Carbohydrates and Diabetes ~ Part II

I really struggle sometimes wondering what goes on in the minds of the staunch low carb advocates.  Something comes along that's just their sort of "red meat" revelation -- you know a "what if everything you thought you knew was wrong" sort of bombshell -- and they just seem incapable of wrapping their head around it because it goes against what they've been told by their LC heroes.  Instead of even trying to reconcile the cognitive dissonance, it seems they'd rather just move the goal posts .... just one more time?   I suppose it is easier to believe in fairy tales, to convince yourself that the rebel path you chose on the word of so-called experts is the right one to optimal health and immortality.  The alternative does tend to get rather uncomfortable.  

When I wrote Carbohydrates and Diabetes, my intent was to dispel one of the more common remaining myths about carbohydrates.  This is one that, sadly, is embraced by the mainstream as well.  I believe this is because there is enough of an intuitive connection between blood sugar and food sugar, and it is technically correct that all starchy carbohydrate is effectively "sugar" as it is broken down into glucose.  

Commemorative Low Carb Guru Teaspoons
And then you have your teaspoon crowd, the ones that fixate on the capacity of your circulatory system to carry glucose as if this is in any way meaningful with regards to how much dietary carbohydrate you can consume.  Simply put, the fact that normally the glucose in your bloodstream amounts to about 1-to-2 teaspoons (closer to 1 fasted, perhaps approaching 2 after a large carb load), really tells us nothing about the role of carbs in diabetes.  Put another way, this is no more relevant than the amount of fat in your bloodstream, or amino acids for that matter.

Statistically every human eats more than 5-10 grams of carbs at a time, and it's not like we have to eat a few grams every half hour to keep blood glucose levels steady.  The same goes for fat.  Statistically every human eats more than a half to 1 gram of fat at a time.  And yet most humans don't have "damaged metabolisms" as a result.  This is because of insulin.  Insulin doing its job -- or one of its various jobs to be more accurate -- of clearing excesses of all three macros from circulation so as to maintain a relatively steady supply regardless of the state of nutrition at any given time.   

Insulin does more than facilitate nutrient uptake, however, its most important roles appear to be its action in the liver to suppress the liver's glucose production (glycogen breakdown and/or gluconeogenesis).   This is real reason why the hyperglycemia of diabetes has very little to do with dietary carbohydrate.   A pancreas that produces insufficient insulin, and as a result too much glucagon is the likely primary problem.  I am convinced by the various review articles that I've discussed this past year or so, that insulin deficiency is the primary defect in the etiology of diabetes.  Hepatic (liver) insulin resistance (or the adaptation/dysfunction we call IR) is perhaps a secondary cause, while peripheral IR is almost assuredly a symptom, if it even exists (again, as it has been described and defined to date).  

Embedded image permalink
All that said, the fact that hyperglycemia isn't due to eating carbs does not absolve the macronutrient entirely.  Carbs could still be implicated if it were shown that they cause the insulin deficiency.  Indeed, this is still the major charge of those like Wiezen Wampe (hehe ... that's Wheat Belly, ever since I found it in German I just kinda like that name better!)  when he implores us to baby our pancreata.  The purpose of Carbohydrates and Diabetes was to discuss a smattering of the wealth of evidence against this "exhausted pancreas" model vis a vis carbohydrate intake.  Using your insulin is not like driving a car that will eventually wear out.  Insulin in your body is not like odorous fumes in a room that you cease to smell if you're in the room for a while.  

If carbohydrate consumption caused diabetes, then the traditional Pima would have become diabetic ... they clearly appear to be genetically predisposed ... but they did not.  Nor do their Mexican "cousins" that still consume a more traditional diet including not just carbs, but grains.  If decreasing carbohydrates was required to treat, put in remission or reverse diabetes, then we would not see improvements on a high carb diet.  Yet we do, with Ma Pi 2 as discussed in the blog post, and others like DASH, Pritikin, etc.  
Why am I writing this follow-up?  Well, because of some of the feedback and responses to that post.  First and foremost, Fred Hahn commented.  That's the full screenshot that you can click to enlarge, but I'll post it chopped up to break up my wall of text and keep you from having to scroll up and down.

