Tuesday, August 05, 2008

AGE RAGE and ALE: low fat!

Just to finish on glycation before moving on to signaling molecules, I'd like to add to Dave Dixon's comments about meal timing and chylomicron peaks after the segragation post. Let's just have a quick think about a serious low fat diet, using real food, say as eaten on Kitava or by the non vegetarian Bantu. These people are up at 70% of calories from carbohydrate. They tend to have the typical elevated fasting triglycerides of carbohydrate based diets, but not the heart disease associated with similarly elevated triglycerides in Western populations. Fasting triglycerides are VLDL particles released from the liver to move carbohydrate derived lipid to adipose tissue or muscle. They may have some PUFA from chylomicrons which have been taken up by the liver. They're certainly not chylomicrons in healthy people.

What's happening on the glycation front here? Post prandially there will be a marked glycation hot spot in the portal vein. This is unavoidable on a high carbohydrate diet. Insulin will rise and insulin promptly inhibits the release of VLDL particles from the liver. Same principle as we went through in this post, using all night glucose bingeing to "treat" hypertiglyceridaemia.

So, post prandially there are minimal chylomicrons due to the low fat content of the diet and VLDL secretion is inhibited. This is a neat way of separating glycation after a carb load from contact with any apoB containing lipids. As glucose uptake tails off, insulin falls and the processed glucose beyond acute needs can be shipped out as VLDLs, primarily as saturated fat which won't generate lipid peroxides anyway.

So there is some scope for genuine low fat diets to avoid glycation problems. You can have your fasting VLDLs up at 3.0mmol/l, just so long as they are full of palmitic acid and don't have sugar all over their apoB100 tags. You'll barely have a chylomicron anywhere to be seen at any stage, so who cares about that apoB48 tag?

It's the three times daily mix of sugar and soy oil (with fridge raid at 3am) which sets the scene for vascular catastrophe. The apoB counts might be the same in Kitava as in the USA, but the sugar coating and rancid fatty acid contents on and in those apoB tagged particles may be very different.



Dave said...

I would guess the Kitavans don't get much fructose in their diet either. Fructose apparently bypasses a regulatory step in liver carbohydrate metabolism, resulting in increased VLDL production. Nice discussion n this paper: http://www.nutritionandmetabolism.com/content/2/1/5

Dumping a large fructose load into circulation when lipoproteins are high is asking for even more trouble. Isn't fructose the "big daddy" of glycation damage?

Lisa said...

Please forgive my ignorance - I do not understand most of your analyses and I have not read every post from prior years. This is my favorite blog though!

Your soy oil and sugar mix sounds like the JK 'piggish' eating pattern while the Kitavan diet sounds like the JK 'Japanese' eating pattern which JK finds can work although is not 'optimal'.

So my concern is shooting and missing. If I shoot for optimal but end up piggish, I could end up very sick. Recent studies of low carb diets (which are really moderate carb) seem to indicate increasingly better parameters as you lower your carbs - like a continuum. So is there a continuum, or could I end up with a carb/fat mix that is much lower carb than the typical Western diet but still very unhealthy for me?

Jennifer said...

I'm so glad you're back! I'm enjoying my daily serving of brain food again! Although it's often more than my brain can digest in one sitting! And I work in biotech/biochem!

mtflight said...


Genial as always. Great work putting this together. So what does this mean in terms of cheesecake?

On one side of the coin, high fat lowers glycemic response when carbs are involved (vs a low fat equivalent). On the other side of the coin, we're talking about how fats can turn evil (add sucrose). Amazing.

Have you ever had a large low carb, high fat meal, then ruined it with something high carb? Suddenly one feels like he ate a ton of bricks. I wonder what is going on at that point.

Anyway, excellent blog--definitely my favorite. Keep it up!


Cristian said...


Evidence that the etiology of the syndrome containing type 2 diabetes mellitus results from abnormal magnesium metabolism.
Wells IC.

