Man walks after removing wheat

No, this isn't some National Enquirer headline like "Woman delivers alien baby."

Tom is a 26-year old man with a complex medical condition, a malformation he was born with and has had reconstructed. Aside from this, he leads a normal life: works, is married, and is, in fact, quite intelligent.

He came to me for an opinion regarding his overall health. Tom was worried that his congenital condition would impair his long-term health and longevity prospects, so he wanted to optimize all other aspects of his health.

But, when I examined Tom, he could barely get himself up on the exam table without wincing in pain. When I asked him to walk, he hobbled a few steps, again clearly in pain. When I asked him what hurt, he said "everything." He said that all his joints hurt just to move.

He told me that his several doctors over the years didn't know why he was in such pain: It wasn't rheumatoid arthritis, gout, pseudogout, or any of the other inflammatory joint diseases that might account for virtually incapacitating this 26-year old man. Even the rheumatologists were stumped. It was also unrelated to his repaired congenital condition. So Tom went on with his life, barely able to even go for a walk with his wife without pain, slowing him down to the pace of an 80-year old.

So I suggested that he eliminate all wheat products. "I don't know for a fact whether it will work, Tom. But the only way to find out is to give it a try. Why not try a 4-week period of meticulously avoiding wheat? Nothing bad will come of it."

He and his wife look perplexed, but were so desperate for a solution that they agreed to give it a try.

Tom returned 6 weeks later. He walked into the room briskly, then bounded up on the exam table. He told me that, within days, all his joint pains had completely disappeared. He could walk, stretch, do all the normal physical things with none of the pain he had suffered previously.

Tom told me, "I didn't think it could be true. I thought it was just a coincidence. So I had a sandwich about 2 weeks into it. In about 5 minutes, I got about half my pains back."

Tom now remains wheat-free and pain-free, thankfully with no discernible joint impairment.

So, yes, Tom walked freely and without pain simply by eliminating wheat from his life.

Is it an immune phenomenon? Does wheat gluten trigger some inflammatory reaction in some people? There is surely something like this underlying experiences like Tom.

Wheat contains far more than gluten. Modern wheat is a collection of hundreds of different proteins, though gluten is the most plentiful, the one that confers the "viscoelasticity" of dough. But there's plenty more to wheat than gluten or celiac disease.

AGEing gracefully

Advanced Glycation End-products, or AGEs, have the potential to change our entire conversation about diet.

AGEs come from two principal sources:

1) Endogenous--Glucose-protein interactions that arise from high blood glucose levels

2) Exogenous--From diet

The first is sensitive to glucose levels: the higher the glucose level, the greater the AGE formation. The second depends on the quantity of AGE in the food consumed.

A compelling body of evidence points towards AGEs as an agent of aging, as well as kidney dysfunction, dementia, and atherosclerosis. Some of the observations made include:

--If AGEs are infused into an experimental animal, it develops atherosclerosis, kidney disease, and other "diseases of senescence" within weeks to months.

--In endothelial cells (cells lining arteries), AGE induces expression of adhesion molecules and inflammatory signals. In fibroblasts, AGE provokes collagen production. In smooth muscle cells, AGE triggers migration and proliferation. In monocytes and macrophages, AGEs induce chemotaxis and release of inflammation mediators. In short, AGEs have been implicated in just about every step leading to atherosclerosis.

--In humans, greater quantities of AGEs are present in diabetics, pre-diabetics and people with insulin resistance. We all know that these people develop atherosclerosis, kidney disease, cataracts, and other conditions at an accelerated rate.

--Foods containing greater quantities of AGEs cause endothelial dysfunction, i.e., artery constriction via blockade of nitric oxide and other mechanisms.

Short of taking agents that block AGE activity, how can you minimize the absorption or production of AGEs? There are two general strategies:

1) Keep blood glucose low--The Whitehall study demonstrated increased cardiovascular mortality with a postprandial (actually 2-hour post- 50-gram glucose challenge) blood sugar of 83 mg/dl. Lower blood glucose, less glycation. Less carbohydrates in the diet, the lower the blood sugar, the less the glycation. Studies like Whitehall demonstrate that glycation begins with glucose values within the normal range. Thus, aging occurs even with normal glucose levels. It occurs faster with higher glucose levels.