Really?  Not a single one?  It would be far closer to the truth to state that every single one does, compared with the truth in this statement!  To then call ME disingenuous?   I tweeted this out with a link to the most obvious statement I could find:

Screenshot of this post

Or how about with a more modern paleo bent?  Diane is Diane Sanfilippo of Practical Paleo fame.  She's tickled pink that Amazon searchers seeking paleo information land on her stuff rather than that outdated low fat Cordain/Wolf stuff.
Screenshot of this post
Nahhh ... no implication that carbs give you diabetes.  It seems to be stated pretty clearly here by Hahn's friend and "expert", Gary Taubes:
Over the years, prominent diabetologists and endocrinologists— from Yalow and Berson in the 1960s through Dennis McGarry in the 1990s— have speculated on this train of causation from hyperinsulinemia to Type 2 diabetes and obesity. Anything that increases insulin, induces insulin resistance, and induces the pancreas to compensate by secreting still more insulin, will also lead to an excess accumulation of body fat.   (GCBC, Kindle Location 8027)
I could go on, but I won't bother.  It seems silly that one should even have to refute such nonsense, but I felt the need to call out the utter stupidity of Fred's comment.    What's even funnier, is that in the next lines he appears to be making the case for how carbs cause diabetes.

OK so let me get this straight.  On the Ma Pi 2, 70+% carbohydrate diet, in one study, all of the subjects who were taking insulin at baseline were no longer taking it after 6 months, because ... what?   Eating carbs forced their pancreata  to produce insulin??  Gee if only it were that easy, eh?    Here is the link to the study he then cites:  Mechanisms of β-Cell Death in Type 2 Diabetes.  So what Fred is saying is that eating carbs will eventually kill of your beta cells ... so it's only a matter of time for those no-longer diabetic Ma Pi dieters until they need their insulin again.   You'd think that only glucose is implicated there, but ...

Whereas some free fatty acids and lipoproteins have been shown to be pro-apoptotic for the β-cell, others are protective. Thus, long-term exposure to saturated fatty acids such as palmitate appear highly toxic ...
Oh and ...
Lipoproteins may affect β-cell survival in a similar way, whereby VLDL and LDL are pro-apoptotic ...
But I digress because that paper discussed possible mechanisms by which diabetic hyperglycemia -- as in uncontrolled frank diabetes, not transient glucose spikes from a carby meal -- can contribute to cell death.  Since the Ma Pi dieters had restored their insulin function, I don't think they need to fear this.   Still, if all you need to do to cure diabetes is to *force* your pancreas to secrete more insulin, why wouldn't you just do that?    

In his last ditch effort to alleviate whatever cognitive dissonance he might have had, Fred claims:

Fred has emphatically stated many times that carb restriction is the only and best way to treat diabetes.  He is not alone.  It matters not that the Ma Pi 2 studies suggest otherwise.   If you can't eat a small potato without your blood sugar spiking through the roof then you have not cured your diabetes.  The subjects in the Ma Pi 2 studies were consuming almost 400 grams of carbs per day.  So the purple highlighted comment is also wrong.  Since the carbs were starch, they likely were eating less sugar, but not less total carbs.  Contrary to LC propaganda, the SAD is not particularly high carb by percentage.  In most dietary studies where weight maintaining "usual intake" is verified, carb intake tends to be 45-50% of calories, in a diet of equal caloric value to the Ma Pi 2, this only amounts to only 250-275 grams of carbs.    These dieters likely increased their carb intake during this study.  

So Fred, if you're reading this, you really need to read the studies, etc., so that you can avoid such gross errors in the future.  

Next up, Peter D/Hyperlipid.  In a blog post on the 3 month study, making fun of it's "macrobiotic" thing.   (Hat tip to Charles Grashow as I don't read that blog) .  To refresh, in that study the subjects had all meals prepared for them and served at a clinic for the three weeks, followed by instruction to follow the diet for two more months at home.  Peter first focuses on the fact that the blood glucose levels rebound slightly during the months at home using this diagram from the paper.

So ... the diet is not sustainable?  Perhaps.  Is this ANY different than what we see for many other diets?  I mean it's not like LC has any better track record in this regard.  Remember Shai?  

