Sunday, March 18, 2018

Eating lots of meat and nothing much else


Wooo has posted a couple of times about Dr Shawn Baker who eats an all meat, very high protein diet, maybe over 400g/d protein intake. His HbA1c is reported as 6.3%. Personally I have absolutely no interest in this style of eating but the underlying mechanism is obviously interesting.

How about this for a hypothetical marked protein ingestion scenario:

A person eats a lot of meat. In response to the insulinogenic amino acids present they secrete insulin. This will be amino acid specific, I’ve not looked in to how amino acids trigger insulin secretion in detail but it will NOT be through pancreatic glucokinase and subsequent glucose metabolism, as is the case for glucose triggered insulin secretion. So they secrete post prandial insulin but not using glucokinase. The insulin will be exactly in balance with the glucagon for that specific protein meal.

The expression of the gene for generating pancreatic glucokinase is controlled by the carbohydrate content of the diet. Glucose means glucokinase is required. All amino acid diet, no glucose, down-regulate glucokinase.

So, as glucose is subsequently and gradually produced from gluconeogenic amino acids and then released from the liver over several hours (in the presence of only basal insulin), there is only a mild glucose derived stimulus to trigger insulin secretion, and this slow release of glucose by the liver also provides only a minimal drive to express the gene for pancreatic glucokinase. Also hepatic glucose output shouldn’t trigger any of the gut derived insulin secretion potentiating hormones (GLP-1 and the like).

So pancreatic glucokinase is mothballed. Modest glucose release from protein metabolism won’t trigger insulin secretion without the glucose sensor. End result is low insulin with moderately elevated glucose, especially during the time protein is being processed. Which I'd guess is pretty well all of the time on greater than 300g/d. How high should glucose go? High enough to allow a slow trickle to be taken up by constitutive transporters and so deal with hepatic glucose output in this way, without insulin facilitated augmentation. Facilitated by exercise if you like that sort of thing.

How toxic is glucose in the absence of hyperinsulinaemia, given that HbA1c over 6%? Dr Baker will let us know over the next 15 years!



Of course exactly the same happens on LCHF eating, just fat does not provoke chronic glucose release from its metabolism outside of a little glycerol derived gluconeogenesis… It probably happens too in some of the weird sucrose based weight loss diets where the mice (it's mostly mice but we all know that you can do "carbosis" in humans too) are hypoinsulinaemic (otherwise they would be fat!) but glucose intolerant. A diet based on a non-insulinogenic sugar (fructose) and its palmitate derivative will mothball pancreatic glucokinase too.

Peter

56 comments:

Unknown said...

good chance to call him a 'hypercarnivore' eh?

raphi said...

someone get that man a CGM!

i'm damn curious

Peter said...

Unknown, more of an explorer. I wonder if mTOR and IGF-1 will be kind to him?

raphi, I have a minor plan. I don't use glucokinase much. Might buy some chicken fillets.

Peter

Rattus said...

Rosedale seems to place an even higher priority on protein restriction than on CHO restriction, though he advocates for both to ketogenic levels. I think he puts a lot of emphasis on protein bc of mTOR.

Ned Kock said...

The elevated A1C may be benign Peter, reflecting a higher-than-average blood glucose level but without spikes (e.g., above 200 mg/dl). The glucose produced via gluconeogenesis, combined with that released by the liver reserves in response to glucagon, ends up not being properly “processed” because the liver is busy dealing with all the protein (a bit like its response to ethanol + glucose). His intake seems like an unnatural amount of protein though, with a possible long-term problem being gout. I don’t see insulin resistance necessarily being a problem for him, but I guess we’ll have to see.

George Henderson said...

How harmful is glucose at these A1c levels?

Not very, if the epidemiology of glucokinase mutations is any guide. Lower rates of micro and macrovascular complications than the "normal" BG population; fairly high retinopathy (though less severe than in T2D) but this would mainly be due to the post-prandial glucose spikes which Shawn is avoiding.

https://hopefulgeranium.blogspot.co.nz/2016/08/glucokinase-mutations-diabetic.html

raphi said...

