LDL cholesterol, statins, and plaque regression

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.


Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.


Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:





The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:





The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.



Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

Comments (12) -

  • J Michael Nicholls

    4/13/2008 6:49:00 AM |

    Dear Dr. Davis,
    I have read your blog for some time now, and I consider it to be the no 1 in the nutrition-health-cardiology field. A couple of years ago I became interested in the “cholesterol theory” and I have studied the development of the statins in detail. Having a background in the “hard sciences” I am appalled at the lack of sound science in this field in particular, as well as in some other areas of medical research.

    To my knowledge there is zero evidence that the lowering of any of the cholesterol levels has anything to do with preventing heart disease or reversing plack. On the contrary, an anti-inflammatory mechanism is probably the reason for the little protective effect there is, while the lowering of the cholesterol levels probably causes more harm then good (as can be suspected from the extensive list of side effects).

    Reading this post and the statement, “LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal”, I couldn’t help feeling that some readers would get it all wrong, especially since “cholesterol lowering” is the healing mantra that is being communicated to the market (and even most doctors seem to advocate).

  • Anonymous

    4/13/2008 11:50:00 PM |

    "Having a background in the hard sciences"? In the "hard siences" they call plaque "plak" ? That was a dead give away that you have no idea what your talking about even before you made the ridiculus statement"to my knowledge there is zero eveidence that the lowering of any of the cholesterol has anything to do with preveting heart disease or lowering plak(sic)" You should read some of the studies, they're easily found on the internet or in journals. By the way did you look at the pictures Dr. davis put up in the article? As Dr. davis always says I don't work for the drug companies and statins certainly aren't miracle drugs but they do have a place. Ever hear of the Framingham Study, just a small study thats been going on for over 60 years now and has studied over 10,000 people( now in its third generation) and they have NEVER had a recorded heart attack in ANYBODY with a cholesterol level under 150. So much for "your knowledge"

  • Anonymous

    4/14/2008 4:40:00 AM |

    Dear Dr. Davis,

    In reading this and about vitamin D, if you have a plaque problem, but your HDL is high and your Vitamin D level in normal, would it still be helpful to take the suppliment?

  • J Michael Nicholls

    4/14/2008 1:56:00 PM |

    Dear Anonymous, there is no need to be so sarcastic, and I apologize for spelling plaque plack. Do you mean to say that all of medical science is of high quality, and that it shouldn’t be questioned? Most of the serious critique against the cholesterol hypothesis comes from medical researchers by the way. I am waiting to be enlightened, please show me the evidence that the LOWERING of cholesterol by it self (per se) is the protective mechanism of statins.

    From your writing it appears that you still believe in the old dogma of high cholesterol CAUSING atherosclerosis. Only a few of the fiercest statinators in the research community still maintain that, and probably so for financial reasons (most statin-advertising is doing its best to communicate just that). Most GPs seem to believe that cholesterol causes atherosclerosis too. It is trivial that in any academic context “correspond to”, “linear relationship” or “associated with” do not mean “direct effect of” or “directly caused by”. With this simple understanding we would have better doctors and better scientist in the medical field, and consequently less treatment of SYMPTOMS such as high cholesterol, high blood pressure and high blood sugar. By the way, is there any proof that atherosclerosis is not causing the higher cholesterol levels instead of the other way around?

    The problem with many defenders of the cholesterol dogma is that they don’t read the scientific literature in a scientific way. I personally don’t know of anyone still believing in the cholesterol hypothesis after having studied it in depth from strictly scientific principles. There is simply no evidence to motivate all the “lowering” of “levels”. It is nothing more than a highly profitable market concept ($30 billion in 2007).

  • Anonymous

    4/14/2008 2:25:00 PM |

    Great write up.

    As  a diabetic, with all of my numbers under very good control, I have been on statins for 8 years and my last two heart scans (5 years apart) had a score of 0 plague.  My question is the following:

    Are you saying that statins are good and should be part of a comprehensive approach?

    Many websites that push your blog are against the use of statins in any approach.  How do you respond to that type of thinking?

    Should you continue taking drugs to reduce your plague if your score is zero?