Nah, no rebound in that fasting glucose in the diabetics there (blue is LC, gold is Mediterranean).  But this is interesting:
Everything improved when you have a real macrobiotic cook serving you. Do it yourself and by twelve weeks things are already starting to fall to pieces
I'm not sure "fall to pieces" is fair, but Peter has just acquiesced that a 70% carb diet to the tune of over 350 grams of carbs improved everything.  So it is a matter of adherence, not the evilness of the carbohydrates.   However Peter would prefer to distract than address this inconsistency with his advocated diet.   No, it is best to claim they are metabolically broken and then speculate that by a year or more, they'll be worse off because ...
There is no answer for diabetics other than LCHF    ~PeterD/Hyperlipid
OK ... because he says so I guess.  My other reason for linking to that post is that George Henderson commented on my initial post, and there, regarding HbA1c.    Now in the 3 month study, HbA1c's were not supplied, but they were in the 6 month study.  However blood glucose levels were reported.  So in comments, in response to George, Peter expands on his thoughts:
I’ve been thinking a great deal about what an HbA1c really means. My own view about glucose is that resisting insulin is where maximum health comes from. The level of glucose in the blood stream is probably then actually irrelevant, if you are keeping that glucose out of cells.
Uhhh, OK.  In my opinion, anyone who believes that cells are healthier if they can resist insulin, really needs a reality check.  I mean a T1 diabetic is apparently Peter's desired metabolic state.  The brain still gets its glucose and there's no insulin around to bother the other tissues or make you fat.  It's a low carber's ideal.  (shakes head)    By resisting insulin, Peter is actually referring to the mistaken notion that without insulin cells cannot take up glucose.  I again refer you to  this post as to why I call that notion mistaken.  If you have elevated blood glucose, it is getting into your cells, and where it probably causes problems in diabetics is that it isn't effectively stored (and comes with a hefty dose of fatty acids).    But, the Ma Pi dieters had lowered blood sugar so I don't really get what he's trying to say.  Enough of the chocolate picker anyway, but I'll leave you with an excerpt from George on his blog:

George Henderson said...
A raw food vegan diet might work better, because then you'd be starving, and starvation probably does cure diabetes, if you didn't die or lose your mind first.
HbA1c is a red herring, because you need hemoglobin and reasonably long-lived red blood cells to have elevated HbA1c, so veganism will lower it even if glycation is increased.
George posted these two "rebuttals" on this blog as well, and I'd like to addess those in this post because they demonstrate, yet again, how low carbers are constantly moving goal posts and/or ignoring inconvenient facts.    We'll do the blood sugar thing first, I've cobbled together two replies in one image:
I had blogged about unusually low HbA1c's and apparently he got this idea from the paper discussed.  It is true that hemoglobin glycation is an imperfect measure of glycemia in some disease/dysfunctional states.  George seems to have taken that and ran with it by presuming that all of the subjects on this vegan diet, what, perhaps didn't really improve glycemic control?  Rather, he surmises sans facts, that they all became anemic with blood cells turning over faster than Fred Hahn can talk himself through his first circle.  He is implying that they had low HbA1c despite high glycemia.  Well, in the study that provided both parameters, both HbA1c and fasting blood glucose declined considerably.  I'd say that there's no reason to question that the decline in HbA1c was indeed due to the decline in glucose levels.  Still, this rebuttal is not so much moving goal posts as it is a display of the mental gymnastics required to reconcile one's dogmatic stances.  I have again cobbled together the two relevant comments into one image.

As you can see, George repeated the notion that this diet was some sort of "fast".  I responded in my comments that it might, indeed, be like a fat fast (one where fat other than that accompanying whole foods is abstained from, not the Atkins kind) and could help "drain the swamp" of  fat buildup despite the caloric intake.  However, there really is no way to look at this diet as any sort of modified fast.  While it was obviously somewhat hypocaloric (effectively) as weight was lost, in general the calorie intakes were quite a bit higher than normally prescribed, at roughly 2150-2200 calories/day.    Some sort of cult diet??  Really??  Yeah and this so-called "nutritional ketosis" is perfectly normal ;-)  C'mon George!!   In between these comments, Charles had pointed out the calorie levels of this supposed "modified fast" which elicited that second comment.

