What am I missing here? Has it not been proven that Statin + Niacin combo is like 90% affective in stopping plaque progression in its tracks? Why does that not say that LDL reduction AND particle size reduction,(Niacin for LP(a),works best? Its not just LDL, I developed heart disease with a 90-100 LDL before my Dr discovered  high LP (a). Treated with 10mg statin,1500 Niacin, diet,I am at a30/30 count. OVER&OUT

Let's just summarise. First there was Keys with his total cholesterol. This turned out to be garbage. Then there was LDL vs HDL. But LDL is calculated and, as we know from this site, tells us nothing about anything. Then we have LDL particle size. Small dense is bad, big fluffy is good, noting that big fluffy contains lots of cholesterol per particle and can increase your calculated, or even absolute, LDL. Two factors, most studies use calculated LDL. The bin is there, file promptly.

The second is that something controls your LDL particle size. How, on a practical basis, does Dr Davis control LDL size and density? No wheat and no sugar. Does wheat and sugar elimination alter anything in the body? Wheat contains both an insulin mimetic and two insulin potentiators, plus starches and sugars both increase blood insulin levels per se. Perhaps there is a message here. It's been known for decades that insulin drives the proliferation of the arterial media we call arteriosclerosis.

If insulin also controls LDL particle size (I have no information on this, but I'm willing to bet it does) then Yudkin and Stout are correct, Keys is wrong and the cholesterol hypothesis, what remains of it, describes the effects of insulin on blood lipids. While insulin and glucose do the damage to the arteries.

Just a cholesterol skeptic view.

Peter

Statins are anti-inflammatory, antioxidant, anti-proliferative and probably anti other things too. Unfortunately they drop cholesterol levels (in humans anyway). Zetia, like torcetrapib and clofibrate, does the cholesterol dropping thing without the anti everything else that statins bring along. No wonder they killed so many people in the clinical trials. Clofibrate. Torcetrapib.

If a drug company develops a drug which converts small dense LDL to light fluffy LDL without affecting insulin sensitivity or glucose, I predict it will go the way of clofibrate and torcetrapib. There's the bin.

I especially find it interesting that, among the so-called pleiotropic, or non-lipid, effects of statin drugs is a modest rise in 25-OH-vitamin D3 levels.

I think this just once again shows that statins DO reduce heart disease but NOT because of the reduction in LDL. I'm always amazed at the Dr. who say you don't need to be on a statin your LDL is fine. Statins have been proven to reduce death rates in cardiovascular disease by 30 to 40% and yes with niacin by 90%!!!!!!!! Anybody worried about heart disease should be taking them. And save me the "side effects" alarm of statins that is so over blown. The fact is we invented a drug to reduce LDL, it does that but thats not why it reduces heart attacks and we're still not sure why they do. We accidently created a great class of drugs.

I remember in Taubes reading that small LDL are the result of particles being formed in a high-triglyceride environment--if so there is a more direct link to diet than through insulin.

About the merits of statins, can't we at least say that through reducing the number of all LDL particles and hence the number of small particles arteries are protected?

Keith

The drug company slanted this study so that they'd get a wonderful result, that they didn't and the lengths that they went to hide or misrepresent the data that came out of the study has to make you suspicious of what ELSE they have learned.

Did you catch that they also suppressed other study results showing liver damage from Zetia?

Also, did you catch the BMJ story today about the calcium supplementation trial that lowered LDL raised HDL and increased cardiac and stroke events in older women?

While that too isn't a death blow to the LDL hypothesis, it certainly doesn't bolster it.

Peter,

Good post; you have an impressive grasp of the literature on this!  I have a question for you, though:  Besides the epidemiology (which I know you don't buy), aren't there still tons of animal studies linking atherosclerosis to dietary saturated fat?  In fact, to promote atherogenesis in lab animals so they can study it, don't they feed them a diet rich in palmitic, stearic, myristic and lauric acids from animal and tropical plant fats, which works predictably?