    Thanks for your time

  • Anonymous

    4/14/2008 6:23:00 PM |

    Playing devil's advocate, I'm not sure if science has proved cholesterol to be a cause of heart disease. What if it's a marker and not a cause?

    Those in the Framingham study with low cholesterol values might not get heart attacks due to lifestyle/genetics, and their low cholesterol is a reflection of their overall good health?

    Those who take high dose statins obtain benefit from less inflammation, but not because of cholesterol reduction?

    I'm not saying the above two statements are true, but it could be possible. It could also explain why statins, as a single treatment, usually don't work for most people, and why the Vytorin/Zetia/Torcetrapib trials failed so miserably.

    Or it could be that the reduction in LDL wasn't enough to matter, or that particle sizes for LDL/HDL wasn't taken into account, or some other factor? It appears that  right now, there isn't hard data that proves what causes heart disease exactly, but simply a lot of risk factors and disease markers instead.

  • Anonymous

    4/15/2008 1:52:00 AM |

    I never suggested that Cholesterol by itself caused heart disease. Clearly many things do, inflamation, CRP, Lp(a)... On the other hand to suppose that cholesterol has NOTHING to do with heart disease is foolish. Show me a cardiologist that believes cholesterol has nothing to do with heart disease and I'll show you a quack. It may not even be the main cause of heart disease in most people but the fact of the matter is reducing LDL lowers the the chance for heart attack in a good number of people. Have you ever heard of Dr. Agagston ? He of the South Beach Diet fame, a cardiologist in South Florida, who by the way the way of scoring calcium scans is named after. See what he thinks of statins and reducing cholesterol levels. and as Im sure you know it gets much more complicated than that when you get into particle size. Take a person who's scans keep going up because he has small LDL and nothing in Dr. Davis program has worked for him 9I am such a patient of the good Dr.s) The best you can do for such a person is lower his LDL as far as you can since its all going to be small particle anyway. I would also refer you to Dr. Greg Browns HATS Study for examples of lowering cholesterol and lowering heart disease or Dr. Davis' example that started this discussion. I apologise if I came off a bit sarcastic in my earlier comments I think this is an important issue to get all points of view on.

  • Anonymous

    4/16/2008 3:32:00 AM |

    Great thead.

    So what are you really saying about statins?  Is there value taking statins in combination with other treatments for men and women?

    How do you address the comments that states statins don't work?

    Thanks for your time.  Your comments are really appreciated.

  • Anonymous

    4/16/2008 6:14:00 PM |

    There is NO DOUBT that statins reduce the chances of a person having a heart attack, NONE. There is question as to what about the statins does that, is it lowering LDL, is it stablising plaque, is it reducing inflamation . . .? Or is it all of these ? And there is no doubt statins have side effects, some serious, but the fact that they reduce heart attacks, that argument has been settled.

  • J Michael Nicholls

    4/16/2008 7:26:00 PM |

    I will not go deeper into the science of atherosclerosis except to say that it has been known for several years now that cholesterol per se does not initiate atheroma, or plaque. You find cholesterol in the lesions but you also find calcium. We find cholesterol and calcium because it is available in the bloodstream. Cholesterol does not have a mind of its own, and it doesn’t one day decide to develop plaque by raising “the level”. Neither does calcium.

    We need cholesterol for many important processes in the body, and it is a part of almost all of our cell membranes. Mother’s milk is packed with it because the baby needs it. Eggs are full of the stuff “because it takes a hell of a lot of cholesterol to make a chicken”. The body has the level it needs at all times, and a higher level could indicate that something is wrong, i e, it is a marker, like someone said. Lowering of levels makes no sense at all.

    It is just dumb luck that the cholesterol lowering statins happen to be anti-inflammatory and therefore have some preventive effect, and may reverse plaque in some cases. The higher the dose the more anti-inflammatory effect, and reversal of atheroma. The higher the dose the bigger the lowering of the cholesterol level, because that is exactly how statins are designed to work. However, there is NO evidence in the scientific literature that the lowering of the cholesterol level has a protective effect, and I am very sorry if this upsets anyone’s religious beliefs. Dumb luck, as I said, the rest is coincidence and correspondence. Big Pharma will do its best to uphold the “religion” though, since it is so profitable. Levels will always be too high, and everybody should be statinated. Statins should be distributed in the drinking water, no less.