Biological Chemistry and Medicine, Creighton University School of Medicine, Omaha, NE 68124, USA. ibertwells@yahoo.com

Evidence is reviewed supporting the presence of an inherited structural defect in the plasma membranes of somatic cells of humans who have type 2 diabetes mellitus and sodium-sensitive essential hypertension. This magnesium-binding defect (MgBD) consists of a decreased content of tightly bound Mg2+ ion in the cell membrane and limits the amount of Mg2+ that enters the cell, some of which combines with ATP4-, produced by the cell, to form MgATP2-, the currency of metabolic energy. Consequently, in both prediabetes and overt diabetes, the intracellular concentration of the interdependent Mg2+ and MgATP2- ions is significantly less than normal. These 2 ions are required as cofactors and (or) substrates for some 300 enzyme systems in human metabolism, many of which are involved with insulin. Thus the decreased activities of particular ones of these enzyme systems due to the decreased intracellular [Mg2+] and its dependent [MgATP2-] are responsible for (i) insulin resistance and (ii) decreased insulin secretion and (or) production, the 2 pathophysiological processes required for the occurrence of type 2 diabetes mellitus. These 2 processes can account for all of the morbid symptoms associated with this disease. Thus, the decreased intracellular concentration of the interdependent Mg2+ and MgATP2- ions constitutes the etiology of genetic predisposition to type 2 diabetes mellitus and can be corrected by 2 identified peptide Mg2+-binding promoters that are derived from the carboxyl terminal of the tachykinin substance P and occur in normal blood plasma. Decreased intracellular [Mg2+] and [MgATP2-] can also result from a dietary deficiency of magnesium or from an abnormal accumulation of saturated fatty acids in cell membranes, which inhibits the entrance of Mg2+ into the cell; thus it is also the etiology not only of diabetes caused by magnesium deficiency, but also of the "lipotoxic" type 2 diabetes mellitus. Although these pathologies cannot be corrected by the Mg2+-binding promoters, they can be corrected, respectively, by dietary magnesium supplementation or by exercise plus dietary caloric and lipid restriction. Theoretically, the disease syndrome containing type 2 diabetes mellitus may involve approximately 30% of the population.

PMID: 18418443 [PubMed - indexed for MEDLINE]

ItsTheWooo said...

I wonder how much of atherosclerotic conditions are caused by lifestyle.

My line of reasoning is that the real risk is in having a metabolic state that is abnormally catabolic, damaging-inflammatory, with impaired anabolism.

Those who get heart disease are all people who are in a hypercatabolic, inflammatory, deficient-anabolism type state. Think of the list of people who really get these types of diseases.

Smokers (chronic low grade hypoxemia/hypercarbia, healing processes are impaired, tissues are damaged, skin and vessels break down)
Chronically stressed out people (cortisol, enough said)
Sleep deprived people (Sleep loss often goes hand in hand with chronic stress, however the sleep state offers a unique metabolic death-march from additional high cortisol, reduced growth factors, reduced thyroid hormone, all of which work together to cause damage to vessel wall).
Diabetics (deficient anabolism and abnormal catabolism, also fits the profile for "chronic stress" as above)
Men (more reactive to stress hormones in males as compared to those with female hormones)
Obese (see diabetics, as well as chronic stress/sleep deprivation, as obesity is often the result of sleep deprivation metabolic abnormalities, secondary to leptin signalling deficiencies - deficient leptin signalling in obesity contributes to sleep apnea, which contributes to sleep loss and abnormal stress response and diabetes and more obesity in a cycle)

I always thought the real issue here isn't so much what's going on with the cholesterol, but the damage to the body's blood vessels. The cholesterol is just a repair substance, and depending on what is going on inside depends on how that cholesterol acts. It's like blaming tourniquettes for a gang violence induced gunshot wound epidemic.... the solution isn't to get rid of supplies to control bleeding, that might actually do harm (and indeed the hypoinflammatory state associated with very low cholesterol levels increases risk of "accidental death" and hemorrhagic strokes, because trauma response and recovery is deficient under those conditions so associated - e.g. very low fat intake and very low calorie intakes).

I haven't done much research on it but it seems the real problem is the abnormal/excessive catabolism, abnormal/deficient anabolism, and the inflammation produced from it. Cholesterol just seems to imply what's going on, like a triage center implies where natural disasters might be occurring, you know?

Gyan said...

Discovered an interesting paper by B.Lands (Progress in Lipid Research, 47 (2008) 77-106).
He is able to correlate CHD mortality to %n-6 HUFA in tissue HUFA (HUFA is highly unsaturated fatty acid) across ethnic diversity (Greenlanders, Japanese, North Europeans, Americans).

