Another superb abstract, hot off the press, on LCHF diets. The data are suggested to be utterly clear cut, solid, and supportive of the physiology of LC eating which I have been espousing for many years now.
The conclusions are criminal. There are 13 authors. None seems to have read Kinzig et al's 2010 paper showing not only this very effect but also showing its complete reversal by a few carbohydrate based meals.
That omission, by 13 people on the author list, is what is criminal. The lack of understanding of the basic physiology of carbohydrate restriction even without Kinzig, by people in what claims to be nutrition research, is criminal. The blood on their hands, from dialysis patients, is criminal.
If even one of the authors has read Kinzig it leaves you wondering about the ethics in the group. If they haven't read the literature...
Disclosure: I haven't seen the full text.
Peter
BTW I just Pubmeded "ketogenic" + "insulin" + "resistance" and Kinzig was hit 24, primarily because 2010 is ancient history and the hits come in date order.
Hat tip to Liv for the link.
EDIT
Laura gave us this in the comments: "They actually cite the Kinzig 2010 paper in their discussion saying that their results match and that the results "could" be reversible... and then they leave it at that".
You have to ask what the lead in time to a study like this is. It strikes me as possible that Kinzig pipped them at the post by 3 years but they went on with the study as they had the funding but couldn't add a re feeding arm because they had no study ethics approval for this. Just trying to be kind, probably a mistake. Or perhaps they are just LC bashers as per usual. The cardinal sign, of using the name "Atkins" in the abstract, is not a good marker for an ethical group. But Kinzig is correct. Reversal is absolutely nothing a newbie LCer wouldn't pick up in 10 minutes on the internet.
END EDIT
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26 comments:
I feel your pain..
On a happier note, following on from your "Ketones, without the side order of Danish Pastry please" post.
An extract from EXERCISE HYPOGLYCEMIA IN NONDIABETIC
SUBJECTS
"...In addition, it has been more recently reported that,
at least in humans, training also reduces muscle glu-
cose transport. This adaptation seems to be related to
the training-induced increase in muscle mitochondrial
respiratory capacity. It has been described to be often
quantitatively just as important as the decline in
muscle glycogen utilization in accounting for the
overall carbohydrate-sparing effect of training [91].."
Hypoglycaemic training improves mitochondrial respiratory capacity. Who-hoo.
Bad news, avoiding some form of endurance (>2hr) training hypoglycaemia without carbs looks a tad optimistic. Boo!
This is what happens when people are too uncreative / unintelligent, are behind the wheel mastheading research.
If not uncreative then a vested religious like prejudicial interest in promoting a myth that HFLC diets promote metabolic disease, and the one true way is bland hydrophillic unflavored starches and fibers.
At this point in time it is simply inexcusably religious to write the LCHF diet causes insulin resistance in the same fashion as conventional diabetes. It is well known this is a transient metabolic adaptation to low dietary glucose and lower insulin levels accordingly, and if anything improved mitochondrial health and densities are the result for adopting a LCHF diet for months and years (with correspondingly better glucose tolerance when consuming a glucose based diet).
They actually cite the Kinzig 2010 paper in their discussion saying that their results match and that the results "could" be reversible... and then they leave it at that.
Hi Peter,
Been lurking for years, but this time I have a question.
1) LCHF diet causes physiological insulin resistance, which is easily reversible. In some people, this is accompanied by higher fasting blood glucose.
2) In LCHF metabolism, without any intervening period of adjustment, an OGTT may cause a pretty major blood sugar spike.
My question is whether the postprandial hyperglycemia described in (2) is eo ispo harmful. Is the BG spike in context simply a marker of LCHF metabolism or is all that glucose in the blood doing some kind of neurological/metabolic damage?
Despite asking on PaleoHacks (shame-face), I haven't been able to track down a definitive answer. Which is weird, considering the the popularity of the whole "carb-cycling/backloading" bag (full disclosure: I do something along these lines).
I don't understand your question. Could it be in #1 you meant LFHC, not LCHF?
I just had an OGTT with 100g glucose and my 1 and 2 hour BG was very high, but my insulin was reasonable. I have been strictly LCHF for over 2 years.
My understanding is that the damage is predominantly from insulin, not glucose. See: Diabetes Epidemic & You by Joseph R. Kraft
Josephus S. I'd also be interested in Peter's take on your question but my understanding (as a Type 2 Diabetic) is that while a transient higher than normal Blood Glucose (BG) is toxic, what may be more important is the duration and frequency of high BG levels. Unless the high BG is accompanied by excessive ketones, to the point of keto-acidosis (unlikely in my estimation, assuming you have a functioning Pancreas) I doubt that you are in acute danger... so an analogy might be passing your hand quickly though a candle flame: you might feel nothing, or some heat, or maybe get a slight redness on the skin. Do this every now and then with time in between, without any likely consequences. Repeat this often enough in a short time span, or hold your hand over the flame longer longer, or closer to the flame, or use a bigger flame; then you might get redness, pain and blisters that take a few days to heal up... if you give it time. Continue without allowing the blisters to heal and you risk ending up with permanent damage (scar tissue) that never heals... or worse. Same with high BGs.
