Hi Dr. Davis.
I’m actually both pleased and troubled with the link to Dr. Diamond’s presentation that you’ve provided.

On the “pleased” side, Dr. Diamond’s analysis is:
•  An excellent/very well done presentation
•  Fact based (e.g. cites numerous studies, documented references, named experts, etc.)
•  Spans the test of time (e.g. references from the 1800’s thru the present day)
•  Ferrets out the major drivers of our present-day obesity epidemic & debunks other commonly held beliefs
•  Synchs with some of the Track Your Plaque (TYP) tenants (e.g. TYP guidance on triglycerides, diet, sugars, etc.)
•  â€œFlags” potential issues like conflict of interest which might have a tendency to creep into the science on occasion (e.g. the Keys report, the errant conclusions resulting from the NCEP report and supporting studies, etc.)

On the “troubled” side, Dr. Diamond’s analysis seems to:
•  Fly in the face of some of the foundational tenants of TYP
•  His analysis/conclusions, and that of other experts he cites, is that cholesterol of any kind is NOT correlated with Coronary Heart Disease (CHD) – at least as a root cause of heart disease (see Myth #2 and Dr. Diamond’s related analysis)
•  That LDL cholesterol – and although not stated by Dr. Diamond I’m inferring – the “sticky kind”, i.e. the small particles that actually adhere to artery walls (not the fluffy LDL particles that bounce away), are actually good!! On his “Final Issues 2” slide, and later in his related pictorial slides (entitled “What Causes Coronary Heart Disease?”), he makes reference to [LDL] cholesterol as a “Misunderstood Hero”?
•  That small, sticky LDL particles actually help the body recover from the damage created by the real culprits… sugars that work in concert with certain bacterias to create micro-tears in our artery walls
•  That small, sticky LDL actually results in the belt-and-suspenders, Rube-Goldberg “spackle” [which again I infer from Dr. Diamond’s presentation ultimately becomes plaque], that fixes (admittedly in a suboptimal and too-late manner) the damage already done by the artery-tearing, sugar/bacteria combo.  Plaque caused by LDL is actually the ‘finger in the dike’, last ditch effort, to fix the artery tears!  Kind of the last line of defense. [see slides on page 53 and Dr. Diamond’s related YouTube discussion.]

As a result, just curious about your thoughts on Dr. Diamond’s hypotheses.  
1.  Am I getting Dr. Diamond’s message(s) right?
2.  If yes, do you concur with – or tend toward – the theory(-ies) supported by Dr. Diamond and other cited experts about the role of cholesterol in CHD?  I gather from your blog post that you sympathize with his glycation theory(-ies), but how about the rest?
3.  If yes again, does that change some of the TYP direction?  For example, a significant part of the TYP approach is to reduce, as much as possible, small LDL particles. If LDL – and thus the resulting plaque – is indeed a suboptimal last line of defense, does reduction of LDL particles lead to a sub-optimization of the body’s last-ditch defense/“back-up plan” to deal with arterial microtears?
4.  Also, knowing that plaque/“spackle” is admittedly a suboptimal last ditch effort, what consequence does reversing plaque ultimately have given that the real damage – the tears in the artery walls (the seemingly real CHD culprits) – has already occurred. Are we pulling the finger out of the dike… without addressing the real root cause of the problem?  â€¦and if yes, what’s the back-up plan to the body’s back-up plan? If we reduce LDL and plaque, and the arterial damage is already done due to years and years of sugar abuse, what plugs the dike then?  I’m not talking about the preventive approaches of avoiding glycation in the first place… obviously that seems to be the real, preventive answer. I’m referring to those of us – for whom preventative measures are too late because the microtears are already there – who might be already living with the consequences of years of potentially errant diet/health guidance (by Keys, NCEP, etc.) and thus “spackle” in our arteries?  If the "spackle" is removed, does the dike start leaking again?

Although I thought I was “on the path to CHD righteousness”, I’m now confused again as a result of Dr. Diamond’s insights. Thanks for any clarifications Dr. Davis!

Dr. Davis,
I'm also anxious to hear what you think of the "hero" role of LDL in plaque.  I'm hoping he didn't go too far off the reservation on this point because the entire hour long presentation was so well done (comprehensive, well-explained, and credentialed) that it will be a powerful aid in spreading the word on both carbohydrates and how messed up the typical GP is with cholesterol treatment (not their fault - but the ATP-III as you say).  It was the tipping point for me.  I'm going off Lipitor now, which I"ve been on for years and will look into your TYP program to ensure I'm doing the right thing.