He also has a graph showing that " Food energy inbalances which elevate blood cholesterol may be fatal only to the degree that n-6 exceeds n-3 in tissue HUFA.

Would love your comments.

Jonathan said...

Peter, please pardon my imposing, but is there any chance you could explain this more directly? I've always wondered if PUFA plus carbohydrate together cause damage that neither of them can effect individually, and it sounds like your post might explain a mechanism for this, but I just can't read between the lines well enough to figure out what you're implying.

mtflight said...


I've heard this analogy before. Is there evidence that cholesterol is high when there is a repair process going on?

Any input on this, Peter? I know you've mentioned your cholesterol is high (LDL--as is mine, but I think you said yours was higher than mine).

I know PUFAS indeed lower cholesterol, and since I try to eliminate them deliberately, this may indeed account for higher than average LDL (and therefore, total cholesterol).

Peter said...


Yes, response to injury (assorted) is how I view atherosclerosis. The whole adaptive physiological process is distorted by modern foods. I guess when the system is allowed to work correctly it works correctly! I'll get round to this when I've finished with the broken process (eventually)


Peter said...


The lowering effect of PUFA on VLDL and LDL is about 2 or 3 posts away. Gettin' there.

BTW do you realise much of this set of posts came from your query about lipid numbers... Not exactly a straight answer! But then I don't have straight answers....


Peter said...

Hi Lisa,

Yes, I see what you mean. Ultimately adding carbs to the OD give Piggish nutrition. Probably a lot more fun than Pasture eating but ultimately quite dangerous. JK talks about the woman for whom the OD wasn't working, but she was eating kilos of cherries per day on top of all that fat.....


Peter said...

Hi Christian,

I find Mg problems quite important. As far as I can see Mg is far more important for glycolysis than beta oxidation and both hyperinsulinaemia and hyperglycaemia cause Mg excretion in the urine. If you have a Mg handling problem LC can again side step this. But it also makes me think that the 30% of the population with Mg handling problems would have no problem if they were eating LC. ie carbs expose metabolic problems which just aren't there when humans limit carbs or eat tons of Mg...

The bit about lipid restriction sounds misguided, but then I would say that!


Peter said...

Few more replies when I get chance


Gyan said...

How does glycation relate with the risk of eating equal calories from fat and carbs (called I believe Forbidden Zone in Optimal Diet).
Does that risk still exist when one consumes minimal PUFA?

mtflight said...

Thank you Peter. I look forward to your posts. Such great insights that you have. They are usually eureka moments for me. Thanks for the answers :-)

Stan Bleszynski said...

Re: Cristian Stremiz quoted paper about magnesium

This is interesting but since Ca and Mg are required in carbohydrate metabolism it is logical that an impairment in their transport through genetics or deficiency (of Mg) in food can impair glucose metabolism.

The primary problem is probably excessive glucose supply while other issues related to Mg may be secondary.

Kwasniewski mentions also an interesting detail:

- pentose phosphate shunt which is the most atherogenic form of glucose metabolism (according to him) requires more Ca than Mg, whereas the more normal (hexose) pathway requires more Mg. Therefore in a situation of a chronic Mg deficiency the body will naturally favor pentose pathway. Pentose pathway is what dominates in diabetes. It also conserves the oxygen which is useful when blood flow is impaired, as happens in diabetes. Again, Dr. K tells about one method to test whether an individual has pentose pathway dominating in his tissues: - the lack of hypoxia symptoms in a leg when blood flow is temporarily suppressed.

The reason I mention all this in this context is because I was able to find the bit and pieces of what I described above, in the published papers but never in a comprehensive way, the way Dr. K interpreted it in his book. Have you found a good published review about pentose/hexose pathway in that context?

Stan (Heretic)

Peter said...

Hi Jonathan,

I'm not sure that anyone has ever lived on a high omega 6 PUFA based diet until 100 years ago. Moderate omega 6 diets probably began with the Egyptians. Fish based diets with relatively high omega 3 levels seem quite well tolerated, whether LC as the Eskimo, or high carb as the fishing Bantu/Kitavans. It's the eating every hour that eliminates segregation and omega 6s and fructose that desperately require segregation, especially if eaten in USA amounts.