2) Choose and prepare foods with lower AGE content. Food content of AGEs is a major determinant of blood AGE levels. Fats and meats are the primary dietary source of AGEs, particularly if cooked at high temperature (broiling, frying). While this does not mean that meats and fats need to be avoided, it can mean that limiting serving size of meats and fats, while being selective in how they are prepared, are important. This can mean cutting your meats in thinner slices or smaller pieces to permit faster cooking, eating rare when possible (not poultry, of course), avoiding cooking with sauces that contain sugar (which enhances AGE formation). Is this an argument in favor of sashimi?

Minimizing exposure to AGEs, endogenous or exogenous, has the potential to slow the aging process, or at least to lessen the likelihood of many of the phenomena of aging.

More on this to come.

Small LDL: Simple vs. complex carbohydrates

Joseph is a whip-smart corporate attorney, but one who accepts advice at his own pace. He likes to explore and consider each step of the advice I give him.

Starting (NMR) lipoprotein panel on no treatment or diet change:

LDL particle number 2620 nmol/L (which I would equate to 262 mg/dl LDL cholesterol)
Small LDL 2331 nmol/L--representing 89% of LDL particle number, a severe dominance of small LDL

I advised him to eliminate wheat, cornstarch, and sugars, while limiting other carbohydrate sources, as well. Joseph didn't like this idea very much, concerned that it would be impractical, given his busy schedule. He also did a lot of reading of the sort that suggested that replacing white flour with whole grains provided health advantages. So that's what he did: Replaced all sugar and refined flour products with whole grains, but did not restrict his intake of grains.

Next lipoprotein panel with whole grains replacing white refined flour:

LDL particle number 2451 nmol/L
Small LDL 1998 nmol/L--representing 81.5% of LDL particle number.

In other words, replacing white flour products with whole grain products reduced small LDL by 14%--a modest improvement, but hardly great.

I explained to Joseph that any grain, complex, refined, or simple--will, just like other sugars and carbohydrates, still provoke small LDL. Given the severity of his patterns, I suggested trying again, this time with full elimination of grains.

Next lipoprotein panel with elimination of whole grains:

LDL particle number 1320 nmol/L
Small LDL 646 nmol/L
--48.9% of total LDL particle number, but a much lower absolute number, a reduction of 67.6%.

This is typical of the LDL responses I see with elimination of wheat products on the background of an overall carbohydrate restriction: Big drops in precisely measured LDL as LDL particle number (i.e., an actual count of LDL particles, not LDL cholesterol) and big drops in the number of small LDL particles.

You might say that wheat elimination and limitation of carbohydrate intake can yield statin-like values . . . without the statin.

Is Cocoa Puffs no longer heart healthy?

Until recently, Cocoa Puffs enjoyed the endorsement of the American Heart Association (AHA) as a heart-healthy food.

For a price, the AHA will allow food manufacturers to affix a heart "check mark" signifying endorsement by the AHA as conforming to some basic "heart healthy" requirements.

Odd thing: The list of breakfast cereals on the check mark program has shrunk dramatically. When I last posted about this, there were around 50-some breakfast cereals, from Cocoa Puffs to Frosted Mini Wheats. Now, the list has been trimmed down to 17:

Berry Burst Cheerios-Triple Berry
Cheerios
Cheerios Crunch
Honey Nut Cheerios
Kashi Heart to Heart Honey Toasted Oat Cereal
Kashi Heart to Heart Oat Flakes & Wild Blueberry Clusters
Kashi Heart to Heart Warm Cinnamon Oat Cereal
Multi Grain Cheerios
Oatmeal Crisp Crunchy Almond
Oatmeal Crisp Hearty Raisin
Quaker Cinnamon Life
Quaker Heart Health
Quaker Life
Quaker Life Maple & Brown Sugar
Quaker Oat Bran
Quaker Oatmeal Squares - Brown Sugar
Quaker Oatmeal Squares - Cinnamon


According to sales material targeted to food manufacturers, the American Heart Association boasts that "The American Heart Association’s heart-check mark is the most recognized and trusted food icon today . . . Eighty-three percent of consumers are aware of the heart-check mark. Sixty-six percent of primary grocery shoppers say the heart-check mark has a strong/moderate influence on their choices when shopping."

So, is Cocoa Puffs no longer heart healthy?

I suspect that agencies like the AHA, the USDA, the American Diabetes Association as starting to understand that they have blundered big time by pushing low-fat, having contributed to the nationwide epidemic of obesity and diabetes, and that it is time to quietly start backpedaling.