HI, Joe--

This "hero" thing, to my knowledge, is extrapolation and supposition. It is an interesting notion. I, too, was impressed with his presentation, but I think that the "hero" thing paints LDL as an entirely innocent player and I don't believe it is. We have only to look at people with heterozygous familial hypercholesterolemia who can have heart attacks in their 30s with pure large LDL to know that there is more to LDL's behavior than a protective function.

Hi, G--

By providing the link to Dr. Diamond's wonderful talk, I didn't mean to suggest that everything he says should be taken as gospel.

Virtually everything he said up until the "spackle" I do agree with. The spackle argument is pure supposition. It makes sense, but only to a degree and ignores the quantitative (e.g., heterozygous familial hypercholesterolemia) and qualitative (small, oxidation- and glycation-prone LDL particles with unique conformations that differ from larger LDL) differences in LDL particles.

Nonetheless, Dr. Diamond's recounting of how this mess was created was enlightening and well-presented and I still enjoyed it.

Dr. Davis,

I watched Dr. Diamond's presentation in its entirety.  I agree that he's done some great investigative medicine, especially looking into long-established research on carbohydrate intake, and, more recently, digging into questions of research funding and conflicts of interest.

His presentation leaves me with a major question about the role of cholesterol.  Diamond claims that high cholesterol levels are not harmful, so long as they are below 300 mg/dL, and that cholesterol has a helpful role.  It is used by arteries to repair themselves after the arterial lining is torn, infected by bacteria, or otherwise damaged.  This is why, he says, we find cholesterol in atherosclerotic plaques, together with white blood cells and dead bacteria.  Yet, we know from your reports and others that an elevated LDL particle number *is* correlated with coronary events.

What's going on here?  Is cholesterol itself harmful, or is high particle number just another symptom of high carbohydrate intake, which causes glycation and loss of elasticity in the arterial walls, leading to damage?

I just read the other comments, so the above question has been answered.  Thanks for all the info!

Hi Brian--
While I truly enjoyed Dr. Diamond's presentation, I think this particular path leads us down a dead end.

I don't think cholesterol per se is harmful; I believe that the particles that contain, among many other things, cholesterol can be harmful, especially small, oxidation-prone, glycation-prone LDL particles. I believe it would be an incredible stretch to say that small LDL particles are somehow protective.

I have inherited cholesterol and just learned from my health store guy that all the grains I have been eating are likely responsible for the high numbers of my small LDL(527) particles.  I thought oatmeal and other whole grains would squeege-mop the bad guys out of my system.  This news is also likely why I haven't  lost any weight (I eat lots of veggies and apples, fibrous fruits and protein.)  I do not use processed foods at all.  I walk a mile to work each day and I am still 10-20 # overweight (and yes it is right in my middle.)  My health guy is the one who directed me to this blog.  Any other information is most welcome.  I am trying to figure out what to fix everyday (supper/dinner) is the hardest.
Joan phillips

Without in any way wishing to contradict the idea that fructose is even worse than glucose readers here may enjoy reading this article on the perils of a diet high in
fermentable carbohydrates.
Dietary Carbohydrates and Dental-Systemic Diseases"
The paper was written by a dentist after reading Taubes Good Calories Bad Calories. Readers who find GCBC hard work may like to start with this Medical News Today article based on the above paper.
If A Diet Is Bad For The Teeth It Is Also Bad For The Body

Don't forget agave syrup/nectar.  That is the latest "low glycemic" sweetener temping sugar addicts, particularly to those interested in health.  Agave sweeteners are VERY high in refined fructose, with some brands much more fructose than HFCS (I've seen figures as high as 92% fructose).

Even more worrying, agave sugar products  are labeled as safe for diabetics, who are particularly prone to damage from frequent consumption of concentrated fructose.

The people I see using or recommending agave sweetner products seem to think that because they can't detect an immediate post-prandial BG rise, that agave syrup is somehow better (therefore healthier) than sugar and safe for liberal and/or frequent use.  Not so.  All refined/concentrated sugars need to be limited in both quantity and in frequency, including concentrated fructose.