I'll chase the paper you posted when I can, but re the worst ratio of fats to cabs, my guess is that glycoxidation would be less of a problem (stable lipids) but straight glycation (of all tissues) would be the problem. Insulin resistance from the fat plus hyperglycaemia from the carbs. JK looks at things in his own way, as Stan comments about the pentose shunt. The pentose shunt provides reducing power to generate LC fatty acids and ultimately cholesterol from sugar, freeing up oxygen under hypoxic tissue conditions. Locations such as the media of large arteries... It's another view of the development of atherosclerosis; the body doing the best it can under bad conditions. PUFA seem more involved in frank patching of the damage done and need to be oxidised to do the job effectively. ApoB lipoproteins glycoxidise for a reason...


Because Mg is an element I tend to look at input and output as controllers of tissue availability. What then controls your dietary needs (ignoring stupid practices like eating whole grains to bind Mg to the fiber/phytate which of course go down the loo) are your urinary losses. Hyperglycaemia and hyperinsulinaemia both cause magnesuria. I like to think of people eating to the Food Pyramid as urinating/pooping their bones down the loo. Obviously urinary calcium and and phosphate losses are affected similarly, so calcium phosphate and calcium oxalate urinary stones are strongly associated with metabolic syndrome. Hence JK's correct assertion that the OD treats all forms of urinary stones... I'll try and dig the papers out and put them up as a post so I can find them when I want them more easily.

Anyway, I think urinary losses markedly contribute to multiple problems including type 2 diabetes, which of course markedly increases urinary losses...

Re Pentose/hexose, not so far. Just any dribs and drabs say JK is correct.


Bryan - oz4caster said...

Sugar and polyunsaturated fat - definitely a recipe for bad health!

emil henry said...

What do people think of cultured butter? It's quite common in Norway. There is an unsalted version (makes very good ghee), and a (cheaper) salted version, with added vitamin D (from sheep suet, D3; 320 IU per 100 grams). It's really taste.


Peter said...

Butter, germs, D3... Do you ship to the UK?


emil henry said...

Did I mention they have a variety with sea salt?

They don't ship. It's made by the largest Norwegian dairy co-operative, TINE. It's our revenge on you guys for feeding your cows all that delicious grass (we feed them mostly pasture in summer; lots of hay, and ugh, soy/corn based "soy feed"). The Omega-3/-6 ratio is 1:3-4, but Norwegians eat fish 2-3 times a week, so we do well.

Of course, we have a organic variety. In Norway, organic cows must be fed largely on herbs, grass, and hay, and be on pasture as much as possible. They get no antibiotics and aren't selected for un-natural traits. It runs for about £7 per kilogram. In summer time, it would probably be Weston A. Price certified. The same dairy, which is independent from the co-operative, sells fermented, non-homogenized whole milk. TINE makes kefir with organic whole (homogenized) milk exclusively, using kefir grains instead of freeze-dried cultures.

In-season, we get really cheap mutton (used in our national dish, "fårikål," meaning "mutton in cabbage") for about £3 a kilogram (if not slightly less). Pasture goodness!

Raw milk isn't too hard to find. We're currently having a session on wheter we should sell raw milk in stores. I'm crossing my fingers, obviously!

Wild game isn't too hard to come by, if you live near a farmer (they tend to own the hunting rights).

My main problem is the lack of decent lard/suet outlets (I will ask a farmer next time he butchers something!) and butchers in this city. This region is known for its rather "nihilistic" apetite. If it's sugar, it's good!

Pros and cons to living everywhere, it seems. We pay £1.4 for a liter of petrol.

Gyan said...

In Optimal Diet theory, the diseases are caused by wrong carb:fat ratio. If the ratio is close to 1 then pentose cycle is activated and that causes diseases.
This is called being in Forbidden Zone.

Now where is PUFA and wrong omega-6/omega-3 ratio in this?

Is there any empirical evidence behind Optimal Diet theory and Forbidden Zone?.
IS there is a population of PUFA-avoiders that lie in Forbidden Zone?.

Peter said...


JK has no concern about PUFA ratios at all. He barely mentions omega 3s ever. His main comment re PUFA is that whatever PUFA you do get should come from food sources, nuts etc (lard too I guess), not refined oils. He also has no concerns about D3 or gluten, but I cannot make this tally with my own experience. The forbidden zone has undoubtedly been used by humans somewhere, at some time, before the development of industrial/agricultural based diets, presumably without problems. I think the need for the OD goes up in direct proportion to your personal degree of damage. No problem with eating this way if you are still healthy, but I feel the need to conform gets higher as your level of illness increases.