Whoa?!  Macrobiotic roughage??  I have been hearing since the 80's from both sides of the white rice/brown rice fence, cereal fibers arguments, glycemic index, and all that jazz.  Pretty much, glycemic index is a bust and has little if any meaning to anyone except diabetics looking to better manage glycemic excursions with insulin, etc. 

Roughage?   Is it really too much to ask that people think a bit critically before commenting such as above?   It's not like I didn't screen cap and include the make-up of the diet involved in addition to describe it.  You know, 40-50% whole grains, which was itemized as being mostly brown rice ... 350 grams of brown rice to be exact.  Here's's take on the nutritional content of that roughly half of the diet.

By my calculations, that fiber clocks in at less than 5% of the carb content, making the rest of it, minus less than a teaspoon's worth of sugar, easy to assimilate starch.   We are so waaaaaaaaaaay past that 151st insidiously fattening gram of carbohydrate already with the rice here.  But George's take is interesting ... that our Ma Pi dieters were actually on a severely calorie restricted diet, though I must say, I've NEVER seen the roughly 50% assimilated figure before!   Scam Feltham and his nuts notwithstanding.  (See here for that reference!)

Carbohydrates do not cause diabetes.   Using your pancreas does not wear it out.  Of these things I am sure, and I have a boatload of peer reviewed scientific research, billions of human people-years worth of long term free living observation, and at least as many unverifiable anecdotes as any other advocate out there to back that up.  It's just that the first two carry a lot more weight.

Ahh ... I feel better after that mini rant.  I'm sorry dear readers, but I get so sick of this dysfunctional mix of unsubstantiated claims, denials, exaggerations and flat out fraud.  This idea that carbs cause insulin resistance is erroneous.  I have tracked down the other source of Taubes' quote above and what I have found out there is that Berson (and Yalow) said no such thing about the etiology of diabetes (or its link to obesity for that matter).  I await one one other citation from Berson & Yalow, just to confirm that Taubes did not simply mis-attribute to the citation itself while getting it correct about the researchers.  If history is any guide, I'm thinking this won't be the case, especially since we are talking about more than just the single quote in GCBC.    Indeed it is interesting how much the view of diabetes in the 60's reflects my own and that of most diabetes researchers.   Stay tuned.... 


Healthy Longevity said…
The Papua New Guinean highlanders were found to consume as much as 94.6% of energy from carbohydrates, predominantly from sweet potatoes which have a relatively high sugar content, yet diabetes, heart disease, stroke and obesity were very rare.

The Arab Bedouins also traditionally consumed a very high carbohydrate, with about 750 grams of full-grain wheat per day, yet diabetes and heart disease were also very rare. Their wheat bellies were flat, not fat.

These conditions have become highly prevalent among these populations as they moved away from their traditional diet and lifestyle demonstrating that these populations are certainly not immune to these conditions either.
As a side topic, would you say that avoiding or reducing foods with a high Glycemic Index or Load has any merit?
George said…
Just to clear up, I do believe the Ma Pi dieters got glyceamic control. I don't doubt that. There are a few ways to get glycaemic control. The only reasons I wouldn't recommend a macrobiotic diet or vegan diet are related to its poor nutritional value, and maybe some poorly tolerated foods/bad fibre/phytate issues for some. The HbA1c issue is about the lack of definite meaning in relatively small differences in HbA1c, given the role of anaemia, which is something you yourself exposed to our attention a few posts back.
A paleo diet like Paul Jaminet's may well give results as good as VLC while being equally as nourishing. So far this hasn't really been tested to the same degree, VLC having been compared with a variety of competing diets but not the PHD (etc). It's about standards of evidence, you can't expect to convince the medical establishment without RCT comparisons and at present those favour VLC. The evidence for VLC is better than that for competing systems, but that by itself doesn't mean one of those competing systems, one which hasn't been tested properly (or is still wrongly formulated) won't one day scoop the pool.
However, if you're a doctor you generally go with the thing already shown to work best, unless you're a brave person convinced they know better (or a quack). At present that does look to be VLC. But maybe we'll know better when we start counting amputation rates and blindness in diabetic populations on various diets long term.