You might also do a search on Glucotoxicity.
After one year of meat only diet Vilhjalmur Stefansson and his fellow explorer were given an OGTT test, the fellow explorer got a pneumonia right after despite being perfectly healthy for the whole year. It looks like glucose spike may play a role.
I guess it is better to be prepared for the test(eating higher carbs for three days prior to it) and be aware of the high spike, and avoid the test if you feel like fighting a virus or infection, or migraine is possible due to whatever makes a person more susceptible to it, or any condition you are treating with ketosis is on a high alert.
Surely the OGTT is unnecessary in this scenario, and will not exactly match what will happen if one is forced to eat carbs by survival contingencies.
I have heard it is sustained high glucose that does most damage, not freak exposure to spikes.
Unless one catches something as a result, like poor Andersen.
But of all potential spikes, the OGTT one is surely the easiest to avoid. If it is essential for insurance purposes or for renewing a commercial pilots license or something, then preparing for it seems wise.
Dr. Eades tweeted recently:
This tells me the 'experts' don't really know what true risk factors are. Cholesterol anyone? http://mead.es/1agJR1c
Similarly, in the abstract you quoted:
Therefore, use of LC-HFDs for weight loss or other therapeutic purposes should be balanced against potentially harmful metabolic side effects.
The authors obviously have no idea what any of those words in that particular permutation means. Not sure how they randomly put those words into a half way coherent sentence.
The obvious logical fallacy is that a diet cannot be therapeutic and not therapeutic (harmful) at the same time. Doesn't take a lot of qualifications to nutritional research, I suppose. Probably a bunch of mouth breathers...
Mind-numbing paper. No one is that stupid and still able to type.
So I agree with Wooo, this paper is religious and the result of vested interests.
Meanwhile, I still haven't heard of a published human trial demonstrating the reversibility, even though it is ridiculously easy to do. So this may be fun IRL after all.
Also, it's possible that the commonly heard suggestions to prepare for three days for an OGTT by eating a medium carb diet maybe falling short if the person has been on a ketogenic diet and not just on LC. They need to make sure they are also not fasted for too long for this test, because someone adapted well to ketosis can easily begin entering that state even after 13hr-16hr fasts (my own experience) and see a high BG and physiological insulin resistance. It's also reversed more quickly than one might otherwise expect, with just one day of medium carb eating (~100-120gm).
Of course, Peter says I have terrific mitochondria, and I'll happily agree :)
But anyone who fasts regularly or enters ketosis regularly (and certainly if both plus HIIT) may well see the same physiological insulin resistance after only the overnight fast demanded by the OGTT - so should maybe keep it under 12 hrs to be on the safer side.
Has anyone observed something similar and tried to track the earliest onset time?
Great analogy, FrankG. And js290, every therapeutic intervention has its potential downside, but which is best for the patient?
Good to have an intervention where avoiding metabolic side effects is as easy as avoiding a 100g bolus of glucose, methinks.
@George Henderson: every therapeutic intervention has its potential downside,
In the context of so-called "evidence-based medicine" that may be true. However, if as Chris Masterjohn puts it, our “common sense” took for granted diets associated with health rather than those associated with disease, then there cannot be any harmful side effects from a carefully formulated ketogenic diet that solves many metabolic diseases.
It would be a logical fallacy to suggest otherwise. I definitely believe there are many problems with so-called "evidence based medicine" as it relates to health.
@ marie c
it's true n=1 stuff, since I've only done it the once, but I recently checked my BG after 12hrs & 16 hrs fasting. Numbers (respectively):
90 (highish for me - roughly my 2hr)
99 (roughly my usual 1hr number)
so maybe your final comment is borne out (once).
Marie c,
In my case I didn't notice any particular PIR after 3 years on a LC diet, but adaptation to fasting and especially exercising in a fasted state got me there. In real life it feels like hiding inside a source of unlimited energy. What a nature trap, adaptation to a tireless exercising made me ill adopted for OGTT test! Just fasting doesn't give me high BS numbers ,my BS slowly drops from fasting level (110 mg/dl) during the day, but exercising would quickly provide me with 121 mg/dL (I guess it is like 6.6 mmol/L).
It looks like an adaptation to LCarbing could be very useful for the people who have tendencies to have too low BS.
Their conculsion are: "These data show that lack of dietary carbohydrates leads to glucose intolerance and insulin resistance in rats DESPITE causing a reduction in fasting glucose and insulin concentrations."