Drug companies are actually scrutinized fairly closely, though plenty of shenanigans still go on.

What scares me even more is what may have been going on BEFORE the intensified scrutiny began a few years ago.

Nowadays, the return on investment for treatment of chronic diseases like cholesterol, osteoporosis, and hypertension are so substantial that it is causing them to see a blur between right and wrong.

Yes. I believe that the evidence for that effect of statin drugs is quite confident.

When I question the Lipid Hypothesis, what I really mean is that I question the wisdom of the simple "high cholesterol means more atherosclerosis" philosophy, a belief that is clearly oversimplified, though it contains a germ of truth.

For anonymous,

Of course statins reduce cardiac mortality and obviously it's nothing to do with LDL cholesterol lowering. But before you pop one on the off chance (they are available OTC in the UK) go very carefully through this paper.

You need the full text, the abstract tells you nothing, so here's a summary:

There were 2913 patients in the placebo group. A total of 306 died during their 3 years of not taking a statin. That is 10.5% died. In the treatment group there were 2891 patients and 298 died, that's 10.3%. Bear in mind that these were high risk cardiovascular patients, the sort for whom statin therapy is supposed to be effective in saving lives.

There was undoubtedly a significant improvement in cardiac mortality WITHOUT improvement in overall mortality. To sum up the PROSPER trial, you can have the cause of death changed from heart attack to cancer, but not the date on the death certificate. You choose. Perhaps you're too young to be in the PROSPER trial, but live long enough and you won't be!

PS if you EVER see a statin trial without the overall mortality figures, just assume there was no benefit or worse. If there is even a miniscule benefit it will be broadcast far and wide.

Keith,

Thanks for the pointer. Obviously high triglycerides are a classic marker of hyperinsulinaemia and insulin resistance. I'll follow that one when I get that far in to Taubes' book. Seems it's looking good for Yudkin.

bad_crc,

Yes, there are thousands of papers like that. They usually use D12451 or something like it. High fat alright, 45% calories from lard. As the rest is? A bit of corn starch, a mass of maltodextrin and an even bigger mass of sucrose!!!!! But of course it's the lard that kills....

Whereas using a real high fat diet you get this paper. I would suggest the 60% of calories from fat us a little low for a rodent. Choosing for themselves they can go to around 80%, get plump but don't develop insulin resistance.

Peter

My understanding is that studies show that statins are effective in reducing heart attacks ONLY in people who have already HAD heart attacks. Not in the general population.

This would confirm the growing suspicion that statins work by limiting the inflammation associated with heart disease. Not through their effect on lipids.

To get back to Zetia/Vytorin, what Dr. Nissen pointed to, which IS in my mind worth noting, was that while the variation in individual endpoints did not rise to statistical significance every single endpoint measured went in the wrong direction. That argues against random effects in my mind.

Beyond that, we know that in most people heart disease develops over a longer period than that spanned by this study, which only lasted 2 years. If all these parameters measured were trending negatively at 2 years, what happens at 5? Or 10? This is one of those drugs that once they put on on it, you take them forever. So the 5 or 10 year result could be devastating if this turns out to be a significant finding.

My suggestion would be continue testing this drug in small studies involving people who are very well informed of the risks, but end the writing of the current 1 million prescriptions a month. That's a LOT of guinea pigs, and if there turned out to be an accelerating pace of problems with it, a lot of people could die unnecessarily.

Statins reduce the number of LDL particles, which is very poorly represented by the conventional (Friedwald)calculated LDL cholesterol.

More importantly, when someone with heterozygous hypercholesterolemia (as in this Vytorin study) has a high number of SMALL LDL particles, then statin drugs, in my view, do provide benefit. But a superior effect would be to specifically reduce the number of small LDL particles, best accomplished with such strategies as elimination of wheat, weight loss via low carbohydrate diet, fish oil, vitamin D, and niacin.