Because VLC treats diabetes doesn't mean carbs are the cause. Pretty sure you need to combine the most processed (fastest absorbed) carbs with the worst oils to get that result, and being a bit choline deficient will help.
Another point is ease of practicing the diet. You can clear fatty liver on a VLC diet (which is surely going to help with glycaemic control) in the time it takes most people to settle among themselves just what foods should actually be in a Paleo diet.
Subcalva said…
I forgot to add the link
carbsane said…
There's really only one way to get glycemic control without exogenous insulin -- restore insulin signaling. Managing blood sugars by not eating carbs, and in many cases limiting protein, is not getting "control" because you can't eat like billions of normal humans. So I don't see what you are getting at there.

There is no evidence that VLC diets reduce any of the comorbidities/complications of diabetes in the long term, and VLC has not really been tested in most clinical trials. Where it has, it predictably reduced insulin requirements but not metformin, etc.

As to fatty liver, if VLC induces rapid weight loss, it will reduce liver fat, but I've yet to see a long term study in maintenance. Interestingly to your interests, I came across a paper the other day (if I find it, I'll shoot it to you on Twitter) about fats and liver damage. If you drink, sat fat = protective, PUFA = bad. But if you don't drink, sat fat = bad and PUFA = neutral.

Why did you bring PHD into this? I don't get the connection there.

As to your facetious anecdotes, OK ... so you got called out on nonsense. Most people don't announce such things to their Twitter followers :-) My point re: brown vs. white rice is that there's not much difference either way. If you can really tell the difference in terms of hunger when you eat it, I suggest you have a serious placebo effect going on there!
carbsane said…
Hi MAS! The glycemic index has pretty much been a bust in any diet trials I've seen for weight loss, etc. It's really so variable as to be meaningless. Nuttall and Gannon have done a lot of work with just potatoes over the years and the (average) glycemic response differs between first meal, second meal, with protein, with fat, with mixed meal, etc.etc.etc. Further, that's "average" and varies widely between individuals.

From my discussion with diabetics, most tend to use lower GI foods *for them* as a way to "eat to their meter" and/or dose insulin appropriately.
carbsane said…
Thank you for contributing these!
carbsane said…
ItstheWooo ... it's time YOU stopped stalking. K?

George commented here. He made comments worthy of being called out. He now says he was being facetious, so that only confirms he was rightfully called out.
Sanjeev Sharma said…
> "not a single low carb expert has ever said that carbohydrates cause T2D"

Lustig says it in his speeches describing his collaborative work with Sanjay Basu. He singles out Saudi Arabia and Malaysia IIRC.

two Interesting things about that:

ONE, in Basu's paper it specifically says causation's not established - in his speeches Lustig's playing the same game from his poison video - saying JUST ENOUGH to be able to squeeze out later.

TWO, Lustig's old response to Sievenpiper & others at that fructose conference, that RCTs must decide the fructose issues, has disappeared - causal inference is now enough apparently - ONE SINGLE econometric model (the Basu paper) is now as probative[*], according to Lustig as the mountains of anti-smoking research and global warming research.

Bravo Doc.

I haven't matched up the times & dates to establish exactly when he changed his tune.

[*] your peers wouldn't let you put it in the paper but they're all morons right Doc?
charles grashow said…

The majority of patients with long-duration type 1 diabetes are insulin microsecretors and have functioning beta cells


Most patients with long-duration type 1 diabetes continue to secrete very low levels of endogenous insulin, which increase after meals. This is consistent with the presence of a small number of still functional beta cells and implies that beta cells are either escaping immune attack or undergoing regeneration.

New technology has enabled scientists to prove that most people with type 1 diabetes have active beta cells, the specialized insulin-making cells found in the pancreas. Type 1 diabetes occurs when the body's immune system destroys the cells making insulin, the substance that enables glucose in the blood to gain access to the body's cells.