    So, why bother, the statins seems to work in a few cases? Well, statins are really poisonous substances, and there are many indications that they cause harm to the human body, particularly by the lowering of cholesterol levels. Side effects are plentiful and it is probable that we will witness statin induced cancers in large numbers in the near future.

    The point to be made here is that there are other and better methods to avoid atherosclerosis and to reverse plaque. Dr Davis is one of the leading proponents of such methods. I personally think it is interesting to se the results of the statin study presented here; I just wanted to stress the point of what statins really do. By all means, we should keep an eye our cholesterol levels. But many people having a hearth attack do not have high cholesterol. But did you know that 90% of them have diabetes or in some other way a pathological sugar metabolism? So what level is the more important?

    About the quacks, who don’t buy the cholesterol dogma, there are thousands of them. Some of them can be found at www.thincs.org. If you are interested in how the cholesterol religion was developed and how science was corrupted to that end, I can recommend Gary Taubes latest book Good Calories – Bad Calories.

    By the way, CRP is just another marker for hearth disease, but I wouldn’t be surprised if there will soon be talk about lowering the level Smile

  • Anonymous

    4/18/2008 1:13:00 AM |

    Well by your klogic there is no scientific proof the lowering inflamation is what cause stsatins to lower your risk of a herat attack, the only thing we do know is that ststins DO infact lower your risk, we just all keep guessing as to why. Well heres another piece to the puzzle: double blind study releasesed this week follow groups of people on statins or placebos and by a slight BUT significant margin the statin takers blood oressure was lowered ! So besides all the other things we think statins do we now KNOW they lower blood pressure. 2 ver5y interesting points for all of our paranoid readers 1. Not one of the study members recieving the statins in the 2 year period had to leave bececause of side effects and 2. this study was NOT paid for by the big bad scarry Drug companies, so there goes your default response.

  • buy jeans

    11/3/2010 4:55:07 PM |

    I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:

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Diabetes: Better than hedge funds

Diabetes is where the action is.

While, for virtually all of history, type 2 diabetes was an uncommon condition of adults, the disease has spread so much to all levels of American society that even kids are now developing the adult form. Researchers from the Center for Disease Control and Prevention predict that, by 2050, one in three adults will be diabetic.

The diabetes market is booming, handily surpassing growth of the oil industry, the housing market, even technology. It makes Bernie Madoff’s billions look like small potatoes. In health, few markets are growing as fast as diabetes—-not osteoporosis, not heart disease, not cancer.

Americans are getting fat from carbohydrate consumption, becoming diabetic along with it. While kids hanging around the convenience store gulp down 26 teaspoons of sugar in 32-ounce sodas and 56-grams-of-sugar in 16-ounce frozen ices, health-minded adults are more likely eating two slices of 6-teaspoons sugar-equivalent “healthy whole grain” bread, wondering why last year’s jeans are too tight.

The U.S. is not the only nation affected. Globally, 2.8% of the world’s population are diabetic, a number expected to double over the next 20 years.

Pharmaceutical companies boast double-digit growth for diabetes drugs, growth rates that keep profit-hungry investors happy. Merck’s Januvia, for instance, introduced in 2006, recently catalogued 30% growth in sales, with annual sales approaching $1 billion. Recently FDA-approved Victoza, requiring once-a-day injection, is expected to reap $4 billion in sales per year for manufacturer Novo Nordisk. Such numbers can only warm a drug company CEO’s heart.

Most diabetics don’t just take one medication, but several. A typical regimen for an adult diabetic after a couple of years of treatment and following the dietary advice of the American Diabetes Association includes metformin, Januvia, and Actos, a triple-drug treatment that costs around $420 per month. Two forms of insulin (slow- and fast-acting), along with two or three oral medications, is not at all uncommon.

“Collateral” revenues from the other health conditions that develop from a diet rich in “healthy whole grains,” such as drugs for hypertension, drugs to slow the progression of kidney disease in diabetes, drugs for “high cholesterol,” and drugs for high triglycerides, and you have a pharmaceutical drug bonanza. You, too, would throw all-expenses-paid, fly-the-entire-sales-force-to-the-Caribbean sales meetings.

