American Heart Association diet makes a monkey out of you

21. February 2011 William Davis (38)
Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?
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Comments (38) -

  • Anonymous

    2/21/2011 3:48:54 AM |

    Back in 2004 I was seeing a Cardiologist because of AFib (since "cured" by an ablation).  The good Doctor wanted to put me on a Statin for reasons having to do with unexplained multiple "risk factors". Not being a big fan of legal drugs, I asked if I could try diet first. He said, "Sure, you can try the American Heart Association diet but...it never works".  Undaunted I tried it anyway and sure enough 3 months later I had gained 15 lbs and my LDL was even higher (I couldn't stop eating).  BTW, I quit the Statin 2 years ago and have been Paleo since. - Jay

  • Sara

    2/21/2011 5:29:27 AM |

    No thank you,
    bananas spike my glucose above 140, he he!!!

  • Anonymous

    2/21/2011 8:56:27 AM |

    I think you are taking the article completely out of context. The monkeys were on the American Heart Association diet and then they added in high frutcose corn syrup. The monkeys got fatter because of the carbs from the corn syrup, not from the AHA diet. Personally I am paleo, but you are pulling a Glenn Beck here.

  • Aerobic1

    2/21/2011 3:28:48 PM |

    The point is not whether HFCS or wheat was the cause, but rather that all simple and refined carbohydrates will create the pot belly that Shiva and most of Americans have.  The animal cruelty police should spend their efforts in Washington protesting the plethora of garbage advice that is forced on us by organizations like the AHA and cut their funding.  By doing so, it will have a significant positive impact and help reverse the upward trends of obesity, diabetes and heart disease that your tax dollars go to perpetuate.  The AHA is one of the most corrupt and lobbied groups by special interests agriculture, the same folks who bring you the refined carbs.  Once the agriculture industry checks clear in the AHA bank account, the AHA "heart Healthy" seal of approval is on the box.  If you bother to look most of the AHA "Heart Healthy" cereals have refined cereals grains and high fructose corn syrup.

  • Anonymous

    2/21/2011 4:35:17 PM |

    Researchers in England and Singapore have developed a device which can assess the risk of heart disease.

    http://insideireland.ie/2011/02/21/watch-like-device-to-assess-heart-disease-risk-9317/

  • Anonymous

    2/21/2011 6:08:36 PM |

    I have followed this blog for sometime. I do appreciate Dr Davis's efforts and the comments made in the blog.
    But I think he needs to address the criticisms made in the previous blog entry. Completely ignoring the comments and questions and moving onto a new topic seems to point toward an unseemly arrogance and a lack of respect for the readers.

  • jean

    2/21/2011 6:41:17 PM |

    Um, click on the link, but prepare for a very sad sight, the poor guy, (or girl) looks miserable.

  • Anonymous

    2/21/2011 7:28:25 PM |

    What's Dr. Davis' alternative to AHA? Is it in a book or something?

  • Anonymous

    2/21/2011 8:23:41 PM |

    As an alternative to the AHA and the ADA dietary guidelines,see Jenny Ruhl's two sites for a start.

    Blood sugar 101
    http://www.phlaunt.com/diabetes/

    Low carb dieting
    http://www.phlaunt.com/lowcarb/index.php

  • Anonymous

    2/22/2011 12:13:08 AM |

    To all the entitled anonymous douchebags, if you don't like what Dr. Davis says in his blog leave! Dr. Davis doesn't work for you.

  • Anonymous

    2/22/2011 12:35:43 AM |

    Two weeks after no dairy, no wheat and some really delicious juicy steaks I am five pounds lighter and feel great.
    I don't give a rip what my lipids are because I am not going to do anything any differently anyways!

    Blood sugars never break 100.

  • Drs. Cynthia and David

    2/22/2011 1:07:42 AM |

    @second Anonymous- try reading the article before criticizing Dr. Davis for mischaracterizing it.  You'll see he was correct.