It was previously thought that all of these cells were lost within a few years of developing the condition. However, new research led by the University of Exeter Medical School, which has been funded by Diabetes UK and published in Diabetologia (the journal of the European Association for the Study of Diabetes), shows that around three quarters
of patients with the condition possess a small number of beta cells that are not only producing insulin, but that they are producing it in response to food in the same way as someone without the condition. The study, which was supported by the National Institute for Health Research, through the Exeter Clinical Research Facility, tested 74 volunteers. Researchers measured how much natural insulin they produced and whether it responded to meals, a sign that the cells are healthy and active. They found that 73 per cent produced low levels of insulin, and that this occurred regardless of how long the patient was known to have diabetes. Researchers studied the response of the insulin production to a meal to prove that the low level insulin production was coming from working beta cells.
George said…
Why do you think we mill grains to remove the bran? Why does most of the world's population prefer white rice over brown? There is a storage issue with flours, but I doubt this applies to whole grains.
In any case, you could always try the macrobiotic diet and see how it works out for you.
I mention the PDH as an example of a low-GI diet that claims the same benefits as a VLC diet. Thus, it could be compared with VLC to see if it's as good or better. So there are studies that could be done that would test VLC claims in useful ways. There are other possible examples - low-fat diets and so on - but the point is that further comparative RCTs will be needed if you don't want to accept the existing evidence.
The VLC camp claims that, on the evidence, VLC should be the first thing that's tried. This doesn't mean it needs to be the only thing, but that it's the place to start.
If PUFA was neutral in people who don't drink, we wouldn't have NAFLD.
And we wouldn't have had comparatively low rates of NAFLD back in the days when people ate much more butter and meat fat than they do today.
PUFA from fish, meat, fish oil, nuts, olives and so on, possibly even some unheated canola oil, I don't think would be hepatotoxic in absence of alcohol, or perhaps large intakes of sugar, up to say 30% of fat, provided that n-3 and n-6 were more or less in balance, and there was a good variety of very long chain fatty acids. Bear in mind that ALD research counts MUFA as saturated fat, because it has 99% of the stability of SFA.
Oh, and the ALD mechanism also protects against acetaminophen toxicity.
A lot of people who don't drink do use acetaminophen.
George said…
My personal experience of the fatty liver question is due to having HCV genotype 3, which does cause steatosis. When I stopped using oils, reduced carb intake and ate more SFA and MUFA from animal sources, and some coconut, I felt better.
Last year, after 2 or 3 years eating high SFA/MUFA, low PUFA (but with some fish), I went into a trial for new oral antiviral meds. Before the trial, I had a CAPSCAN, which is an ultrasound that measures steatosis in dB (same machine as a Fibroscan, which measures scarring). I had moderate detectable scarring, showing the effect of long-term viral exposure, but no steatosis. I suspect this would be an unusual finding in someone with HCV genotype 3, that is, that fibrosis would usually be accompanied by steatosis. My ALT/AST were 30.
After the trial, which seems to have worked, the scarring has significantly reduced, AST/ALT are 18. I am pretty confident that restricting carbs and omega 6 countered the effects of the geno 3 HCV (having this infection is comparable to being at high risk of NAFLD for genetic reasons). "Genotype 3 was the independent predictor of steatosis in all patients."
George said…
Eating like billions of normal humans - why would you be wanting to eat like the normal humans that are getting diabetes?
What about taking no medication like billions of normal humans too? The trouble and expense of medication is a factor just like the discomfort of resisting peer pressure.
I believe that reductions in meds on VLC trials also includes blood pressure meds, BP may be a good predictor of future complications.
charles grashow said…
Can you show any reference that indicates that billions of people have diabetes as you assert above.
Lighthouse Keeper said…
Two U.K. doctors (twins) embark on two separate diets, one high fat low carb, the other high carb low fat. Watched this documentary when aired on wednesday. At the same time the cherry picking fingers of the U.K.'s low carb bloggers must have been hovering over their computer keyboards in anticipation of another ' The Men Who Made Us Fat ' or the patently absurd Catalyst ' Heart Of The Matter' . Looks like they were disappointed . Might be because one of the supervising doctors told the low carb twin at the end of the trial " What is worrying is your body is not responding to insulin as well as it did, if you eat too much fat, that can stop your body responding to insulin and it also can tell your body to produce more glucose, what we have seen is your blood glucose has climbed from 5.1 which it was before the diet - which wasn't great to start with but still in a healthy range to 5.9. Now you are only .2 away from being pre-diabetic. It's not good for you, you should stop that diet."
charles grashow said…
charles grashow said…
carbsane said…
Why are you deliberately twisting words? Eating like billions of normal humans as in humans that do not get diabetes.