@George

I remember that blog post of yours and am a bit disappointed in myself for not thinking of it as a possible explanation.

Peter said...

Yes, the comparator I had in my head was Essential Fructosuria. Huge levels if plasma fructose but no possibility of metabolism. Always made a mockery of the "reactivity" of fructose cf glucose. Never could find out what it did to HbA1c. Also made me think that glucose phosphate might be more of a reactor with Hb than glucose per se. If unphosphorylated fructose reacted with proteins the HbA1c rise would be marked in Essential Fructosuria and I'd expect it to be a differential for high HbA1c...

Peter

jesrad said...

Too bad he did not post any number for liver function, he only mentioned they are "out of whack"... Even though the iron / ferritine is low, his liver could be on fire as far as we know.

I've seen one person with high fasting glucose on a LC diet before - and he was on statins. The day he stopped taking statins, the HbA1c and fasting glucose started normalizing. Cannot quite wrap my mind around this yet...

Another thing with high-ish chronic glucose, is that it seems to ramp up schizophrenia. I have mild schizophrenia and I know from testing (back in my pre-diabetic days) that I start getting interesting, ah, visions when my glucose climbs upwards of 110-120. At 140+ I suspect I would have God on speed-dial in my mindphone, LOL.

ctviggen said...

I've been following Shawn for a while. There is an entire subculture of people eating nothing but meat. Because of them, I've been looking into this and also eating higher protein for low carb and less fat. I bought a CGM specifically to see if I could find a delayed blood sugar spike due to eating too much protein. I could not. I ate meals with >120 grams of protein, and could not find a delayed blood sugar rise. In fact, if I ate "normally", such as eating a pound of ground beef or a steak, my blood sugar was so flat, I could show it to you and you could not point out when I ate. If I ate a lot of seafood with (some) carbs in it, I would get quick "spike" of maybe 10 or so (US units), then it would go down. No delayed blood sugar increase I could find.

I am eating close to but not 100% meat, however. I also only workout twice per week (weight lifting to failure + some HIIT, only 35-40 minutes total). I'm also still overweight, though down over 50 pounds. My HbA1c was 5.0, everything else via blood work is (mainly) fine, though my last insulin was a tiny bit high (10). Due to higher protein? Unfortunately, I don't have an insulin monitor, so I can only get this done when I get an actual blood test taken.

As for eating this way, I think it might have benefits. Or at least I haven't been able to find detriments as of yet. I've already been keto or nearly so for 4+ years, so maybe that affects things.

ctviggen said...

By the way, one of the issues I've found with the CGM I used (Freestyle Libre) is they have poor data analysis and aren't meant for people eating low carb. For instance, this is what I wrote in my "diary":

"Fasted from Wednesday, November 29th after dinner until Friday, December 1. Body by Science workout at about 6am. Ate at 9:15am-9:55am. 1 can pink salmon (180 cals,3g fat, 36g protein), shrimp (not sure how much), 1 package mussels, 1 can anchovies w/oil, olive oil, vinegar, 2 chicken thighs."

The accompanying graph shows 5.3 (European units) at about 8am, after getting to work, 5.4 at about 10am, after eating, and then 5.3 at 11:15, (4.5 at 1:30pm/1330; gradually decreasing until 4.1 at bed time and below 4 overnight).

When you download data, the Freestyle Libre puts a "dot" and the corresponding blood sugar level on a graph. In between downloading data, the data is shown but it does not show values for highs or lows. So, I don't know the highs or lows unless I happen to download data at that time.

The scale on the graph goes from zero to 21. On that scale, a 10 point US unit (about 0.5 European unit) rise is small and difficult to see.

Peter said...

ctviggen, interesting. If my surmise is incorrect that sort of implies he might actually have a beta cell deficiency... Not so good. When I get the chance to I'm thinking of a 300g protein load at breakfast time with nothing else then track through the day. Work gets in the way so it'll be a few days yet before I get chance.

Peter

Shaza said...