This raises the question of how well the two groups in this study were matched for the number of small LDL particles. To my knowledge, this was not measured.

Let me also remind everybody that the measure obtained and used for comparison was carotid IMT, not carotid plaque.

I'm certain I'm not alone in feeling bewildered that such a dominant theory of the disease could turn out to have been so wrong for so long at such great cost in lives and treasure.

Just as a question of historical interest, how far back in the history of science do we have to look to find this kind of reversal of understanding of what the facts are with such broad and great consequence?

Hi, WC--

I'm not sure, but it's not the first time.  

Is the earth still flat?

Hi Dr. D.

I was thinking of Galileo also and his remarkable discovery that the earth orbits the sun.

But then I thought "surely we don't have to go that far back do we to get to such a broad and consequential paradigm shift?"

Maybe we do.

Could zetia be interfering with the absorption  of simvastatin?

Hi wccaguy,

You may enjoy this discussion article from PLoS. The authors intend it to be provocative, put it does pose the question "on which day did medicine stop making mistakes?"

Peter

In response to Jenny, not all studies on reducing heart attack death havwe been done on people who already had a heart attack. The reduction of 30 to 40% is whether you've had one or not.

Our saturated fat question keeps coming up, but the current common wisdom is that saturated fats are "neutral" in the sense that they raise both LDL and HDL. But do we know what they do to the number of small particles? Of course, if LDL is raised by making particles fluffy then saturated fats are clearly protective.

Keith

Hi, Richard-
No, there was indeed a substantial further drop in LDL with Vytorin over simvastatin.

There is a very modest shift from small to large LDL.

Zetia dropped my very high, inherited LDL to normal, BUT I afer a couple months on Zetia my post-menopausal body stopped making estrogen--my gynecologist remarked on it.  

I also started having a problem with persistent visual afterimages which the ophthalmologist said might also be from having too little cholesterol.

Both problems went away when I stopped the Zetia. I have very high LDL but I also have the "longevity" cholesterol gene which makes for big fluffy LDL as well as very low Apo(b). My doctors--including the cardiologist I saw--are ignorant about the implications of both findings and just obsess about the high LDL.

Since naturally produced estrogen seems to be protective for heart disease, I wonder if some people with inherited high LDL are like me have the large fluffy LDL molecules which give a deceptively high LDL value on tests. For them lowering it with Zetia drops LDL TOO low, so that the body doesn't have the cholesterol it needs for important functions, like making the naturally produced female hormones that may be protective against heart disease.

Hi, Jenny-
Keep in mind that conventional LDL is a flagrantly inaccurate number. In my experience, LDL of 150 when accurately measured (we use the NMR LDL particle number as the "gold standard"), the true number is between 80 and 270 mg/dl.

In my view, conventional LDL is a silly number. It is also the basis of a $23 billion (annual revenue) industry.

In Dec 05 I had a heart scan score of 145.  I went from 10 mg of Lipitor to 80mg of Vytorin and 1000 Niacin, 1 fish oil.  At that time my particle number was 1325 and small particle # 977.  A year later it went to 1503/1277.

In Nov 07 my heart scan went to 291. I then went to 2000 mg of Niacin and 150 COQ10,4 fish oil, 500 mg C, Vitamin D.

My new liposcience profile taken Dec 27 07 shows small particle down to 249 and particle number down to 279.

I dont know why my plaque increased so much but the new lipo profile is impressive in reduction.

Is there anything here that seems weird or is it just the plaque grew fast and is likely now under control with the much improved scores?  All other factors on the profile were great and my Vitamin D is very good and CRP excellent too.  My homosistine was 15.7 is the only thing a bit high.

Thanks!!

Sorry, but I do not assess entire programs on this blog.

I would invite you to participate in the conversations in the Track Your Plaque Forum for detailed discussions like this. There is also a free report on "10 steps to take if your heart scan score increases" on the www.trackyourplaque.com website.