The global diabetes market has already topped $25 billion and is growing at double-digit rates. Forget the Internet, gold stocks, or solar energy—-diabetes is where the money is. This fact has not been lost on the very market-savvy pharmaceutical industry. As with any successful business, they have devoted substantial resources to develop and grow this booming business.

270 lb man in diapers

Alex is a big guy: 6 ft 4 inches, 273 lbs.

On 10,000 units per day of vitamin D in gelcap form, his 25-hydroxy vitamin D level was 38.4 ng/ml. One year earlier, his 25-hydroxy vitamin D level, prior to any vitamin D supplementation was 9.8 ng/ml.

According to the latest assessment offered by the Institute of Medicine (IOM):

Vitamin D need for a 13-month old infant: 600 units per day

Vitamin D need for a 6 ft 4 in, 273 lb male: 600 units per day

I paint this picture to highlight some of the absurdity built into the smug assumptions of the IOM's report. It would be like trying to fit a large, full-grown man into the diapers of a 13-month old. Few nutrients or hormones (in fact, I can't think of a single one) are required in similar quantity by an infant or toddler and a full grown adult. However, according to the IOM's logic, their vitamin D needs are identical, regardless of age, body size, skin color, genetics, etc. One size fits all.

Just as the original RDA assessment by the Institute of Medicine kept thinking about vitamin D somewhere in the Stone Age, so does this most recent assessment.

90% small LDL: Good news, bad news

Chris has 90% small LDL particles.

On his (NMR) lipoprotein panel, of the total 2432 nmol/L LDL particles ("LDL particle number"), 2157 nmol/L are small, approximately 90% (2157/2432).

Bad news: Having this severe excess of small LDL particles virtually guarantees heart attack and stroke in Chris' future.

Good news: It means that Chris potentially has spectacular control over his lipoprotein and lipid values, achieving statin-like values without statin drugs.

Typically, extravagant quantities of small LDL particles are accompanied by low HDL, high triglycerides, and pre-diabetes or diabetes. Chris' HDL is 26 mg/dl, triglycerides 204 mg/dl; HbA1c 5.9% (a reflection of prior 60-90 days average blood glucose; desirable 4.8% or less), fitting neatly into the expected pattern.

Chris' pattern tells me several things:

1) He overconsumes carbohydrates, since carbohydrates trigger this pattern.
2) He likely has a genetic susceptibility to this effect (e.g., a variant of the gene for cholesteryl ester transfer protein, perhaps hepatic lipase). Only the most gluttonous and overweight carbohydrate consumers can generate this high a percentage small LDL without an underlying genetic susceptibility.
3) Provided he follows the diet advised, i.e., elimination of all wheat, cornstarch, oats, and sugars, he is likely to have an extavagant drop in LDL particle number. Should he achieve the goal I set of small LDL of 300 nmol/L or less, his LDL particle number will likely be around 500 nmol/L. This translates to an LDL cholesterol of 50 mg/dl . . . 50 mg/dl.

In many people, this notion of taking statin drugs for "high cholesterol" is an absurd oversimplification. But it is a situation that, for many, is wonderfully controllable with the right diet.

The American Heart Association has a PR problem

The results of the latest Heart Scan Blog poll are in. The poll was prompted by yet another observation that the American Heart Association diet is a destructive diet that, in this case, made a monkey fat.

Because I am skeptical of "official" organizations that purport to provide health advice, particularly nutritional advice, I thought this poll might provide some interesting feedback.

I asked:

The American Heart Association is an organization that:

The responses:
Tries to maintain the procedural and medication status quo to benefit the medical system and pharmaceutical industry for money
240 (64%)

Doesn't know its ass from a hole in the ground
121 (32%)

Is generally helpful but is misguided in some of its advice
79 (21%)

Accomplishes tremendous good and you people are nuts
6 (1%)


Worrisome. Now, perhaps the people reading this blog are a skeptical bunch. Or perhaps they are better informed.

Nonetheless, one thing is clear: The American Heart Association (and possibly other organizations like the American Diabetes Association and USDA) have a serious PR problem. They are facing an increasingly critical and skeptical public.