I did Shawn's 90 day meat trial, it was easy as I had been Low carb for years. All my blood panel was excellent, including Mg and Folate. I remained on this way of eating as I felt so good. BUT I did have a similar observation, I have a blood glucose monitor, every day I checked it was 4.3 - 4.9 , mainly 4.6. YET my Hba1c last week was 5.3. Now I know that is fine but I DID expect to be in the 4 range. I have no other test to compare that too. My LFT was perfect as was everything else. LDL went up but subractions fine, hdl was 2.3! Trigs.7

The difference between Shawn in I is that I eat a huge variety of meats and I can not eat more than 120g of protein in a day ( I average 80ish) , I cook in butter etc! I also eat tons of seafood, shellfish and offal once a week. SO I shake my meats up, love pork! I donate blood 3 times a year so my ferritin is very low and I am not sure that is natural or confounded. I have done so since 1997, so not sure ... Lp(a) was 12, I forgot to mention. Nothing at all is out of whack. Shawn actually suggested I get Fructosamine done a few days ago when I remarked I thought A1c would be in upper 4 range. SO, he is on to fructosamine test. I will post my fructosamine as soon as I get results. All my labs pre and post trial were posted on twitter. My last fasting glucose was 4.6 but I did not have insulin done as my Kraft test last year was excellent. HbA1c is Australia is only allowed once a year if not diabetic. I will probably start adding some plant foods back in as winter comes..... I feel wonderful I must say . I do a lot of exercise. Ketones are up and down, but never high at all. I actually don't test them anymore much..

Shaza said...

** I forgot to add, that using Dave Feldman's Remnant Cholesterol tool am super low as well, 4 whilst Shawn was 2 ... super low! also, Remnant Chol to HDL: 0.04 >>> Lowest Risk Quintile, I am Pattern A for Particles. Everything from the lab is honestly great.

ALl chemistry panel was perfect too....

Peter said...

Hi Shaza, 80ish sounds very reasonable for protein intake from my perspective, maybe just a little high. I do the same. I'd just point out that everyone talks lipid numbers. Why? Do people believe lipids cause CVD? Or are they looking at lipids as a marker for hyperinsulinaemia? Why not measure the substance which is driving the intimal thickening? Nothing specific to yourself, just people seem hung up on lipids and it puzzles me as to why. The longest living mice in the world have appalling lipids but very, very low insulin. The equivalent humans also have appalling lipids but very low CVD rates. To paraphrase someone (Ivor?) "It's the insulin, stupid!"...

The dwarf humans https://academic.oup.com/jcem/article/91/6/2093/2843401

Peter

Shaza said...

Oh Peter, I could not agree more! It is just that people are so stuck on Lipids and that is their first line of questioning! So I just put it out there.

Like I said my Kraft test very good! Could not be much better! I will have that every 2 years ie 2 hour OGTT and Insulin over 2 hours, for those who do not know Kraft assay.

No Intimal thickening BUT CAC score of 10 a few years back, this is what started my journey off SAD diet.

I will repeat CAC in a year. I totally agree INSULIN is the key. That is why with my all meat diet I ate lots of fatty meats , thus making it hard to squeeze in more protein! That is where Shawn and I diverge I think. Protein over 80 starts to make me feel nauseous.

On a mediterranean diet my natural feeding seemed to be 60g Protein and I felt very good at that. I weigh 60 kilos, 173cm tall and waist is 27. My2 hour insulin on Kraft assay was 29. Peak 2 hour insulin on Australian number is looking for under 60, I was well under at 29. 2 hour glucose was 6.1 with Aussie lab looking for under 7.8 . So that was good too. I am in 50's. ( the 2 hour Insulin series was after drinking 75g glucose, YUCK) So that is my big reveal. I am paranoid about raised insulin. My husband is tpe1 diabetic, a terrifying disease to watch and SAD diet, as he was for most of his 'diabetes' career.

On the trial a typical day included: Eggs, Ribeye and Lobster tails. Or eggs , salmon and Pork . Every day 2 eggs, some seafood and some red or white meat. I cooked in Butter, ghee or olive oil. I also ate some cheese if needing a snack, just no plant based food.

The only lab I think I missed out on was Omega3 Index . I did track on Cronometer and posted many times on Twitter and I managed to keep the ratio pretty good! Eating should not be such hard work!

Shaza said...