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

Probably probably the most helpful in addition to up-to-date info I came across on this topic. I am positive fortunate that I noticed your article by chance. I¡¯ll be subscribing to your individual rss feed in order that I can have the most recent posts. Take pleasure in all the pieces here.

Probably probably the most helpful in addition to up-to-date info I came across on this topic. I am positive fortunate that I noticed your article by chance. I¡¯ll be subscribing to your individual rss feed in order that I can have the most recent posts. Take pleasure in all the pieces here.

I could see this might be a problem if gut health was compromised; exogenous AGEs would then have a pathway to get into our tissues.  Assuming someone is on a low carbohydrate paleolithic style diet, what evidence is there that the exogenous AGEs do anything other than merely pass through the digestive system?

Hi August, I echo the same question. Is there any research on exogenous AGE's absorbing in to our bodies?

Dr. Davis,

Are palm oils/hydrogenated oils a significant source of AGE's like butter?

What about clarified butter (ghee)?

Dr. Davis, now you're delving into the unknown with your suggestion of an anti-AGE diet. You don't know. You're suggesting we eat that diet but you haven't any data to support such a suggestion. Don't do like they did with saturated fat. Think of the alternative we adopted then that brought us here. Think of the alternative we will adopt now that will bring us who knows where.

If the advice of the day is to avoid AGEs in food, what kind of food will we eat then? Since meat contains a boatload of AGEs, that's out but what will replace it, soy? See how your advice is already turning on itself?

Stick to what works on the TYP program as a good doctor should and leave the speculation to the speculators.

Martin, there have been numerous studies connecting the association of AGEs with various health issues. There is nothing novel or or new about this.

Avoiding AGEs doesn't mean you can't eat meat. All you have to do is eat good fresh meat and don't over cook it until it is well done or overbrowned. If you like your meat chared and well done, then you may have to make a sacrifice.

Yes even properly prepared meat has some AGEs in it. But no one food or diet is perfect. You just do the best you can and try to avoid the big mistakes. Just my opinion for what it is worth.

Doc - with regards to exogenous AGEs, it sounds like this could be the new cholesterol-is-bad-for-you theory. My apologies if I have overlooked something in your post, but I don't see any logical argument leading to the conclusion that exogenous AGEs affect your health. Your previous post on butter also makes you sound like an alarmist. Of course, if you have a diet coming up, this is understandable.

what do stomach acid and bile do to ingested ages?? ...and the rest of the digestive process? sss

One of the primary AGE components of milk products is pyrraline:

Glycation in food and metabolic transit of dietary
AGEs

Here are some quotes from this study:

"Given the data for pyrraline excretion, it
can be concluded that dietary pyrraline is nearly completely
released and resorbed during digestion, followed by rapid
elimination via the kidneys, thus leading to nearly complete
recovery of dietary pyrraline in the urine. This indicates that,
in contrast with Amadori products, of which only up to 5%
are recovered in the urine [24,25], pyrraline obviously is not
metabolized within the body."

"Above all, however,
it has to be realized that the term ‘AGE’ comprises a large
number of individual amino acid derivatives, of which only a
minority have been identified and quantified either in foods
or in vivo."

Now that everyone is speculating in the last two posts, is it possible that some AGEs are much more harmful than others? (As the previous study indicates?)

Are we distinguishing the types of AGEs when we measure them? (Or are we lumping them all together like what was done with cholesterol?)

Are food derived AGEs eaten as part of a meal less harmful then analogues produced in a lab and fed in isolation? (Like most AGE studies I've read?)

Again, if butter is as bad as these measurements indicate, why hasn't it been identified epidemiologically as such a bad food? Those with the highest butter consumption tend to be the healthiest (although I suppose because it displaces margarine).

I can understand why all AGEs might be harmful to someone with compromised kidneys, but I agree with Martin Levac that we're really delving into the unknown.