I don't feel the OD is the complete answer to all problems, just it gets a lot closer than most.

JK never gives you empirical evidence. That's why I grub around for it. It's quite possible he's just so far ahead of everyone else's thinking that I'm wasting my time thinking about relatively unimportant things like glycation and insulin. I'm here where I am and I have to view the world from my own viewpoint!


Stephan Guyenet said...


Kitavans eat plenty of fruit, according to Lindeberg's papers. All the fruit I've ever looked up contains a fair bit of fructose. Then again, I don't know whether their intake changes seasonally. Lindeberg may have gotten a seasonal snapshot.

Anonymous said...

"Isn't fructose the "big daddy" of glycation damage?" (Dave)

No, actually cooked fat and protein are the grand-daddy. They are 13-29 times worse than carbohydrate foods on average. Glycation is a misnomer when you realize 13-29x more damage is caused by cooked meats and fats. (I assume PUFAs are much worse than MUFAs and SFAs in this context, but the study doesn't say what types of fat were tested.) Fructose is not a problem if you balance it with more or less equal glucose, e.g. grapes. The problems come when you over-eat fructose, as in apple juic.


Anonymous said...

"Have you ever had a large low carb, high fat meal, then ruined it with something high carb? Suddenly one feels like he ate a ton of bricks."

I've never had that experience, but the main carbs I eat are "unheated" honey, grape juice, strained orange juice, white rice (unenriched), and sourdough bread or potatoes. I feel best on a no-fiber diet. Eating too much potatoes make me tired. I have given up the 85% chocolate and feel better than ever. Dark chocolate is too high in fiber, IMO. It's around 7.5% fiber by weight.

After eliminating 85% chocolate for two months, I tried adding it back. Immediately, I felt hunger increase and energy drop. I think it best to avoid even dark chocolate, due to a gross excess of fiber. Cocoa butter would be better, IMO. I'ver found a direct effect of fiber on my health and it's not beneficial. I've tried various experiments, and my results were paradoxical. I found that 100% juice strained of all fiber gave me stable energy and no hunger, but if I used juices with some pulp, there would be more nausea, energy crash, and hunger. I concluded that it was not the carbs that were the problem but rather the fiber. Even the most minute traces of fiber degrade your digestion and energy, IMO.

So I get foods that say 0g of fiber per serving and feel great.

Peter said...

Hi Bruce,

I think we'll have to differ. Diabetics glycate their proteins and lipids because their blood is full of sugar. A diabetic doesn't suddenly start eating chargrilled meat on diagnosis to crank their HbA1c from 4% to 13%.

From this paper particularly this table: People eating to the SAD have 40-50units of AGEs in their blood stream, unless they are diabetic. Early diabetics have about 70 units and renal failure diabetics 80 units. The last figure is particularly high as we excrete AGEs through our kidneys. Artificial high AGE diets were made in the study using fructose to glycate albumin in the absence of lipids.

You may consider that filling your portal vein with fructose is fine provided you mix it with an equal amount of glucose, as you propose, but for me, the fructose will just do what the glucose does, only 10 times faster.

You can take a saturophobic American, let them eat their PUFA and olive oil but normalise their blood glucose, Bernstein style, and the glycation of their Hb will plummet. Glucose glycates. Fructose beats it hands down. Normalising blood glucose normalises glycation of HbA1c. Probably the rest of the body's proteins too.

Certainly PUFA glycoxidise if they are in the right situation, but assuming fructose and glucose are innocent is not remotely how I see the world!



Anonymous said...

"All the fruit I've ever looked up contains a fair bit of fructose."

Cranberries are over 80% glucose. I think we also need to factor in the ratio of other sugars in the fruit. Some fruits have a lot of sorbitol, while other fruits (like grapes and pineapples and oranges) have little or none. Some fruits are have high ratios of fructose to glucose, like apples. Others hae more/less equal glucose and fructose, like grapes. Some fruits are high in sucrose and others have 1% or less (like grapes and blueberries). You can't lump it all together. Every fruit is unique and should be considered on its own with a controlled study, not flawed studies using refined sugars.

Anonymous said...