RE: Cholesterol. It is amazing how stuck on stupid we are as a population about that! We are well enculturated. Even though I know TC is useless and that women with the highest Cholesterol live the longest, I am also guilty of looking at those number first! Pop culture is a powerful thing!

HS-CRP On a very rigours non plant, meat diet one of the best thing I noticed was no aches and pains! Joints that were getting a bit inflamed I guess calmed down. That was noted a lot in people on the trial. Pre Carnivore my HS CRP was 1.4, by January it had plummeted to 0.6 That was a surprise! I note that Shawn also has v low CRP. I was LCHF/keto before trial.

Troponin was 2 and 2 after 4 hours! ( that was a curiosity test) so super low...

I guess that about covers it, the CAC will be the real tell-tale next year. I will post score.

Shaza said...

Kraft Test is really well documented in Ivor Cummins new book, Eat Rich, Live Long. He is the guy that pushed me in to the CT Scanner for CAC score, I am glad he did! I have zero'd in on Insulin ever since!

Shaza said...

Correction: When I said no intimal thickening, I mean Carotid Intima

Amy Berger said...


jesrad: regarding statins interfering with glucoregulation: it's becoming increasingly recognized that statins confer increased risk for T2 diabetes. There may be multiple mechanisms involved, but one is that statins inhibit/reduce protein prenylation, and this step appears to be required for glucose-stimulated insulin secretion from pancreatic beta-cells. It doesn't surprise me that glucose levels started to normalize as soon as your friend quit the statin. I blogged about this awhile back. You can find relevant links regarding this mechanism in the post: http://www.tuitnutrition.com/2015/04/statins-and-diabetes.html

(Warning: I am not as succinct as Peter. I am pathologically wordy. My apologies for the long post, but it might be interesting for you if you want to dig into that mechanism.)

Eric said...

Wow, what a flurry of comments, seems more tangible a topic than the mini-series on adipocytes.

Wonder why noone has mentioned this pioneer:
https://en.wikipedia.org/wiki/Vilhjalmur_Stefansson

Apparently, he did not thrive on prime cuts but only when offal and animal fat were added into the mix.

Eric said...

Peter, have you posted on Essential Fructosuria and reactivity of unphosphorated fructose before? I thought that was cut and dried, but apparently not.



Shaza, CAC has a radiation dose of 0.7 to 2.0 mSv, with the EBCT method being at the low end, i.e. you will be receiving your yearly natural exposure or 10 return flights SYD-LAX within a few seconds.

While I am ready to tosh the LNT model and I do believe radiation hormesis exists (just think of the high rise in Taiwan that had radioactive structural steel - have there been new follow-ups?), I am weary of
- flash exposures
- anything that gests ingested.

While the chest is not a particularly cancer prone area, the effect of radiation on CVD is documented. Personally, I wouldn't not get a CAC scan just to satisfy my curiosity.

Jay said...

@Eric, @Shaza Chest is a cancer prone area in a woman! and I believe Shaza is a woman (picture/ name, Aussie short for Sharon amiright?)
Currently resisting pressure from my dr to have some kind of investigation on those lines because I have 'high cholesterol' (eat LCHF and have been for about 10-12 years).

Peter said...

Eric: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5347275/

Enjoy study two on plutonium inhalation... Study one is more like the Taiwan steel episode

Peter

Peter said...

Nope, never got to write about essential fructosuria. It was always on the to-do list. I'd not realised other folks had written. Is it Good or Bad?

Ta

Peter

Eric said...

Jay, apparently mammary tissue is not that sensitive to gamma and x-ray. The biological dose, as measured in mSv, takes into account the susceptibility of the tissue in question. Quoted CAC doses are indeed about 20% higher for women, but not more.

Peter,

I am not aware of any piece about essential fructosuria except that wikipedia says there are no adverse health effects. My comment was that I was previously under the imperession.

The paper was very interesting. I am a physicist by training, but not nuclear physics. I had to refresh and read up when one of our suppliers was affected by the 2011 earth quake and I had to travel there a few months after the Fukushima disaster. Their problems were related the earthquake and inappropriate resumption of processes, but they were in a city that maintained 200 µS/h at that time.