"Martin, there have been numerous studies connecting the association of AGEs with various health issues. There is nothing novel or or new about this."

Please give us a study. This sort of broad statement is hard to counter argue otherwise!

I'm not really convinced AGEs you eat are a problem. But if you're enamored of low temperature cooking, looking into Sous Vide cooking. It yields delicious results by cooking at much lower temperatures than normal.

Speaking of endogenous AGEs, caused by high blood glucose levels, here is an interesting factoid - blood glucose levels in birds are very high yet their HbA1c levels are low:

http://healthcorrelator.blogspot.com/2010/10/blood-glucose-levels-in-birds-are-high.html

There are a few possible reasons for this. One of the most interesting mechanisms is vitamin C synthesis. Not only is vitamin C a powerful antioxidant, but it also has the ability to reversibly bind to proteins at the sites where glycation would occur.

All humans cook food and have done so for thousands of years. This is natural for us. If you've ever cooked meat on a camp fire, you know that the some of the meat becomes very crisp. Paleo people didn't have temperature gauges so I'm very sure there were plenty of exogenous AGE's. In fact, I would suggest, since these pieces of foods tend to taste very good to humans that they are an important piece of our nutrition not the opposite.

"High blood glucose (any blood sugar above 100 mg/dl) will permit glycation"

I would love to know some research that backs this claim. I have seen it numerous times but have not been able to find any research that specifically deals with it.  Also, just guessing, but I would bet that damage occurs at considerably lower blood sugar levels for those eating a conventional, nutrient sparse diet as compared to those replete w/ vitamins, minerals, phyto-nutrients etc who eat a diet containing very large amounts of "real food" particularly non-starchy vegetables

Has anyone ever taken an A1C of a grain-feed cow?  Maybe that high AGE butter was from a diabetic cow!

I don't know if AGEs are harmful either, but a pressure cooker is great for low-temperature cooking. It's also much faster and keeps in the juices better than oven roasting.

Re: sausage (from the last post), the list of ingredients from the chorizo I eat is pork, water, salt, paprika, spices and garlic powder. "No nitrates, MSG, preservatives, sugar or soy," reads the label. I don't understand why this is worse than any other meat.

Sausage could be a problem because,

1)The meat is ground up so more of the surface area was exposed to oxygen. More of the meat is oxidized.

2)Sausage unlike unground cuts of meat must be cooked through because of bacterial contamination. The more you cook meat the more you get AGEs.

3)Some sausages as with hot dogs are pre cooked. Then you cook them again. This should also increase AGEs.

There are indeed studies that 1) measure serum levels of AGEs in humans after consumption of exogenous sources, and 2) relate AGE levels to biologic effect, e.g., endothelial response.

There is no question that the exogenous AGE conversation requires more exploration. I've followed this conversation for some years, but I believe it is gathering real momentum and looks and feels like a genuinely meaningful issue.

We need more info, no doubt. The notion of endogenous AGEs already fits quite nicely into our observations of the benefits of a low-carb diet. But  exogenous AGEs have potential for taking us one step farther in crafting an ideal diet. Recall that the "Paleo" approach is one reconstructed to mimic ancient behaviors, not necessarily one to achieve a new set of modern goals, such as reversal of coronary disease or osteoporosis.

It's clear that in the US we eat lots of carbs and get lots of heart disease and diabetes.  But there are lots of traditional cultures that eat even higher percentages of carbs (cassava, beans, rice and others) but that don't get those diseases.  How does the AGE theory explain that?

Dear Dr Davis,

I know your opinion against butter, but disagree, based on a lifelong experience, as a skin chronic healed by milkfats and (land)animal fats.

For the first 40 years of my life I was never free of allergic reactions and imflammated skin symptoms. Raw food helped not, vegetables and salads helped not, and the official healthy lifestyle helped not either. 10 years ago, when the stsart of Zonish lowcarb (much like your style) finally helped me incredibly much... Yet my skin has healed fully only after I switched to very, very buttery and egg-yolky diet close to Jan Kwasniewski.