  • Lori Miller

    2/22/2011 1:20:03 AM |

    @Anonymous #2, the group on the HFCS drinks (among other things) and the group on the AHA diet were two different groups of monkeys:

    "Dr. Grove [of Oregon Health and Science University] and researchers at some other centers say the high-fructose corn syrup appears to accelerate the development of obesity and diabetes....

    “'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat', said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio.

    "Still, about 40 percent do not put on a lot of weight.

    "Barbara C. Hansen of the University of South Florida said calories, but not high fat, were important. 'To suggest that humans and monkeys get fat because of a high-fat diet is not a good suggestion', she said.

    "Dr. Hansen, who has been doing research on obese monkeys for four decades, prefers animals that become naturally obese with age, just as many humans do. Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate 'nothing but an American Heart Association-recommended diet', she said."

    The article goes on to refer to the first diet as "high fat," even though it's only 33% fat, and the way the article is written, it's hard to tell the groups apart.

  • Might-o'chondri-AL

    2/22/2011 1:49:54 AM |

    Take the banana; a banana a day for one year offers hormetic (small bit of bad does good) low dose radiation of +/- 3.6 milli-rems for the entire year. Low dose radiation boosts the cytokine activity of NK (Natural Killer), the tumor stopper. A chest x-ray doses out 10 milli-rems by comparison.

    Potassium Kiss, found in bannanas, is 0.0118% K40 isotope potassium. It emits mostly gamma radiation (when proton snags an extra electron) and some beta particles (when neutron mass spins off an electron and neutron becomes a proton); which are "slow" in collision with things, like a cell.

  • Anonymous

    2/22/2011 2:00:22 PM |

    To a recent "Anonymous":

    Dr Davis does have have an obligation to his readers. By convention, he is expected to explain himself and respond to polite and appropriate questions regarding his blog. That is why the interaction is provided, and he seems usually to encourage the dialogue. Dr Davis could have just as easily established this blog without the interactive feature. Currently, among usual glowing reader comments and often enlightening questions has come some criticism. His response to this criticism is what is currently lacking ... of course, this is only my opinion.

    By the way, I am not exactly sure what "entitled anonymous douchebags" have to do with anything.

  • John Townsend

    2/22/2011 3:11:15 PM |

    RE: “blah blah ... completely ignoring the comments and questions and moving onto a new topic seems to point toward an unseemly arrogance and a lack of respect for the readers.” by anonymous.

    Fortunately, commentary on this excellent blog is for the most part constructive and informative. However a comment like this is frankly annoying because it’s mean-spirited, disingenuous, cowardly, and clearly not helpful. The poster is not obliged to read this blog, let alone dump on it like this anonymously!

  • Misty

    2/22/2011 4:13:12 PM |

    Interesting!  I have been advising a woman who works in a chimpanzee sanctuary in the North West.  There is one chimp who had blood sugars of 1000.  

    Sadly, they have put this chimp on Crystal Light and Tofu as a remedy.  

    Chimps share 99% DNA with humans.  We know that aspartame and soy are both dangerous to the human body.  

    The most interesting thing is, she rebelled when her goodies were taken away.  

    They too are addicts just like us.

  • Flavia

    2/22/2011 7:20:22 PM |

    You're the only doctor I trust. The more i see the changes in my BP and overall health following your advice, plus the more I learn about what should first be done to treat hypertension, the more pissed off I get.
    What jerk puts a young woman on atenolol without even asking for some tests or if she eats too much salt or if she's wound high at the dr's office!!?? What the hell!?

    BTW, my blood pressure has dropped even more- an average of around 121/81- from 151/102. This is with 12mg of atenolol which I should hopefully kick to the curb soon Smile

  • Might-o'chondri-AL

    2/22/2011 7:40:32 PM |

    Hi Misty,
    Although chimps and humans share 96% identical proteins the implication of our intervention is complicated. Here's why.

    We actually have 40 million genome variables, including 500
    DNA repair/apoptosis pathway proteins. 5% of proteins show different splice variations; we have different arrangements of coding regions on the chromosomes we share.