Back to the paper, two of the authors are with companies (medical equipment or other?) and one is with the university of Düsseldorf, a state that is home to nuclear energy giants that were very upset about the Merkel governments decision to phase out nuclear energy post Fukushima.

1. Introduction is pure polemics and mostly self-referential: "low-level radiation scare", "Radiation exposure has never been demonstrated to cause heriditary effects in human populations" (are humans different from animals, finally?), "health consequences of the precautionary evacuations ... in Japan".

However, the signalling stuff should be right up your alley...

(continued)

Eric said...

2. Gamma study:
The raw data show a decrease in lifespan from the smallest dose of 0.3 cGy/d (which for Gamma and full body exposure is the same as 0.3 cSv/d or 3 mSv/d, so the smallest dose the dogs were getting was more than a full year's worth of background radiation. Figure 2 is neat in that they resoundingly trash the LNT model and offer a threshold (i.e. contradiction of linear NO threshold) or hormetic model. The hormetic model makes sense and places the optimum dose at about 50 to 80 mGy/y, with the short lived dogs profiting the most with about 30% extension of lifetime. However, can we safely assume that most short lived dogs will be the same at all doses???
Then they make a big deal about those short lived dogs also being more resistant to high doses. When you look at the graph, there is a small area between 700 and 1200 mGy/y where the short lived dogs seem to thrive (again assuming it is the same dogs), and it is essentially based on one lone data point. There is a much larger area between 2000 and 30 000 mGy/y where the long lived dogs to better.

Takeaway? Should we all get some cobalt doped steel installed like those (un?)fortunate Taiwanese did? Some observational facts:
- the Japanese are long lived, and in spite of all their nuclear power plants and love for seafood they have a very low background radiation.
- there are aras in Iran and Greece where the natural background dose is on the order of 20 mSv - without any proof of extended lifetimes!

3. Plutonium inhalation

What did the original researchers do with the deceased dogs? Bury them in the Mohave desert?

Their analysis yields very similar results to the gamma study. There does not seem to be a high dose area where the long lived dogs do better than the short lived. All in all, I find this very surprising, as there are studies from KFA Jülich (a traditionally nuclear friendly lab, today known as KIT) that show that even minute doses of plutonium invariably lead to bone cancer in dogs after 10 years, possibly due to local accumulation. The authors do not mention these but note that the effect of the inhaled plutonium is purely local to the lungs but seems to have an overall effect on lifetime suggesting powerful signalling.

4. Recommendations

They do stop short of suggesting preventive irradiation or inhalation (I have seen others suggest these!), but they suggest to raise the protection limit to 300 mGy/year and increasing the residential radon limit.

Hmm, I suggest they find new jobs with the cleanup crews in Japan. On top of gamma radiation, there is plenty of cesium and iodine to be had. Let's wait for the hormetic effects of concentrating them in their bones and thyroids....

Eric said...

While we have allowed the comments to drift, here's something I posted at Malcolm Kendrick's that has not drawn any replies. What are your thoughts on antibiotics vs. mitochondria?

Eric


----------------------------
original post:
Don’t antibiotics also damage mitochondria throughout the body and hence cause (lasting?) damage and accelerated aging? It is also well known that they decimate gut bacteria and I have always wondered why folks aren’t given new seed bacteria after a course of oral antibiotics. What about the iodine protocol, wouldn’t one expect that to also have these effects?

On the other hand, the odd course of antibotics has been known to help the CVD situation by clearing out chronic nests of infection and hence lowering overall inflammation.

There was also some hype about old broad spectrum antibiotics killing cancer cells a few years back but it seems the initial promising results did not translate into that much of a success:
https://www.ncbi.nlm.nih.gov/pubmedhealth/behindtheheadlines/news/2017-06-12-antibiotics-and-vitamin-c-could-kill-cancer-cells/

Peter said...