I live far up North, but have no symptoms of vitamin D deficiency, in spite of not eating the pills and not having much sun for the better part of the year. Furthermore, I cannot eat fish, and do no longer supplement with fish oil either, due to problems induced by it. Yet my skin has never been as good as now, fully without irritation or other symptoms. And unlike my frends and colleagues, I no longer seem to catch seasonal colds, either.

So far the only thing I can blame for the last few years of well-being is increased use of milkfat and non-muscle parts of animals (fat, marrow, liver and skin collagen). Of these the milkfats make up a major part of the daily calories, often more than 50 E%.

I'm interested to hear your thought on possible causes, which make this butter strategy work the best of all that we've ever tried; both for myself and for others in our family

With regards,
LeenaS

I am a Type 2 Diabetic with normal blood sugar who takes -0- drugs and -0- insulin.

I experienced tremendous benefits from going low carb primal. I won't detail them here but I have not been sick in 20 mos.

This summer I performed a one week dairy fast (I'd been off milk for almost a year) and then added back butter.

Butter was very inflammatory. I no longer eat it. Clarified butter or Ghee and Cheese are not inflammatory and I eat it occasionally.

So for me, I agree with butter.

Anonymous, thanks for the info on sausage. I buy raw sausage and I'm careful to avoid over-cooking any meat, mostly because it gets like shoe leather.

Another question: is cream high in AGEs? Does the churning action required for butter contribute to oxidation or AGEs?

What's the consensus on carnosine ? I've read some articles claiming it helps with AGE factors.

Dr. Davis, it's fine to have data on a diet that contains AGEs, but where's the data on a diet that avoids AGEs? Where is the justification for adopting such a diet? Avoiding something leads to adopting something else. What will that be? You can't predict. Nobody can predict. This is the danger of advising to avoid something just like that was the danger of advising to avoid saturated fat and pretty much all animal fat altogether in one big swoop.

If we can't eat fat, we must eat sugar. There's no other alternative. If we can't eat meat, we must eat some other form of protein. What will that be, soy, wheat, any other grain, legumes? If we can't eat meat, we must eat some other form of those essential nutrients like B12 and EFAs. But where can we get such a high quality source of those nutrients but in animal flesh? The quick answer is nowhere.

When you advise to avoid AGEs without giving us a safety threshold, the safe course is to avoid all AGEs, not just a little bit. When you give a safety threshold, it doesn't matter because the substance has been declared bad entirely anyway so the safe course is the same.

We can see this with animal fat and pretty much any kind of fat. Fat is bad, so any fat is bad, so less fat is good or better, but no fat is best. That's how it works in spite of having some form of safety threshold we can abide by like say 10g of saturated fat per day maximum. Why is that? The safety threshold is declared as a maximum with no minimum.

So tell us Dr. Davis, what is the maximum and the minimum amount of AGEs you advise we eat? But more relevant to the discussion, how can we find out exactly how much AGEs is in the food we eat every day so that we can make an informed decision on exactly how much AGEs we eat every day? Is there a tool that will allow me to find that out? The point is that even if you give us a precise number on how much AGEs we can and cannot eat, we can't even control how much AGEs we eat. Accordingly, the best course of action is to avoid all AGEs and not just a little bit just to be safe because the contention is that lots of AGEs is worse than none.

With endogenous AGEs production due to high blood glucose and other simple sugars like fructose, the problem is much simpler. That's because this AGEs aspect of sugars is merely the last installment of How Sugars Kill Us Slowly. We already know that sugars kill us slowly and we already know just how much of it will do it and how long it will take and etc. But until you find out exactly how much exogenous AGEs we must avoid and exactly how much we can get away with and how to measure the AGEs in the food we eat, this problem will remain unresolved and unresolvable.