I see "moderation" used a lot in reference to sugars and agave products whenever criticism of sugars is made.  But what is "moderation"?  Do we even have a reference point anymore in our sugar-drenched culture?  "Moderation" in the 21st century is still at least a hundred pounds per capita more sugars than most humans consumed just a few hundred years ago, and much more than our paleolithic ancestors consumed. Even "moderation" needs to be considered in moderation.

Wow, that's really interesting.

In the past I've wondered if something real simple (like removal of soda/sugary drinks) from society would have a major impact on both heart and general health.  Apparently it would.

It's also weird how cardiologists (in general) overlook sugar intake almost completely. When I last saw my cardiologist, I was sort of baffled that they were offering the patients waiting for infusion therapy snacks while they wait. The nurse commented how  the patients go  first for the peanut butter/jelly sandwiches and they run out fast. And I'm there thinking... are they crazy, giving  sugary food to heart patients?  Then I remembered most cardiologists tend to be fat intake oriented only.

Question for Dr. Davis -- what amount of fructose, daily would you consider safe? Is any amount  safe? As certain fruits do provide health benefits even if they do contain fructose. Berries are still acceptable? What gycated hemoglobin level do you aim for with your patients and have you noticed any differences in plaque progression based solely on this value?

Hi Dr Davis,
Could you tell us more about beer? Do you mean that beer has fructose added to it? Or that it contains a lot of fructose naturally? In general, how high up is beer on your list of things that we shouldn't eat? I ask because I'm having some success cutting down on sweet things and on wheat, and beer is one of my chief culinary pleasures. I don't mean that I drink a lot or that I drink everyday, just that I thoroughly enjoy the 3 or 4 beers a week I do have. (I generally drink brews made with 100% barley malt.)

So low glycemic fruits (which are high in fructose) like apples, apricots, berries, cherries, grapefruit, plums, and prunes can be hazardous to our health...

I'm starting to run out of things I can eat.

Hi,
Thank you for the link to the JCI
study. I can hardly wait to see how the CRA will militantly respond. As a former research technician I am driven crazy when the CRA claims that sucrose and HFCS are essesntially similar. Take the variant HFCS-55. To the casual observer the 55% fructose: 45% glucose composition looks 5% different than the 50:50 ratio found in sucrose. That is, until you do the math.
55%:45% = 55/45 = 1.22.
This means in every can of Coke
(bottled in the USA) there is, compared to glucose, 22% extra fructose. The CRA can't deny the math; they designed the ratio. To your health.

Did anyone notice that one of the authors of the article is RM Krauss? I love chasing his articles on pubmed.  His saturated fat articles from a few years back are particularily interesting.  I think of him as "small dense krauss" in the age,rage and ldl series on Peter's blog.

Dr. Davis - there's so much great information here, but when we ask questions to try to understand the information, you don't answer them!

Thank you, Curious.

But most of my time is spent in my more-than-full-time cardiology practice, consulting to the nutritional supplement industry, research, and the practically full-time website, Track Your Plaque, in which I engage in discussions with your wonderfully savvy Members. So I have to triage my time accordingly.

Also, I read the comments and I try to cover as many of the points as possible in future posts or in the content we post on Track Your Plaque.

Remember: As I post prominently on the blog: The Heart Scan Blog accompanies Track Your Plaque; it is not meant to be a standalone source of information.

Dr, D.  Those of use who TYP ( "track your posts") on this Blog may not be as "bought in" as the members of your track your Plaque members.

If fructose is added to beer, it will be converted to alcohol so none left in the final product.  If wheat is used in the beer grist, the starches that are extracted are converted (mostly) to alcohol so no residual "toxins" to cause swelling.

It isn't high fructose corn syrup consumption or prepared meals that makes Americans one of the most overweight nations in the world, its eating more calories that you need; it comes down to pure physics

I'd like to see a post about the lie of Calories. Fat is calculated at 10 kcal/gram because if burns (bomb calorimeter) better than sugar (calculated at 4kcal/g, the same as fiber).

But of course sugar is much more available to our bodies as energy than fat or fiber.

This makes the Calorie a big lie and emphasizes even more the low-fat diet (because fat would obviously be easier to cut by calorie than carbs).

When people try to talk about the "physics of losing weight", they need to address the underlying assumptions that make the whole system a lie.

