI's to check, so there might have been some people who were asymptomatic. Given that a lot of people probably would have ended up low calorie, but not extremely low fat, I guess that leans things towards not enough fat.

Denise says a tablespoon of oil ruins things... but what are the operating conditions? Eat some rice. Free fatty acids go down, maybe you're more insulin sensitive while you digest and absorb the rice. Add that tablespoon of fat to the rice--maybe you're not as sensitive.

Or eat the rice first, wait three or four hours, until you're certain you've probably digested it all, then have the fat. Maybe the oil reduces your glucose tolerance--but going in, glucose and insulin are hopefully at basal levels. Going the other way might not be as practical, because eating the fat first, it can take a lot longer for blood lipids to return to normal. All this takes at face value that the person's reaction to that rice really is that of a non-diabetic, as is claimed. Just having fat in the system, at any time of day, can't be the problem, logically--or the diabetes couldn't get better during weightloss itself.

I had to have my gallbladder removed after doing low-fat for a year or so.

Fung talks about insulin pulsatility. The fat with the carb meal would reduce the glycemic index but would reduce the pulsatility along with increasing the IR. A longer fasting period would be required for insulin to come back down.

This is interesting. high GI was better than low GI in this study - even with fat: http://ajcn.nutrition.org/content/63/1/47.short

Looking at the menus in that study... there was a time I probably would have expected a health benefit from the low vs. the high glycemic diet.

Saw this earlier;



The actual area under the curve for insulin wasn't actually that different among groups. There was a significant difference between butter and no butter and potato, but not between plain potato and plain potato with olive oil. Just looking at the graphs though, you can see that the difference between olive oil and butter was marginal, though. Make olive oil the control--all significance would disappear.

What I find interesting, though--40 grams, 80 grams of olive oil plus potato--indistinguishable. 80 grams of butter plus potato was also indistinguishable from 40 grams, when it came to insulin. This suggests that if there's a dose response, it occurs somewhere below the 40 grams threshold.

http://high-fat-nutrition.blogspot....d-dr-davis.html

In this hyperlipid post, adding butter to 40 grams of glucose had such a powerful effect that about two-thirds of the insulin secreted were due to the added fat. There was a much weaker effect in the potato study--I'd guess due to the potato study involving diabetics. The butter and glucose people in the hyperlipid study had insulin return to basal at two hours, and under basal at three hours and beyond, that doesn't sound too diabetic to me. So maybe you get a weaker relative effect in diabetics, since often their free fatty acids are elevated even in the fasted state.

I read insulin resistance and it always bugs me. Nobody ever explained to me in a reasonable way why it's important, or what in fact it actually is. Well, let's see. What's the context? Glucose disposal, plain and simple. But what's the context of glucose disposal? Excess glucose disposal, also plain and simple. So, the only reason insulin resistance is important is within the context of a high-carb diet, just as plain and simple as the rest. What if we eat a low-carb diet, why should insulin resistance be important then? We got no excess glucose to dispose of. Indeed, the most likely primary cause of insulin resistance is excess glucose. So, once we eat low-carb, there is no reasonable expectation of insulin resistance to occur, or if it does occur to a level which would otherwise disrupt proper disposal of excess glucose specifically, to consider it important for the purpose of excess glucose disposal, since we got no excess glucose to dispose of.

The context of low-carb does not fit standard insulin resistance. We need a new standard for this, and a new way to measure this new standard. I propose that a priori, three parameters be used to determine basic insulin resistance: BG, blood ketones, blood insulin. The ratio of the three tells us several things all at once. With standard insulin resistance, glucose is used in several tests. Within the context of low-carb, using glucose does not serve our purpose. We have no need for any information regarding how quickly we dispose of excess glucose, when we don't normally dispose of excess glucose. However, we do have need of other information regarding, for example, how well we regulate ketogenesis in the liver, and for this we would need to use ketones rather than glucose. So again for example, if we inject ketones in the blood, we should expect to see a drop in both BG and insulin. If we don't see this effect, then it's obvious the liver isn't regulating ketogenesis properly, and here we have some tangible information that concerns us. Once we establish a standard for these measures, i.e. dose-response for example, we can more easily determine insulin resistance as it relates to us as a group and to us individually. But until then, we're just talking.