    Chimps have 2.5 splice variations in places where humans only 1.5 gene splicing possibilities. 80 proteins we share similar gene intron segments for the chimp's intron is longer. Humans have more genetic activity post-translation to further modify events.

    Humans don't have Neu5Gc (N-glycolyl-neuraminic acid) which is a sialic acid binding immuno-
    globulin-like lectin (Siglec). This mediates molecules of sialic acid to perform differently. It directs what gets bound; the result is spleen macrophage response for chimps immune system works differently.

    The chimp ligand (thing that binds to something) processing mechanism extends to how they metabolize estrogen and phyto-estrogen iso-flavenoids (like soybeans contain). They pass both ligands, like wheat lectins, and estrogens more fully in their urine than humans do.

    For chimps a high fat diet causes less urinary excretion of estrogen, as well as less of the fragments of peptides from lectin ligands. To be precise high protein and high carbohydrate diets also diminish those metabolites % in chimp urine; just less so than high fat.

  • worldinside

    2/22/2011 8:46:30 PM |

    Dr Davis,

    I have just found your blog because I have only recently begun searching for dietary info in order to guide me in rebuilding my skeletal muscle (and brain) after a so-far-11-month bout of severe adverse effects to a statin.  (When prescribed my readings were: Total Chol 297, HDL 117, LDL 165, triglycerides 73 – after 2 months of little exercise as the result of pneumonia and eye surgery.)

    The widespread acceptance of the "Paleo" diet interested me greatly, because I independently came to some of the same conclusions several years ago.  There is, however, a big Something that I don't understand and that I haven't seen addressed.  I hope you can – briefly, I know – educate me.  Why such severe restrictions on carbs when they were so important in our survival?

    The characterization of Paleo as high protein, high fat, low low carbs doesn't square with my college science courses and subsequent reading.  Early, early man would have grubbed around for whatever he could find, and, yes grubs would have been eaten were he lucky enough to find them, as well as other insects, wounded  small game, carrion, and fruit/berries/nuts.  Early man would also have discovered ROOTS and TUBERS very early on, and wild pea pods and the like, long, LONG before he was capable of running down game alone or in concert, or could even be sure of modest, reliable supplies of protein and fat.

    And once he was a hunter, then what?  Not much fat on wild monkeys and stressed hooved animals (lots of other predators were after them, too), and one had to live between those perhaps widely spaced hunts that were successful and had to be shared.  More ROOTS and TUBERS – because fruit alone tends to leave you hungry for more (the fructose), whereas a nice raw potato, a few carrots, could calm the gnawing in the stomach.

    Yes, I see that we now need considerable protein and a lot of fat (compared to current guidelines) because as we progressed  our expanded diet of increased amounts of protein and fat permitted our brains, especially, and our bodies to evolve to take advantage of such nutrients.  But I can't agree with the demonization of a large segment of our natural food supply.  Cut out grains.  I can see that.  But the sweet potato?  In the skin?  With generous amounts of butter gilding its fiber-rich goodness?

    Why?

  • Anonymous

    2/22/2011 10:09:55 PM |

    This may clarify, in their recent 2010 paper, M Konner and SB Eaton, estimate the ancestral diet (as % of daily energy) composed of
       35-40 acrbohydate,
       25-30 protein, and
       20-35 fat.
    They comment that the carbohydrate source for “hunter-gatherers” (HG) was from fruit, vegetables, and nuts, not from grains. They go on to say that the reduction of carbohydrates to extremely low levels is not consistent with the HG model, but neither is a high-carbohydrate, “meat as a condiment” type of diet.

    Konner and Eaton, both physicians, published their seminal paper on Paleolithic nutrition in 1985. The statistic above comes from their most recent paper of 2010. For those interested in how the popular interpretation of scientific research tends to “spin” the original detail, references to both their papers are below. Unfortunately, the 1985 article in the New England Journal of Medicine is restricted to paid subscribers only, while the recent invited article in Nutrition in Clinical Practice is available free online.