Jammer, Please, it is a fundamental law: you can not create or destroy energy.  Mechanistically the body may deal with fats, sugars and proteins differently but unless you live in an alternate dimension, calories absorbed by the gut are either expended as energy or stored in the body in one form or another.  Belief in some magical effect of being able to "eat all the xyz without putting on weight" is a matter of faith and faith is neither fact nor science.

Anonymous, on the contrary, you are expressing faith in but one interpretation of the Laws of Thermodynamics (LoT).  When tested, results often show that one can eat more calories on a restricted carb diet and be less hungry and lose more weight.  The reasons are many and I refer you to Good Calories Bad Calories should you wish to learn more.  The body is not a closed system, and your interpretation of the LoT imply that it is.  What do I mean?  â€œCalories in = energy expended + fat accumulated/depleted” is correct, but only if one realizes that some calories drive hormonal responses which have an effect on the equation.  Eat more protein, feel less hunger, be more active, thus expend more energy.  Eat more carbohydrate (measured by glycemic load in particular), feel more hunger and behave like hungry people do - rest more, thus expending less calories.

Do teenagers grow because they eat too much or because their bodies are responding to the complex interaction of hormones?

Do pregnant ladies gain weight because they eat too much or because their bodies are responding to the complex interaction of hormones?

Do post-menopausal ladies gain weight more easily because they suddenly begin to eat too much, or because their bodies are responding to the complex interaction of hormones?

Do tall thin people (ectomorphs) just magically match their consumption and expenditure (thus remaining slender despite what appears to be high food intake)?  Or are they genetically programmed to a different hormonal response than endomorphs?  

If you met two people, one tall and thin and the other shorter, wider, with a large pelvis and heavy bones – don’t you already know that one will struggle more with their weight than the other?  You do, and you know it long before you know which one is the least disciplined in the non-food arenas in their lives.  

Are you aware of the research that shows, repeatedly, that the obese consistently eat less than many or most of those who are not obese?

Do those who are heavier than we think they should be eat too much, or are they responding to the hormonal mileu they have created by eating foods which we are not designed to eat?  I think the later.  Obesity is not the result of a character flaw, it is a result of widespread consumption of foods (primarily cereal gains, sugar and agricultural products which have exceptionally high carb content) we are not genetically adapted to.  These foods drive a hormonal response the results in energy accumulation as fat.

Aplloswabbie,notwithstanding the impact on what drives people to consume or expend energy at different rates, all excellent info., the equation is still balanced in the end.

Anon, agreed, but the significance of our agreement on that fact is low, as it provides little utility in assisting ourselves or others with their health.  For me, the realization that "low fat" diets are unnatural and drive metabolic derangement gave me a chance to eat good food to satiety, but avoid the high body fat that plaques my family.  Best regards.

How much fructose does beer have then? From what I could find, the fructose content of barley malt is significantly lower than other sugars.

how about mal;tose from tapioca syrup?

Now if you could get Congress to drop the high tariffs on sugar so it becomes less expensive than HFCS, we all could live longer.

Not much longer, we predominantly have sugar from local beet rather than HFCS in the UK, yet our stats aren't much better. IMO there's little difference in the relative toxicity between sugar and HFCS within the context of a high wheat diet

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So fruit, in moderate portions, is bad for me?
*snort*
I understand targeting HFCS just as you would large amounts of sucrose.  It's the AMOUNT of these substances that can be a problem.  The other nutrients I get from a piece fruit can far outweigh any possible negative of small amount of fructose in the piece of fruit.  Decisions are all about risk vs. benefit. I imagine there are no risk-free food choices.

No risk-free food choices, Anon?  Whole fruits and vege have little risks!

Very good post that busts everything that http://betterworldcookies.blogspot.com/2010/06/why-i-use-agave-nectar-examination-of.html says!

Wow, I had no idea of this. I should start being careful with my eating, I am really worried about my health now due to several conditions and this is a real eye opener

Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).

A point that Robert Luskin makes in his video "Sugar, the Bitter Truth" is that biochemically fructose does not produce Leptin in the body, the "stop eating" hormone.

A great ingredient for corporate food products - the more fructose, the more you eat/drink before feeling "full". Given that the calorie surplus that makes the US one of the fattest countries in the world is only 20 calories per day, high fructose corn syrup could account for that all by itself.

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