In other words, the best course of action with exogenous AGEs is to just ignore them outright. After all, we've been ignoring them outright for the past couple million years without so much trouble.

Bill,

Butter is high in AGEs? Wow - why? What about Ghee?

Do you know what the AGEs are in smoked meats like smoked trout?

Does the canning process increases ages as in canned wild caught salmon?

Hi, Fred-

I believe that smoked fish tend to be moderately high in exogenous AGEs.

One of the difficulties with quantification of AGEs in foods is we have limited data on the AGE content of various foods. It's not like grams fats or carbohydrates listed in plain sight on the label.

I find the AGE conversation a fascinating new potential insight into helping us decide how to best manage food choices, as well as food preparation.

As with all new ideas, it will cause upheaval in preconceived notions.

Given some of the previous blog posts, the largest preconceived notion might be yours toward butter. So, it's no big deal if you aren't up to the challenge of defending what you posted. That's okay. Trying to be coy about it, not so much.

Count me as a skeptic on this one.

Very good review on AGEs. Dr. Davis is 100% right to be concerned.

http://biomedgerontology.oxfordjournals.org/content/65A/9/963.full#ref-109

Chris Masterjohn has the skinny on AGEs in butter:

The Daily Lipid: Is Butter High in AGEs?

People are confusing exogeneous AGEs which are generally harmless compared to the dangerous endogenous AGEs.

Endogenous AGEs are created by proteins in our bodies reacting with reducing sugars.  Practically the only sources of dietary reducing sugars are fructose (table sugar, HFCS) and  cooked starches. The obvious solution is to eat far more meat and butter and drastically reduce carbohydrates.

Humans have been eating cooked food for 1.8 million years and are very well adapted to them. The novel foods in the human diet are large quantities of plant proteins, starches and sugars.

I'm surprised you think kale and spinach are so wonderful. Renowned toxicologist Dr Bruce Ames says that there are considerable amounts of natural toxins and carcinogens present in all food plants.
http://www.fortfreedom.org/n16.htm

Any potential benefits from eating kale is likely to be due to hormesis.

In fact there is absolutely nil direct scientific evidence that eating fruit and vegetable has any health benefits whatseover. The benefits of vegetables have only been found in a few poorly designed population studies. Any observed 'benefits' of eating vegetables are probably just due to confounding variables - people who eat vegetables smoke less, drink less alcohol, are more active and eat less sugar and junk foods.

Gary Taubes is skeptical of the claims about exogenous AGES

http://www.healthcentral.com/diabetes/c/36758/17729/gary-taubes

Hi Apra,

In 'The Diet Delusion' Gary Taubes says that the natural diet of humans is almost purely carnivore with a few berries. Taubes studied physics at Harvard and aerospace engineering at Stanford before becoming a journalist. Because he was properly trained in using rigorous scientific methods he can readily see the flaws in nutrition research.

I've read the sole paper that lists butter as a high-AGE food: "Advanced Glycoxidation End Products in Commonly Consumed Foods" (2004, Journal of the American Dietetic Association, via Google Scholar cache).

The data is in Table 1, which refers to "foods prepared by standard cooking methods" (these include frying), but the table says nothing specific about how the butter was processed. I am willing to bet that the butter in question had been treated at high temperature (maybe used in frying).

Consider these values:

Milk, cow, whole .... 0.05 kU/mL
Butter .............. 265 kU/g

Expecting high AGEs in uncooked butter -- over 5000 times the level in milk! -- would make little sense.

Would you consider revising your post in light of this?

The data table lists butter as 100 gm serving, or over 3 ounces (23,000 - 26,000).  In the serving size database, the amount of AGEs normalize a bit, at 1100 - 1300.  I wish they had done organic vs commercial butters, but maybe next time we can see that data.  No surprise on pan fried bacon at 91,577 for 3 ounces and 11,905 for the serving size (2 slices is the norm).   As with all foods, moderation.  And thank you for your blog - it is very informative!