"Diabetics glycate their proteins and lipids because their blood is full of sugar."

9 times out of 10, their bodies are full of PUFAs, chemicals, and other junk too. Would the same be true if they ate a low-PUFA diet? Would raw omnivores ever get diabetes?

"A diabetic doesn't suddenly start eating chargrilled meat on diagnosis to crank their HbA1c from 4% to 13%."

Most of them are eating cooked meat however, and that is proven to be a lot worse for causing AGEs than raw meat. Unless you cook all your meat in water and cool it before eating. The fact is that some people have low blood sugar and high hbA1c and others have high blood sugar and low HbA1c. There is not a perfect correlation, despite what low-carb gurus maintain. Her's a study that I pointed out a while back, making this point clear. The idea that a high HbA1c is purely the result of eating carbs is nonsense. It's due to PUFAs, cooked meat, and lots of other things. As the other study I gave showed, cooked protein & fats are 13-29 times more likely to get glycated than carb foods.


Anonymous said...

"Artificial high AGE diets were made in the study using fructose to glycate albumin in the absence of lipids."

Those foods are cooked/processed. I would like evidence that raw and/or unprocessed food does the same - in vivo, not in vitro. Cooking protein in the absence of sugars/fats still generates AGEs. As I've said, I can not put any faith in studies using purified fructose. If you show me a study using unheated honey, i will listen. Otherwise, I have to go by what the study showed, and they did not show that natural foods have a bad effect. They showed that highly processed foods had a bad effect.

"You may consider that filling your portal vein with fructose is fine provided you mix it with an equal amount of glucose, as you propose, but for me, the fructose will just do what the glucose does, only 10 times faster."

Proteins and fats get glycated even faster, esp when cooked. So you are doing vastly more damage. The claim that fructose is worse than glucose is based on test tube studies using processed food and/or epidemiology, neither of which I put my faith in. When you show me in vivo studies of people eating Food, I will believe their results. All kinds of effects might be seen with processed foods, that would not happen with the same food raw or unprocessed. I've shown studies that honey lowers trigs and that was heated honey. Raw honey is probably better still.

"You can take a saturophobic American, let them eat their PUFA and olive oil but normalise their blood glucose, Bernstein style, and the glycation of their Hb will plummet. Glucose glycates. Fructose beats it hands down. Normalising blood glucose normalises glycation of HbA1c. Probably the rest of the body's proteins too."

Because they're getting rid of lots of high-PUFA junk foods which cause even more damage. The fact remains, some have high glucose/fructose and low A1c while others have the exact opposite. Can you account for this? I bet the people in Kitava have low A1c scores. Bernstein's diet alters more than carbs. Plus, he's looking at people who are already messed up from eating the high-PUFA and trans fat Western Diet. You claim glucose and fructose glycate, but you don't point out that cooked fats glycate, even more more - esp the PUFAs. And proteins glycate when cooked in the open air. So, if you are anxious to avoid AGEs, eat raw foods.

Gyan said...

Glycation needs both sugar and protein/fat.
Now the question is
1) Does PUFA undergo glycation more readily than SFA/MUFA?
2) Does cooked protein undergo glycation more readily than uncooked protein?
(btw what is the difference once proteins have been broken down into amino acids in stomach?).
3) Does glucose/fructose ratio matter?

The study that Bruce cited, about AGE contents of various foods, the abstract isnt clear at all. What are foods from fat groups?. Prtoein group is I guess cooked meat but food from carb group?.
Bread with butter?. Does it belong to fat group or carb group?

Gyan said...

Wont sourdough bread contain a lot of fiber?
Wheat is probably the highest fiber-containing food that exists (15 g per 120 g whole-wheat flour).

Peter said...

About 10 people achieved HbA1c below 6%, they all had average glucose values below 10mmol/l, on a diet based around the ADA "load up on carbohydrate and load up on insulin" protocol. This is, in its own right, a spectacular achievement for those 10 people. Three people out of 1439 achieved a mean glucose of 5mmol/l. There rest are being mangled.

Anyone eating to the ADA diet, as a type one diabetic, will have a massive rollercoaster of glucose ranging from blood like treacle to hypoglycaemic coma. Checking 7 blood values 4 times a year might reflect this nicely. It might not.