Eric, as a clinician I am very aware that many of the drugs we use are mitochondrial toxins. Classically enrofloxacin, which inhibits DNA gyrase, kills bacteria and in unlucky cats will kill enough mitochondria to produce sudden onset permanent blindness. Many other abs are RNA translation inhibitors so might well have off target effects on mitochondria. The penicillins and cephalosporins are immune to this problem as they act primarily on the bacterial specific cell walls. Unfortunately because they are bactericidal they can provoke a massive release of endotoxin if used under major sepsis conditions. Best avoid major sepsis if at all practical. When that fails choose your mitochondrial toxin with care. Just that sometimes you have no choice...

Peter

Shaza said...

Eric, thank you so much for your comment re: Radiation. You are correct.

Shaza said...

@jay, thanks for comment. I am in the camp of a couple of CAC scores in my lifetime. I am also in the camp of Chol is nonsense and that heart disease is driven by other factors. Shaza is short for Shannon! Yes from Sydney.

Shaza said...

@Eric, you may enjoy this info re Long haul and Polar flights and radiation: https://www.arpansa.gov.au/understanding-radiation/radiation-sources/more-radiation-sources/flying-and-health https://www.nasa.gov/centers/langley/science/polar-radiation.html

Pity us pilots who get Hong Kong to New York routes! I am not flying anymore but son does that exact route based out of HK, yes radiation is a worry at all levels. Management is sending ULP's into those routes to save on fuel costs even as pilots are considered radiation workers.

Jay Rickert said...

Hey Peter,

So I did familiarize myself with some of Rosedale's insights regarding protein restriction, which, as far as I understand, is recommended for middle aged adults (.6 g per kg), and that younger adults ought maintain around a g per kg.

Unrelated, my diet currently has 18 egg yolks in it. I remember you mentioning eating 6 egg yolks in the morning, so I must ask - do you consider larger amounts of eggs, like 18, excessive as far as cholesterol intake?

George Henderson said...

I increasingly see serum lipids as signposts that point back to carbohydrate being eaten or not, and forwards to where the fat from the diet or adipose is going. Higher cholesterol? Congratulations, if HDL is part of that you've chosen fat. Lower TG/HDL? Now you're actually burning that fat. Higher LDL in that context? Congratulations, you're burning a lot of it.
Higher LDL with higher TG/HDL? Sorry, whatever you're eating, and it looks like it's mostly been carbs, that fat is now accumulating, you might want to look at burning some.
Cholesterol the molecule, as far as any risk of that accumulating goes, will basically track with the fat.

Eric said...

George, is that your personal impression or also found by others? Some of it rhymes with cholesterol code, Ian Cummins and Chris Masterjohn, but not all of it.

It certainly reflects my readings from the last two work checkups, even if I am lowish carb at best (50 - 120 g), but then I have been doing 14:10 or 16:8 intermittent fasting for the past three years or so.

cavenewt said...

Sounds like the lipophobes are tying themselves into knots again.

"In conclusion, a 15% increase in energy from dietary protein at constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased CNS leptin sensitivity and results in clinically significant weight loss. This salutary effect of protein may help to explain the paradoxical weight loss observed in subjects placed on low-carbohydrate diets, because an increase in protein intake accompanies the high fat content of such diets (5–7). Our results suggest that less emphasis should be placed on carbohydrate restriction without regard for concomitant increases in dietary fat. Replacing a portion of dietary fat with protein may result in weight loss comparable with that reported with low-carbohydrate diets while minimizing the adverse long-term effects of increased dietary fat. However, further study of the effects of dietary protein intake on renal function and calcium balance will be required before high-protein diets can be widely recommended for weight loss."

https://academic.oup.com/ajcn/article/82/1/41/4863422

Peter said...

Dinosaurs...

Jay said...

@Eric, @George - it chimes in with what I've found too.
When I went more low-moderate carb (after listening to doctor friend)I got those changes exactly as he described. Last time I got the pep talk to really change my diet and stop this silly nonsense of lunching on creme fraiche and dark chocolate. I tried I really tried for a week with green salads and oily fish but after worrying about eating way too much protein I'm back on the cream and chocolate.

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Eric said...