    Eaton SB, Konner M. Paleolithic Nutrition: A consideration of its nature and current implications. N Engl J Med. 1985 312:282-289.

    Eaton SB, Konner M. Paleolithic Nutrition: Twenty-five years later. Nutr Clin Pract 2010 25:594-606. http://ncp.sagepub.com/content/25/6/594

  • Brent

    2/22/2011 10:22:14 PM |

    There seem to be a few anonymous people making posts giving their opinion about how this blog should be run. Some of their assertions remind me of the entitlement mentality ruining this country.

    First, Dr. Davis is under no obligation to answer anyone's comments or questions.  How much do you pay to come here and read? I thought so.

    Second, when he chooses to respond, understand it is taking time out of his day that could go to his medical practice, (Real clients who pay for his services) his family, or without knowing the man personally, his hobbies or other interests.  How much time do you think it would take to write an answer to each person who poses a question in the response section on this blog?  Keep in mind how much slower writing is than speaking! It would take hours.

    Maybe it hasn't occurred to some of you that an answer to one person in the comments section won't be seen by very many people.  A much better use of his time is to write a short blog post at some time in the future that will be seen by many, and will be search-able, rather than answering the same question over and over again in the comments section.

    It's not all about you, people. Get a life.

  • Lori Miller

    2/23/2011 1:20:07 AM |

    Worldinside, first, there's no one paleo diet. At certain times and places, like Cro-magnon Europe, the diet was nearly all meat. Paleolithic humans ate animals (snout to tail, not just muscle meat), fruit (in season), and, yes, tubers when they were available.

    Second, probably unlike Paleolithic humans, many readers of this blog don't have normal blood glucose reactions to carbohydrates. As you probably know, carbohydrate consumption spikes blood sugar even in normal, healthy people. In people with diabetes or metabolic syndrome, eating a tuber can cause BG levels that can lead to organ and tissue damage. Overconsumption of carbs over a month in such people can lead to high triglycerides as well--not to mention weight gain.

    While it's useful to look at how Paleolithic humans ate, we also need to look at medical science and keep our own individual quirks in mind. Humans need to eat protein. We also need to eat fat; we can't make essential fatty acids ourselves, and dietary fats have a unique ability to allow us to absorb vitamins A, D, E, and K. But there's no such thing as an essential carbohydrate (people who have hypoglycemia aside). Our liver can make blood glucose from protein. And just because something is natural and somebody else can eat loads of it, doesn't mean everybody can eat it.

  • revelo

    2/23/2011 1:47:45 AM |

    Assuming your goal is longevity and health in old age, it doesn't matter what our hunter-gatherer ancestors ate, because they didn't live much beyond age 70, which is quite young by modern standards. Living to 100 and being healthy in your 90's is very unnatural, so it follows that those of us who want to live that long should eat unnaturally. All the evidence I've see suggests that being lean and conditioned is the way to go, regardless of diet, but that a mostly vegetables diet is most conducive to longevity. Eating mostly grains is also okay. Eating high-fat or high-meat is NOT conducive to longevity.

    If you are not lean and conditioned, then first priority is to become lean and conditioned, and any diet which helps towards this primary goal is a good diet. Only after you become lean and conditioned do you really need to start worrying about diet.

  • Anonymous

    2/23/2011 4:03:16 AM |

    … as always such enlightening comments …

    In my neighborhood, it is generally accepted that the life expectancy at birth for preindustrial populations was 30-35 years. This was due not to the absence of older people but due to the extremely high infant and child mortality. Deaths overwhelmingly were due to infectious diseases that are now under control, more or less. With the longer average life spans came the advent of the diseases of civilization: atherosclerotic cardiovascular diseases, type 2 diabetes mellitus, chronic obstructive pulmonary disease, lung and colon cancers, essential hypertension, obesity, diverticulitis, and even dental carries. As of 2011, US life expectancy at birth is 78 years.