I'm all for taking no medications. As ALL the subjects in the 6 month study were thanks to their diet.
carbsane said…
I don't have diabetes or glucose intolerance. I don't really care about who eats what. I prefer white rice, but there's no evidence that brown rice is even close to the half indigestible roughage you asserted.

I don't think VLC is a good starting place. It made sense for a while but when you understand nutrition and metabolism and how humans have traditionally eaten, there's just no support for adding excess fat calories and limiting carbs to the levels Pauls suggests. The scientiic literature points way away from anything that high in fat.

Like I said, I'll see if I can find the paper and will shoot it to you on Twitter. Kinda preoccupied with research and real life job and family at the moment.
Screennamerequired said…
Oh no! not the dreaded insulin spiking disease causing wheat!

Speaking on dietary trends and whole wheat
George said…
The assertion is not that billions have diabetes, but that people have diabetes from eating as billions eat.
The WHO estimates that 1.4 billion adults are overweight. Diabetes probably in millions but growing as oils and sugars spread.
I just don't get the argument - were the people in yr 6 month study eating as billions of normal humans do?
That wasn't the impression I got. Eating the normal way, for a diabetic, doesn't work, is the strong impression I get from the literature. A Macrobiotic diet, or a low-fat vegan diet, or whatever - these are not "normal" just by dint of containing carbohydrate.
ExEffectsGuy said…
I subconsciously found myself shaking my head this morning as a read a blog page of one of the low carb heroes. It seems in this particular recent update about the futility of calorie restriction and increase calorie burn. OK, as far as that goes, not too radical these days, but it seems the options are eat carbs but starve yourself or eat "the right way" hi fat moderate protein, grudgingly small amount of carbs if any. It's amazing how all of us at one time or another can get so caught up in our dilemma. As the replies indicate, and the hero himself has indicated in the past, this no brainer easy to stick to low/no carb diet is often abandoned in a moment of "weakness." OK, I agree a concentration camp is a bad diet model, but so is cherry picked science, tenuous causal relationships in nutrition, and the denial of the possibility that there is room for discussion and further analyses. What if there is no one answer? Oh well....I have to stop reading that stuff. I am interested in the inevitable epiphany moment that will undoubtedly come to them if they're honest enough to admit it.
charles grashow said…
Subcalva said…
The high sugar twin lost 1 kg (0.5 kg fat and 0.5 kg muscles) and the high fat twin lost 3.5 kg (though I can't remember now if it was 2.0 kg muscles and 1.5 kg fat or the other way around). The explanation to why both of them lost weight was that both the diets were not that palatable. They talked about a study made on rats being fed in the same way and they didn't put on weight on low fat or low carb. Not until they mixed sugar and fat they say changes in weight and the most palatable mixture were around 50/50 where the rats put on weight very rapidly. On of the twins then made a very short "study" by offering around three types of doughnuts to people in the street. One was an ordinary glazed doughnut, the second was a doughnut with sugar frosting and the third type was a cream filled doughnut. Most went for the ordinary glazed doughnut which supposedly is 50/50.
Craig_in_CT said…
The end point of the show seems reasonable: they argue that it is the combination of fat with sugar (or refined carbohydrates), creating calorie dense, highly palatable foods which is the root of all evil dietarily speaking. It is very much in line with Guyenet's view. Toward the end, they quote a researcher named Susan Jebb who has supposedly done a lot of work on the effect of macronutrient dietary composition on health outcomes. She states that the effects are modest; what matters is whether or not you are overweight. I'm guessing you'd probably agree with above.
charles grashow said…
Jimmy Moore's response

Twin sisters embarked on the Twin Noakes experiment to test
Professor Tim Noakes’ controversial theory about the dangers of a high carbohydrate diet. Here are the results.