The point is anybody who talks about insulin resistance within the context of low-carb doesn't actually know what he's talking about, cuz you know, there ain't no data on that.

I'm not sure that I fully understand insulin resistance, either. I see it as an excess glucose thing, too. If the body can't use excess glucose or store it for short term use, then it gets stored as fat. If it can't do that fast enough, you BG rises to the point where damage is done. I reached that point and I know what the damage feels like. I also know that this was immediately undone when I committed to LCHF. Fortunately, not a lot of damage had yet been done. LCHF ended the extended periods of excessively high BG. But 9 months into this WOE, I was still getting post prandial BG readings peaking above 140 from a simple 10 carb meal. Clearly, not all the damage was yet undone and I was still insulin resistant. As of this month, I have been at this WOE for 20 months. I've raised my carb limit to 40 net carbs (starting October 1) and I've been testing new foods by taking post prandial readings at intervals after the meal. Now I can have a 25 carb dinner and not have my BG peak any higher than 100 following the meal. I certainly have a better tolerance for carbs than I did a year ago. Provided I stick to a carb limit within what my body can properly handle, I don't expect insulin resistance will ever be an issue again. But I would say that it is still an issue -- especially early on in this WOE. Had I attempted to just eat moderate carbs (say 150 or less as the ADA suggests) -- then I would still be exceeding my BG limit and insulin resistance would continue. And so would the diabetes. We don't need to eat zero carbs -- but I think it wise to figure out what our carb limits are at what ever stage we are at -- and keep our carb intake at a level that keeps our BG low and stable as much as possible.

A couple of links regarding physiological insulin resistance:
http://high-fat-nutrition.blogspot....resistance.html

http://www.marksdailyapple.com/does.../#axzz3pG2aOI5T

I agree the terminology is very confusing, and a lot of what they say about it sounds like conjecture at this point. But it has been very helpful for me to mentally shift from BG levels to insulin levels as being the focus (a la Dr. Fung).

Dang, where's that quote about the mice choosing high fat diets? was that here? I really like the idea of studies like that if they can be done with quality foods, rather than industrial processed crap. I've seriously thought about setting up options for my chickens (e.g. suet block, vegetable matter, corn, fish) and measuring what they eat. I know for a fact that the proportions would change depending on season. The cabbage head disappears in spring, but just hangs there in fall. I don't see why humans would haven't some of that seasonality.

Bile is made of cholesterol and that gets all out of whack on SAD so it's possible it contributes to gallstone formation due to changes in chemical makeup of bile. Just an idea, but I think worth investigating. Just look for a comparison between bile on LCHF and bile on HCLF.

A quick search: https://ca.search.yahoo.com/search?...on&fr=yfp-t-715

Second hit: http://www.medscape.com/medline/abstract/1612328

So maybe not just cholesterol, but the general idea of changes in bile composition seems to be plausible here.

Makes sense. Low fat dieters are generally going from the SAD, just because that diet change causes stones, doesn't mean that even a lifetime of living on just sweet potato would cause stones.

We are looking at people with weight to lose though, people who have eaten traditional diets and had never had a weight problem their entire lives wouldn't have the increased efflux of cholesterol from fat cells that you'd get during rapid weight loss.

First result from that second search Martin linked to might shed some light;



Mucin is a crystallizatiion-promoting compound?



100 % cholesterol saturation is the point of maximum solubility of cholesterol in bile, so 90 percent should be safe, with 114% there should be some precipitate. You can see the absolute increase in cholesterol wouldn't have to be that great to increase risk of gallstones, if level of saturation is a determining factor.