    For sure, aerobic fitness is essential to health and longevity in the modern world however, medical science has demonstrated that many of the diseases of civilization would be minimized with appropriate dietary modification. Yes, the same medical science that we are throwing rocks at in the current “cutesy” survey of the AHA offered in this blog session.

    One method of analysis in medical research is the examination of the Paleolithic diet supporting the discordance hypothesis that tries to explain that the mismatch in our modern diet from that what our genome has evolved is the cause of some chronic diseases. As an example, consider the modification of sodium intake. Studies of our ancestors diet estimates their sodium intake at about 800 mg/day, compared to a current adult average of 10,000 mg/day estimated by the WHO. Well-validated computer simulations predict that a reduction of 3000 mg/day (30%) in sodium intake would result in 40,000 to 90,000 fewer deaths from coronary heart and stroke each year in the US. On the other hand, moderate ethanol intake has been shown to reduce cardiovascular risk. Ethanol consumption was probably nonexistence before the invention of agriculture and not part of the paleo lifestyle.

    No one has all the answers but blindly following any particular lifestyle or lifestyle advocate will probably not get you to a healthy 9th decade or simply a healthy older life. However, with a little luck and the judicious adoption of demonstrated healthy habits in fitness, nutrition, and lifestyle we all may get there.

  • Anonymous

    2/23/2011 4:31:32 AM |

    I think the problem people have with The Heart Scan Blog is that they forget the doctor is referring to people who have metabolic problems. I've met many people who are fat and who eat potatoes and fruits yet keep their cals low and lose a ridiculous amount of weight. But at the same time I know people who, if they ate the same way, they would gain weight.

    In general, the info on this blog is really good. Sure there are times where it seems that the doctor has recanted his hate of weight so much that he begins going after the most random stuff (i.e.. butter), but realize that this is a blog and that - as mentioned previously - everyone is different.

    Closing anecdote: My grandfather is 94. He's incredibly healthy (runs a whole mango farm in Asia). His diet would be deemed bad by most of the people on this blog. He eats oatmeal topped with mangoes for breakfast, Hawaiian Bread with SPAM sandwich (because he's out on the farm), and he eats white rice for dinner. His cholesterol is perfectly fine. His heart is perfectly fine. In fact, the doctors are always amazed at how healthy it is.

    So it goes to show, it depends on YOU. Do your research, see what info is out there, don't rely entirely on any one source of info. So a doctor recommended you a diet you don't agree with? Guess what? Go see another doctor! Just be sure you aren't going from one doctor to another until you hear the answer you WANT to hear as opposed to the one you NEED to hear.

  • worldinside

    2/23/2011 10:40:57 AM |

    Thank you to all the  Anonymousi, Lori and Revelo who replied to my question, especially the first responder.  I've downloaded the paper and am looking forward to reading it.  I was pleased to note that, as I believed, those early diets were pretty well balanced.

    And thanks, Lori and another, for pointing out that this site is intended largely for people with CVD and/or metabolic disorders.  (That explains the every 15 min BG readings!)

    I was not questioning because I was confused about which diet to follow, but rather, was confused by the way the term "Paleo" [diet] was being thrown around on this site by several commenters, as in "I've been Paleo for two months now and feel great.  No more carbs for me."  And I wondered if that was the site terminology for the diet plan envisioned by Dr Davis.

    Revelo, I don't think I agree with your statement, " Only after you become lean and conditioned do you really need to start worrying about diet."  First of all, unless you've a metabolic disorder I think you should be mindful rather than worrying about your diet.  Second, I'm inclined to believe that once you're conditioned that's when you can stop worrying, if you were so inclined.  You've cranked up the mitochondria and they're working away at increased effectiveness even while you're not working out.

    By the way, I used to love oatmeal in the morning.   Several years ago I started what turned out to be about two years of oatmeal for breakfast every single morning – with half and half or cream and brown sugar.  Then I stopped as suddenly as I had started.  I think my body needed something the oats supplied, and then it no longer did.  And I stayed slim all that time.  Now I don't touch fructose except in fresh fruit (Thank you, Dr Lustig), so no sugar either white or brown should I ever again get the oatmeal urge.