Jay, protein would be the least of my worries if I crammed oily fish:
http://perfecthealthdiet.com/2011/04/omega-3-fats-angiogenesis-and-cancer-part-i/

I have a green smoothie made from about 50 g of organically grown dark green leaves and the odd fruit (e.g. half an orange). I suppose at least this will give me fiber, magnesium and vitamins C and K but not sure if there is any other benefit (did not really feel much different when the machine was away for repair). Peter does not seeem to be too fond of fiber, though.

Peter said...

I tried protein loading today and managed ~250g between 7.30 and 9.00 today. BG 6.30am 4.7, 8.00am (after about 150g) 4.9, 9.00am 5.2, 2pm 5.5, 3.30pm 4.7.

Nothing spectacular. My normal BG as I get home from work would be about 3.5, maybe 4.0 so I don't know that the protein load really gave a delayed glucose elevation. It looks like it might have done but definitely not in to pathological levels. It wasn't something I enjoyed so I'll stick with my diet based around fat I think...

Peter

Bob said...

Peter, I'm curious what your choice of protein loading was.

Pretty sure it wasn't skim milk.

Peter said...

Chicken fillets and salami (pork)...

Keith Runyan said...

Peter, I am a retired clinical nephrologist with type 1 diabetes and thus have a special interest in all things diabetes including HbA1c. The HbA1c test was "discovered" in the 1960s more than 20 years before home blood glucose monitoring (HBGM). After HBGM was widely available, only a minority of patients would use them often enough to understand a patient's level of glycemic control. Thus, clinicians and researchers in the field had to rely on HbA1c. However if you drill down to the details, you will find that the test does not reliably reflect the average blood glucose (BG) in a significant proportion of the population. I did a blog post on this topic https://ketogenicdiabeticathlete.wordpress.com/?s=hba1c so I encourage anyone interested to look at the accuracy (or lack thereof) the test and the many other factors besides glycemia that affect the result. You will find a similar problem with the Fructosamine test as well. Now that there are several HBGMs that are quite accurate i.e. within 15% of the laboratory value in excess of 95% of the time, the best way to understand one's glycemia is measure it with a HBGM say 5-6 times a day on several different days. The FreeStyle Lite HBGM is one such device. It is the meter I use.
In the case of Dr. Baker, the HbA1c result of 6.3% could have been a lab error which in my experience happened more than nonclinicians could possibly imagine or Dr. Baker could be a "high-glycator" as explained in the blog post above.
Bottomline HbA1c is a convenient surrogate for average blood glucose, but by no means is it not fraught with errors.

George Henderson said...

Eric, we're working on a "multiple lines of evidence" paper including drug trials to support the Cholesterol Code idea.
Basically your body is only interested in regulating two lipids by lipoproteins - it wants there to be the right amount of TGs to supply any shortfall in NEFAs, and it wants to regulate the proportion of cholesterol in its cells. It isn't interested in regulating the lipoprotein particles per se, these can be bounced around as suits regulation of the other 2 things.
Genetic disorders do produce exceptions, e.g. various problems when LDL receptors are blocked (but blocking in response to SFA is serving both TG and cholesterol regulatory purposes, it's adaptive), or easier cholesterol regulation if ApoA1 Milano gene is lowering HDL or other genes lowering LDL.
Overproduction of cholesterol in situ due to excess insulin or leptin driving HMGR - which seems to me to be the main thing tying cholesterol to heart disease - won't always increase LDL (e.g. if it's in an inflammatory context it won't), reducing it won't always lower LDL (e.g. on keto it might not because LDL is also pproduct of fat use), but reducing it with a statin (inhibiting HMGR) will lower LDL.
Hence the way that statins seem to support the lipid hypothesis, when they are really much, much more supportive of the insulin hypothesis of heart disease.

Peter said...

Hi Jim,

Yes, I would agree that both HbA1c and fructosamine are far from problem free, though I hadn’t really thought that the lab tech might have picked up the wrong vial to measure the HbA1c from. I’d also agree that factors which drop A1c, especially high RBC turnover from GI bleeding, will also drop fructosamine as albumin is always lost with RBCs in haemorrhage. I’d be interested to know if the factors which artificially raise Aic (such as slow RBC turnover) would also raise fructosamine as fructosamione would be my go-to to check on an artificially high Aic, assuming no lab error……

Peter

Peter said...