Maintaining a blood glucose of 83mg/dl on waking, continuously after breakfast, up to lunch, after lunch, through to supper and through the night will invariably give an HbA1c below 6% and occasionally below 5%. This is on 30g carbs per day from green leaf veggies, protein around 60g per day and the rest of calories from fat. Dr Bernstein is a saturophile but does not forbid PUFA. He has a driven approach to maintaining his value of normoglycaemia.

To suggest he obtains these HbA1c results by accidental changes to his diet other than those aimed at normoglycaemia is fatuous. The fact that the ADA diet plus insulin leaves most people with almost no control over their blood glucose does not invalidate HbA1c as a marker of hyperglycaemia.

Just throw in to the mix the advice to consume fruit freely, sugar in moderation (by USA standards) and the roll of diabetic sweets based around fructose, there's plenty of scope for any two diabetics with the same glucose to have marked variation in glycation due to fructose intake. Add to that the incidence of NAFLD in diabetics and many but not all will have fructose penetration to the systemic circulation. Add to that the roll of NSAID for arthritis management and persistent subacute blood loss will drop HbA1cs in those poor diabetic unfortunates so afflicted, without dropping their blood glucose. Did I mention the accuracy (more specifically, the lack thereof) of blood glucose meters, especially at higher readings?

There's lots to think about on glycation and the ADA diet before I abandon normoglycaemia and its assciated HbA1c. The orange juice can go down the loo without passing through me, strained or not, thank you very much.

In Kitava of course their HbA1cs and post prandial glucose levels will be normal. Otherwise they would have heart disease.


Bryan - oz4caster said...


What are your thoughts on fructosamine as an AGE marker?

Peter said...

Hi Bryan,

It's our standard marker for veterinary diabetes monitoring. At a two week "hindsight" it gives you very prompt marks out of 10 for your protocol, assuming the patient has not already given you zero marks by hypoing or being glycosuric, both big no-nos in my book. We don't actually use HbA1c much in vet work, it's available but frcutosamine is much more use for assessing management changes.


mtflight said...

On the topic of "urinary losses," experiment:

fasting, drinking water-- urine color: very light, clear yellow

drink lemonade sweetened with a nonnutritive sweetener (optionally a "diet coke") -- urine color: very light, clear yellow

Next, drink water -- urine color: very light, clear yellow

drink lemonade sweetened with sucrose (optionally a Coca Cola) -- urine color: deep yellow (almost like one took a multivitamin).

What is in the urine? Why is it deep yellow when one drinks sugar or high-fructose corn syrup? Is it B vitamins?

Question: would the outcome be different if sweetened with honey?

Peter said...

Alex, immediate thought is food dye, what colour is the lemonade? Also, just try sugar water or honey water...


mtflight said...

This would be home-made lemonade.

I don't think it's dye because diet coke (or any diet soda) would be "as if drinking water" when it comes to urine color (very very light)

Try a regular cola (with sucrose/high fructose corn syrup) and it's a lot more yellow.

The typical explanation of yellow/almost fluorescent urine after taking a multivitamin is that we don't absorb all the vitamins, so the water soluble ones come out in the urine (this happens with the B complex pills too)... so I figure it'd be something along those lines. Don't we need B vitamins in order to digest sugars? Or is that a myth...

Dave said...

Interesting hypothesis on the role of cooking in human evolution:


Peter said...

Hi Dave,

Full text is here.

Not read it yet, but I don't think we started cooking by boiling our meat. Holding a leg of something by the foot and sticking the rest of the lower limb in to an open fire seems much more likely to me. Dietary AGEs and ALEs would have exploded on to the scene. Maybe 200,000 years is long enough to adapt. Who knows, maybe AGEs spurred brain development (joke, maybe, just stirring!). No chance of a barbi with the weather we're having in the UK at the moment anyway.

I'll be interested to see what they have to say in the light of Hoffer's work with B3 and schizophrenia. B3 is a beta hydroxy butyrate mimic and probably throws similar switches to ketosis, which may go some way to explaining the suggestions of its benefit on several fronts. I don't generally much like antioxidant B vits, but ketone bodies... They're interesting, particularly on the metabolism front.



Peter said...

Alex, I think it's riboflavin, B2, which is bright yellow, but quite why sucrose/fructose would put it out in the urine I dunno.... It's B1 which is used for relatively little other than carbohydrate metabolism. I'm open to suggestions as to what's going on.