And of course we must not forget Dr. Briffa

"The fundamental problem with this programme is that it essentially dressed up anecdote as science. It’s not a good idea to judge the impact of different diets by testing them on a limited number of people in this way."

BUT - N=1 experiments are valid!!
charles grashow said…

Do elevated free fatty acids impair glucose metabolism?

If yes wouldn't that be enough of a reason NOT to go on a VLCHF diet?

I ask because of this comment on Dr Briffa's blog
31 January 2014 at 9:03 am
"The poor performance on OGTT taken by low carbers is called the Randle effect which allegedly normalises after 3-4 days of ‘normal’ carb eating. I have been curious about this and the programme seemed to support my experience. I am fit and thin but a year ago thought I’d give low carbing a go for general health and to lower a slightly high (5.5)
fbg. I now notice that I have become extremely carb intolerant and despite introducing more in the way of rice, fruit, yogurt to eliminate the Randle effect I remain more carb intolerant than I was before going low carb. My food choices are more restricted now – has my body ‘forgotten’ how to deal with carbs altogether and how much harm are the
high blood sugars seen after say having plain yogurt and fruit doing? Could it me that in my case (and studies only seem to focus on a certain physiology) a high carb diet has done me no favours at all?"
Elevated Free Fatty Acids Impair Glucose Metabolism in WomenDecreased Stimulation of Muscle Glucose Uptake and Suppression of Splanchnic Glucose Production During Combined Hyperinsulinemia
and Hyperglycemia

Elevated Circulating Free Fatty Acid Levels Impair Endothelium-Dependent Vasodilation

Your thoughts
mike said…
"Why do you think we mill grains to remove the bran?"

because most whole grains don't taste good
eulerandothers said…
I don't think 'most whole grains don't taste good' is the reason.

And George, you're dead wrong:

'White rice is the name given to milled rice that has had its husk, bran, and germ removed. This alters the flavour, texture and appearance of the rice and helps prevent spoilage and extend its storage life. After milling, the rice is polished, resulting in a seed with a bright, white, shiny appearance.'
charles grashow said…
"A Macrobiotic diet, or a low-fat vegan diet, or whatever - these are not "normal" just by dint of containing carbohydrate."

SO - a normal diet contains NO carbohydrates?? Or is there a limit where a diet, by including carbs, is no longer "normal"?
George said…
That's rather obtuse Charles.
Pretty much the opposite of what I said.
To spell it out - normal diets, how billions eat, do contain carbs, normal diets are not calorie restricted, normal diets are not vegan or macrobiotic.
Normal diets are not used as therapeutic interventions for diabetes, except as controls.
George said…
I think the Paleo objection to fish oil is a bit exaggerated. It seems to work better than most supplements in RCTs, though the effect is contingent and vulnerable to being lost through other factors, it still shows.
George said…
Digestibility at various extraction rates was a debate at the time of food rationing in WW2. More bran (lower extraction) meant less digestibility, which was bad (less energy) but more vitamins, which was good. Scientists were split and compromised on medium extraction rate.
George said…
So what happened to the famous water weight loss of low carb? All of a sudden it turned to muscle and jumped down the toilet?
charles grashow said…
"normal diets, how billions eat, do contain carbs"

How many carbs as a %
George said…
Well it would be easy to supply more details from an n=1 than were supplied from the infotainment n=2. All sorts of basic things like triglyceride levels seem to have gone walkabout. Half the data that should have been most easy and obvious for the show to provide was not there. Jimmy has at least given Evelyn screeds and screeds of data to analyse from his n=1.
George said…
What you can get, whatever you like, same with fats. I'm not trying to define normal except to say that restrictions are not part of normal eating patterns which are matters of medically unaware, largely unconscious habits and preferences.
So if someone has glycemic control on a macrobiotic diet that happens to be, say, 80% carb, it's still first and foremost a macrobiotic diet, an unusual diet unlikely to be acquired by following one's natural appetite, it does not predict that person's response to a more normal high-carb, low-fat diet.
eulerandothers said…
I think 'extends shelf life' is a winning argument when it comes to food.
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