George, I'll look fwd to the paper!

cavenewt said...

Never mind me...just subscribing...

Display Name said...

Keith,

His fasting glucose was 127 which is consistent with an A1C of 6.3 when you consider postprandial spikes so both the A1C and fasting glucose would have to be a lab error. Also, he did a home glucose challenge and his results were elevated (see below). The question I have is why not get an immediate retest plus do a glucose/insulin challenge? He now seems to be implying that he lack of CKD in cats with hyperglycemia somehow shows that you can have high glucose and no damage in people even though cats have other adverse effects and they do develop diabetes as Peter will verify.

Home OGTT Results:

172 Hour 1
154 Hour 2
119 Hour 3

Average 148

Peter said...

Cats certainly get diabetes and they certainly get CKD, though the two are not considered related. Cats are also essentially immune to cataract unless they become hyperglycaemic while very young (very rare). Unlike dogs and people they lack activity of aldose reductase in adulthood so never convert the glucose to sorbitol to generate the cataract. I've see exceptions. I've long wondered if the CKD of cats is diabetes in situ but you have to wonder why the hyperglycaemic cats are not more severely affected. I'd be sort of loathe to bet my kidneys on being feline in nature...

Peter

George Henderson said...

@ Display name,

"His fasting glucose was 127 which is consistent with an A1C of 6.3 when you consider postprandial spikes so both the A1C and fasting glucose would have to be a lab error"

But why would there be post-prandial glucose spikes on this diet, and why should FGB and HbA1c always be rigidly correlated in any case given that variation in RBC turnover and no doubt other factors will affect HbA1c?

Check the link in my original comment for risks of complications in GCK deficiency in humans. There is a high risk of macrovascular disease in CKD patients, yet a low rate in GCK deficiency, so the risk of CKD from low GCK activity isn't jumping out from that data.

https://hopefulgeranium.blogspot.co.nz/2016/08/glucokinase-mutations-diabetic.html

Glen Nagy said...

Peter, Baker does a lot of high intensity exercise, would this affect his numbers? He hold a few over 40 records on the Concept 2 rowing machine, mostly sprints of around a minute or two that are very glycolytic. He is 6'4", 240 lbs and lifts heavy weights. He does a lot of things most people would say you would need carbs to fuel, and he does it on a meat only diet.

Display Name said...

George,

I'm not sure has has postprandial spikes. He could be spiking during exercise without knowing and that is why I recommend a CGM.

When in doubt about results they should be retested and a glucometer or CGM should be used to verify the findings. High FBG alone is associated with increased morbidity & mortality so the fact that his FBG is so high is a definite concern (irregardless of A1C) unless it is a lab error.

In his latest article Shawn speculates that he could have MODY:

"These things coupled with my current clinical history certainly point away from on going diabetic pathology to include some of the hybrid types such as MODY (maturity onset diabetes of youth)". 

There are problems with studies of rare mutations so I doubt these results can be applied to either Shawn or the general population.

George Henderson said...

GCK mutations are the most common form of MODY

https://www.diapedia.org/other-types-of-diabetes-mellitus/41040851237/mody-due-to-glucokinase-mutations

So if Shawn has MODY this is likely generalizable; for the general population, low PP and fasting insulin is protective, and probably more protective than low HbA1c within the non-diabetic range. For T1D the story is different because low HbAic means variability, with all its risks, has been minimized, but insulin action is as we know very different when exogenous.

Display Name said...

It sounds like he had repeat tests done but he has only said that he thinks the original A1C of 6.3 is "close" to being accurate. He did reveal his repeat testosterone level, however.

A test for MODY could be expensive. Even if he does have MODY he is still subject to complications. He needs the type of exam Bernstein does to rule out complications (e.g., R-R interval, slit lamp exam and Oscillometry). A CAC is insufficient. Even if his exam is completely normal I would still be concerned about future complications because there is no guarantee that he will not experience them.

MODY seems unlikely given his age and his apparent lack of family history. He is not using insulin but it sounds like he might need it. His extreme diet and exercise are unusual factors that make sense to rule out even if he does have MODY.

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