  • Eric

    2/23/2011 1:15:16 PM |

    To all the "anonymous" posters-

    After reading Dr. Davis' blog for some time now, I can assure you he will respond if the comment is worth his time.

    General bad mouthing is rampant on a blog and if he spent most of his time refuting narrow minded opinions he wouldn't have time to be a cardiologist or write. So chill out or go elsewhere.

    Also- his views aren't directed to just people with metabolic syndrome. It's for people who seem to be the American picture of "health" but are a ticking time bomb for diabetes, stroke, heart attack. His knowledge delves deeper than just a typical lipid panel (LDL, HDL, triglycerides).

    People should know what they speak of, before the pop of at the mouth about topics they aren't well suited to debate.

    Good post Dr. Davis.

  • terrence

    2/23/2011 5:33:37 PM |

    Anonymous February 23, 2011, said "…. after looking it over following a very strong recommendation, I can say that I will not be back."

    Thank you anonymous - based on your silly comment from which I took the quote, you have absolutely NOTHING to say. I am delighted you are going.

    r Davis, thank you for yet another informative, intelligent post.

  • Might-o'chondri-AL

    2/23/2011 7:38:26 PM |

    Some are not abreast of the science and how it is clinically relevant. A 33 year 14,000 patient study of Danes, published 18 Feb 2011 in Annals of Neurology, indicates Doc's insistance is well founded.

    (In case you wonder why neurologists' data are relevant it is because 87% of fatal strokes are ischemic strokes. Now on to the science reported.)

    Danes followed those with strokes over 33 years and found that NON-fasting triglyceride levels were more of an indicator than cholesterol level.
    Specificly: women and men with over 89 mg/dl NON-fasting triglycerides had 1.2 times more stroke risk.

    Doc's rants about blood sugar after eating, including butter induced spike, are in line with NON-fasting triglycerides being
    a risk factor. He does detail
    triglyrerides in other posts and goes into the VLDL mechanism too. My layman's focus on LDL & genetics overlooked what this blog clued me in to.

    Laboratory lipid blood work shows the fasting trigylceride number. Doc pushes home test of
    post-meal blood sugar since it is a surrogate of VLDL and NON-fasting triglycerides getting elevated (or not).

  • Might-o'chondri-AL

    2/24/2011 12:08:16 AM |

    Non-diabetics, like me, think blood sugar science is for the other guy. Doc seems to be trying to hammer it home that it is relevant to some more of us.

    Let's focus on coronary problems, like multi-vessel coronary disease, although it is all tied in to cardio-vascular "events". A meta-analysis of 20 studies covering 90,000 non-diabetics is worth summarizing.

    Over 12 years those 90,000 non-diabetics' heart risk (multi-vessel coronary artery disease) correlated exponentially with both fasting and post-meal blood glucose levels. This was irregardless of the person not meeting the diagnostic criteria for being diabetic; and irregardless of "normal" fasting blood sugar, or even signs of glucose intolerance. In other words, the +/- 2 hour span of blood sugar dynamic is connected to cardio-vascular events.

    (Multi-vessel coronary disease is when the left ventricle functions, but there is +/- 70% stenosis narrowing of blood vessel from plaque.)

    European Diabetes Epidemiology Group's 2003 "DECODE" research shows that the interplay  of blood sugar and cardio-vascular risk can start even in the "normal" blood sugar range. The risk progresses in a linear
    fashion, yet there is no specific point where can say individual has passed the point of no return into danger.

    Again, the DECODE data's
    significance is that post-prandial (after meal) glycemia, and to a lesser extent fasting blood sugar level, is relevant to cardio-vascular events even in some non-diabetics.

    Non-diabetics can still share some of the 30 risky genes with type II diabetics and yet not become diabetic. We don't know which of us has what of those allelo-morphs (a.k.a. allele; a DNA sequence on a chromosome).