Just telling people to "cut the fat and cholesterol" is beginning to fall on deaf ears. After all, the advice to cut fat, cut saturated fat, cut cholesterol and increase consumption of "healthy whole grains" in 1985 began the upward ascent of body weight and diabetes in the American public.

Believe it or not, my vote would be for something between choices 1 and 3. I believe that the American Heart Association achieves a lot of good. But I also believe that there are forces within organizations that are there to serve their own agendas. In this case, I believe there is a substantial push to maintain the procedural and medication status quo, the "treatments" that generate the most generous revenues.

I believe that I will forward these poll results to the marketing people at the American Heart Association. That'll be interesting!

The formula for aortic valve disease?

I've discussed this question before:

Can aortic valve stenosis be stopped or reversed using a regimen of nutritional supplements?

I had a striking experience this past week. Don has coronary plaque and began the Track Your Plaque program. However, discovery of a murmur led to an echocardiogram that measured his effective aortic valve area at 1.5 cm2. (Normal is between 2.5-3.0 cm2.)

Because of his aortic valve issue, I suggested that, in addition to the 10,000 units of vitamin D required to increase his 25-hydroxy vitamin D level to 70 ng/ml, he also add vitamin K2, 1000 mcg per day, along with elimination of all calcium supplements. (I asked Don to use a K2 supplement that contained both forms, short-acting MK-4 and long-acting MK-7.)

One year later, another echocardiogram: aortic valve area 2.6 cm2--an incredible increase.

This is not supposed to happen. By conventional thinking, aortic valve stenosis can only get worse, never get better. But I've now witnessed this in approximately 10% of the people with aortic valve stenosis. The majority just stop getting worse, an occasional person gets worse, while a few, like Don, get better.

Aortic valve stenosis is to the aortic valve as degenerative arthritis is to your knees: A form of wear-and-tear that leads to progressive dysfunction. When the aortic valve becomes stiff enough (i.e., "stenotic"), then it leads to chest pains, lightheadedness or losing consciousness, heart failure, and, eventually, death. Bad problem.

Aortic stenosis typically starts in your 50s with calcification of the valve, getting worse and worse until the calcium makes the valve "leaflets" unable to move. The treatment: a new valve, a major undertaking involving an open heart procedure.

What if taking vitamins D and K2 and avoiding calcium do not just reverse or stop aortic valve stenosis once established, but prevents it in the first place? Tantalizing possibility.

Pressures on my time being what they are, I've not had the freedom to put together a prospective study to further examine this fascinating question. But it is definitely worth pursuing.

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

A blood glucose at this level is typical after, say, a bowl of slow-cooked oatmeal with no added sugar, a small serving of Cheerios, or even an apple in the ultra carb-sensitive. Normal blood sugar with an empty stomach, i.e., fasting; high blood sugars after eating.

Conventional wisdom is that a blood sugar of 160 mg/dl is okay, since your friendly primary care doctor says that any postprandial glucose of 200 mg/dl or less is fine because you don't "need" medication.

But what sort of phenomena occur when blood sugars are in this range? Here's a list:

--Glycation (i.e., glucose modification of proteins) of various tissues, including the lens of your eyes (cataracts), kidney tissue leading to kidney disease, skin leading to wrinkles, cartilage leading to stiffness, degeneration, and arthritis.
--Glycation of LDL particles. Glycated LDL particles are more prone to oxidation.
--VLDL and triglyceride production by the liver, i.e., de novo lipogenesis.
--Small LDL particle formation--The increased VLDL/triglyceride production leads to the CETP-mediated reaction that creates small LDL particles which are, in turn, more glycation- and oxidation-prone.
--Glucotoxicity--i.e., a direct toxic effect of high blood glucose. This is especially an issue for the vulnerable beta cells of the pancreas that produce insulin. Repeated glucotoxic poundings by high glucose levels lead to fewer functional beta cells.

A blood glucose of 160 mg/dl is definitely not okay. While it is not an immediate threat to your health, repeated exposures will lead you down the same path that diabetics tread with all of its health problems.

Indian buffet

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

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?

Construct your glucose curve

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:


In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:


(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.