But here--hopefully the rapid weight-loss period lasts longer than two months. It would be pretty sucky to go through the risks and then the lifetime restrictions necessary after gastric bypass for just two months of rapid weight loss. I wonder if there is a depletion of cholesterol at this time (reminds of Dr. Davis's observation of early changes of serum lipids going in the wrong direction, during early rapid weight loss), making the early part of a very low fat, low calorie diet the riskiest for gall stone formation?

An increase in mucin content of bile sort of raises my eyebrows in the context of a diet that's not only lower in calories, but ideally lower in carbohydrate as a percentage (to make room for sufficient protein) as a percentage as well. But I've always hated Jaminet's mucin-deficiency theory, so that's probably just my prejudice showing. Even if it has the unfortunate side effect of increased risk of gallstones, maybe there's a bit of gut-healing going on post surgery (not from the surgery itself, but of gut permeability that was present pre-surgery).

Very interesting guys! One of the theories of CVD is that cholesterol crystals form when cholesterol is high and the crystals go on to damage the endothelium. That never really made any sense to me because the cholesterol is encapsulated and smaller lipoproteins are more atherogenic than large ones but they take longer to be taken up. If blood cholesterol is changed because of metabolic disease, it'd start to make some sense and would explain why there's little relationship between total or LDL cholesterol and CVD. Ratios are better markers but are really indicators of the metabolic state.

Thanks for the links about the very interesting concept of physiological insulin resistance. It makes a lot of sense why eating a higher amount of protein in a carb-restricted diet causes immediate conversion to glucose to capture it for the brain. With protein becoming the primary source for glucose, one can postulate that LC people are very efficient with gluconeogenesis, as the metabolism is looking capture a glucose source for those tissues depending on it. Cutting back to moderate consumption of protein seems to fix this for many, even when increasing carbs. This is extremely helpful in fine-tuning one's macros to get to the ratio that works for the individual. It also supports the argument that it's the insulin that must be managed, not necessarily the BG.

https://intensivedietarymanagement....-pritikin-diet/

Dr. Fung blogs here about the Pritikin diet, the second part of his response to Denise Minger's carbosis post.

This is actually more what I thought the first post would be like, a bit more open to the idea that the Pritikin diet is just another way of approaching the insulin problem. I think he seems to have brushed aside the idea of dietary fat as a problem with insulin sensitivity. Anyways, that's just mechanism--however it works, if somebody experiences an increase in insulin sensitivity and reduced insulin and blood glucose on this sort of plan, then they do, that's all.

Still can't see a fat-missing/low-protein plan working long term, especially considering the way LCHF provides missing nutrients.

Yes. Playing devil's advocate though--there are some nutrients that are more plentiful on a something like Pritikin--the Rice Diet is more clearly deficient.

I think one value in looking at this stuff--a better understanding of the two ends of the dietary spectrum, very low fat and very low carb might give more options overall than the single view. Even just looking at one side can give insights to the other.

An example is the large body of literature involving food quotient. There are all these studies where they feed people a high fat diet vs. a low fat one. What they found was that when people ate more carbohydrate, they oxidized more carbohydrate for energy, but eating more fat didn't promote the oxidation of fat. They had their low fat goggles on--so of course, looking at this effect, all they saw was that carbohydrate oxidation was self-regulating, but fat oxidation was not. So that eating fat led to fat accumulation. This is actually true. But it's incomplete, looking at this through a low-carber's eyes, it's stupidly obvious that this shows that not only is carbohydrate oxidation sensitive to the level of carb intake--so is fat oxidation. In encouraging carbohydrate oxidation, carbs also suppress fat oxidation. Two sides, same coin, suggesting two approaches that not only fit into the same universe, they are actually corollaries of one another--almost predictive of one another. There's no paradox in opposite approaches working when they work because they're opposites.

Of course low carb won't work as well if endogenous glucose production is too high, and low fat will only work if you can reduce endogenous fat production low enough as well.

Steven Cooksey concluded his experiment. http://www.diabetes-warrior.net/201...3/very-low-fat/

The criticism I have is that it takes three days of eating carbs to reverse physiological insulin resistance. The carb phase was only three days. Therefore, we learned nothing.