    So, non-diabetics (specificly those with the alleles similar to diabetics) may have normal fasting &/or normal post-prandial blood sugar yet be at risk of a cardio-vascular event. Furthermore, non-diabetics with suspiciously elevated fasting blood sugar are thought to be manifesting one of those genetic SNPs (single nucleotide polymorphism, a.k.a. mutation).

    Clinically 35% of diabetics have cardio-vascular events and 5 years later 35% of those go on to have a fatal incident. In comparison 24% of non-diabetics have cardio-vascular events, yet 5 years later 33% of those who share the risky allele(s)go on to have a fatal incident. In other words, everybody who took a first "hit" has virtually the same chance of dying; speculation is the non-diabetics who go on to die share the dying
    diabetics risky allele(s).

    Discussing what (say) grand-dads
    eating habits is annecdotal; as is we non-diabetics assumption time won't alter things for us.
    Many of us do not share genes with any diabetic risk, so Doc's "gluco-phobia" is irrelevant. He obviously
    sees plenty, diabetic and non-diabetic, who come to him so they won't die unnecessarily.

    For you who may live long enough to see routine testing, or doing research, here is a list of the 10 alleles most associated with European ancestry adult onset diabetes relevant to what was discussed above.

    It bears mentioning that each may have up to 3 allele sub-variations for each risk
    gene. In no particular order, they are:
    FTO rs8050136, IGFBP2 rs4402960,
    CDKAL1 rs7754840, HHEX rs1111875,
    SVC30A8 rs13266634, PPARG
    rs1801282, KCNJ11 rs5219, TCF7L2
    rs7903146, CDKN2A/B rs10811661and rs93000039.

  • Dr. William Davis

    2/24/2011 12:20:46 AM |

    Wow. I see I enter a fascinating conversation.

    In response to a question posed by Worldinside: The difficulty with carbohydrates differs substantially from person to person, based on 1) genetics, e.g., apo E2, 2) intensity of physical activity, 3) preceding lifelong carbohydrate exposure, 4) current weight and insulin sensitivity, 5) vitamin D status, 6) lectin content of consumed foods. There are other factors.

    Point: There cannot be a one-size-fits-all approach to diet. This is one of the main reasons I advocate postprandial glucose checks, a means to assess a specific individual's carbohydrate tolerance.

    And thank you, Eric and Terrence, for understanding that this is a blog and that I do my best to respond, given my time constraints. I've just finished a 10 hour day in the office, spent 2 hours starting in the early a.m. editing a new book (to be released by Rodale in fall). I now turn to website responsibilities until late tonite.

    There's only so much you and I can fit into a day.

  • Kent

    2/24/2011 4:13:42 PM |

    Can't wait for the new book, the first one was truly a God send.

    Does it have a title yet?

  • Anonymous

    2/24/2011 5:00:16 PM |

    I find this blog to be very helpful in sorting out what to eat and how it may effect me.  
    I have increased the amount of Vit D and fish oil that I take daily.
    He is providing a good public service with the blog for which I thank him.

  • ArtsyNina

    2/25/2011 1:26:37 AM |

    Dr. Davis- I've been following your blog for a while now and always enjoy your posts! Informative for sure - both the posts and all of the comments.  Your sign off question gave me a good giggle.  Keep up the good work!


    artsynina.blogspot.com

  • Gene K

    2/28/2011 6:22:23 PM |

    @Kent

    You can read the already written chapers of the book if you log in to the TYP site: trackyourplaque.com.

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  • John Gardner

    7/11/2011 5:23:22 AM |

    The American Heart Association had always given good advice on caring for one's heart. It is up to us if we heed them or not.

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Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

2. April 2010 William Davis (12)
Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

1. April 2010 William Davis (11)
The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

28. March 2010 William Davis (16)
Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

26. March 2010 William Davis (20)
Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

23. March 2010 William Davis (24)
Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

21. March 2010 William Davis (19)
No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

Statin stupid

19. March 2010 William Davis (0)
If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

19. March 2010 William Davis (83)
In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

18. March 2010 William Davis (0)
If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

18. March 2010 William Davis (74)
No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.