This is BASIC physiology: when you go on a LCHF diet, you body wants to KEEP the glucose it has in the blood, so it switch ON for "insulin resistance" so the liver, muscle and brain slows down glucose uptake to protect it. It is entirely normal.
And the rest of their results is just what we are looking for: a healthy reduction in fasting glucose and insulin concentration.
Of course, if you screw everything up by injecting glucose, your metabolism needs time to readjust.
Physiology is a logical science; not considering the "time factor" is illogical.
Denis
As Galina L mentioned above, and as I'm pretty sure has been discussed on this blog previously, here are the published results of Stefansson and his colleague Andersen's OGTT following a year of a "solely lean and fat meat" diet. The OGTT was repeated 2 or more weeks later, after the "general diet" had been resumed.
http://www.jbc.org/content/83/3/747.full.pdf
Here we have an human trial in 1929 by respected "establishment" researchers.
Interestingly this article cites related research with human subjects. It seems that low-carb was a valid topic for mainstream interest back in the day :-)
And yet they are still getting it wrong with rodents in 2013 -- or as suspected, consciously misrepresenting their findings.
--
Thanks George. It's hard to see the long-term internal damage caused by chronic high BGs but I think burns to skin are easier to imagine.
I just re-read for the umpteenth time the Tolstoi paper I linked above. It is very refreshing to read someone who does not seem driven by any agenda but is simply making observations, reporting their findings and drawing reasonable (but not final) conclusions.
I recall growing up in the UK in the early days of the BBC and it seems to me that was the way of science in those days... you could trust the white lab-coated experts they trotted out from time to time. No hype or agenda.
Now I find I have to be so skeptical and even the link to WHS from Woo above leaves me cold. The posts there just oooze with agenda and disinformation. He is not a person I can trust without second-guessing their every word and personally double-checking every citation.
Oops "white lab-coated experts"
I just read that and my Canadian super-sensitive PC alarm sounded..!
I meant that the lab-coats were white.
I certainly did not mean to imply anything about the scientists themselves :-(
From personal experience, and being a diabetic, my blood sugars are fantastic on LCHF and very stable.
Any dietary mistakes (=eating carbs/sugars) are not possible without having all diabetes symptoms come back with a vengeance.
This silly carb-loading/treat-day suggestion, or the suggestion to go back to higher carb nutrition would be suicidal at least in my case, and I suspect the same for others to varying degrees.
I decided to stay LCHF for the rest of my life, and I do not miss any carbs/sugars, and I do not miss being sick.
I agree, that low-carb diets have been promoted without sufficiently educating people about the metabolic adaptations taking place, and their disruptions by various diet mistakes.
The conclusions of the authors in the cited article are ridiculous if your choice is being diabetic and dying on a standard diet, or "insulin resistant" with good blood sugars and healthy on LCHF.
Why would anyone WANT to pour out major amounts of insulin? Why would anyone WANT to depend on burning sugar?
Kevin FST and Galina L.,
thanks for the responses!
Kevin, we're n=2 for those particular times now :). My numbers are 82 and 89. If you keep going longer with the fasting btw, you'll likely see fasted BG start to drop. Mine can go to 68mg/dl while I feel terrific, fully switched to ketone metabolism I'd guess at that point.
Galina, yup, I've found fasting with exercising has especially potent effect on BG too.
Apart from noting time factor in fasted BG measurements, I was alluding earlier to the fasting time factor in the BG response to a hi-glycemic meal. There's a difference in BG peak after morning hi-g breakfast, eg. two cups of hashbrowns or two toast and jam, versus after fasting until brunch/lunch and eating potato then (in the name of science!).
That's a type of 'glucose' challenge test anyone can do at home. After 13hrs fast, my BG peaks at ~145mg/dl for a potato, after 16hrs fasting it can go to 195(!) after eating potato. Context: my usual post-prandial BG (for a mixed meal with carbs et al and not fasted) rarely tops 120-130mg/dl.
FrankG, thanks for the link, I'd been looking for it.
Unfortunately, while physicists revere that time period, too many lab-coated colleagues in the health fields disregard pre-war studies as quaint. I mean, what did those old scientists know, they studied 'normal men', not specially bred rats!
@ js290,
My meaning being that, if, granting the terms of the "evidence based" model we must weigh benefits and adverse effects, as the authors seemed to clumsily imply, then temporarily "failing" the OGTT has to be the most minimal of adverse effects, as it relates to an artificial situation which is - by definition - outside the conditions of the ketogenic intervention itself.
@George Henderson: Thank you for clarifying. Obviously, it's hard to tell from just the abstract, but it may be good to know if insulin was measured as part of the GTT. I'm sure Ron Rosedale would remind us that measuring glucose response without also measuring insulin response won't tell the whole story of insulin resistance. The abstract mentions ITT, which doesn't seem to be the same thing.
For anyone interested in full text of the paper, you can get it here:
http://ge.tt/5RRy7Jr/v/0
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