While it's a step in the right direction, judging from the above list of breakfast cereal "survivors" of the check mark program, the criteria may have been tightened . . . but not that much.

Fractures and vitamin D

This is a bit off topic, but it's such an interesting observation that I'd like to pass it on.

Over the past several years, there have been inevitable bone fractures: People slip on ice, for instance, and fracture a wrist or elbow. Or miss a step and fracture a foot, fall off a ladder and fracture a leg.

People will come to my office and tell me that their orthopedist commented that they healed faster than usual, often faster than anyone else they've seen before. My son was told this after he shattered his hand getting slammed against the boards in hockey; his orthopedist took the screws and cast off much sooner than usual since he judged that healing had occured early. (My son was taking 8000 units vitamin D in gelcap form; I also had him take 20,000 units for several days early after his injury to be absolutely sure he had sufficient levels.)

My suspicion is that people taking vitamin D sufficient to enjoy desirable blood levels (I aim for a 25-hydroxy vitamin D level of 60-70 ng/ml) heal fractures much faster, abbreviating healing time (crudely estimated) by at least 30%.

For any interested orthopedist, it would be an easy clinical study: Enroll people with traumatic fractures, randomize to vitamin D at, say, 10,000 units per day vs. placebo, watch who heals faster gauged by, for instance, x-ray. My prediction: Vitamin D will win hands down with faster healing and perhaps more assured fusion of the fracture site.

T3 for accelerating weight loss

Supplementation of the thyroid hormone, T3, is an underappreciated means to lose weight.

Thyroid health, in general, is extremely important for weight control, since even subtle low thyroid hormone levels can result in weight gain. The first step in achieving thyroid health is to be sure you are obtaining sufficient iodine. (See Iodine deficiency is real and Healthy people are the most iodine deficient) But, after iodine replacement has been undertaken, the next step is to consider your T3 status.

I've seen T3 ignite weight loss or boost someone out of a weight loss "plateau" many times.

Endocrinologists cringe at this notion of using T3. They claim that you will develop atrial fibrillation (an abnormal heart rhythm) and osteoporosis by doing this. I have yet to see this happen.

Adding T3 revs up metabolic rate at low doses. The idea is to push free T3 hormone levels to the upper limit of normal, but not to the hyperthyroid range. While an occasional person feels a little "hyper" like they've had a pot of coffee, most people just feel energized, clear-headed, and happier. And weight trends down much more readily.

Taking T3 by itself with no effort at weight loss generally yields only a modest weight reduction. However, T3 added to other weight reducing efforts, such as wheat elimination and exercise, accelerates the weight loss effect considerably. 5 lbs lost will likely be more like 8 to 10 lbs lost; 10 lbs lost will likely be more like 15 to 20 lbs, etc.

It's also my suspicion that more and more people are developing a selective impairment of T3, making it all the more important. I believe that you and I are being exposed to something (perchlorates, bisphenol A, perflurooctanoic acid, and others?) that may be impairing the 5'-deiodinase enzyme that converts the T4 thyroid hormone to the active T3. Relative lack of T3 leads to slowed metabolism, weight gain, and depressed mood. While avoiding or removing the toxin impairing 5'-deiodinase would be ideal, until we find out how to do this, taking T3 is a second best.

The tough part: Finding a prescriber for your T3.

The world according to the Wheat Foods Council and the Whole Grains Council


You might get a kick out of what the Wheat Foods Council and the Whole Grains Council recommend for a sample meal plan:

Breakfast: Whole grain raisin toast
Lunch: Sandwich on whole grain
Snack: Rye bread crackers
Dinner: Whole grain pasta with your favorite sauce

Breakfast: Whole grain waffles 
Lunch: Hamburger on whole grain bun
Snack: Graham crackers
Dinner: Whole grain homemade pizza on whole grain pita crust

Remember Morgon Spurlock's documentary movie, Super Size Me? (If you haven't already seen it, Super Size Me is viewable for free on Hulu.) Spurlock conducts a self-inflicted 30-day experiment of eating at McDonald's fast food restaurants every day. In short, the results on Spurlock's weight and health are disastrous. 

How about Wheat Belly: The Movie? We would chronicle our star through a 30-day course of meals served up by the Wheat Foods and Whole Grains Councils, all featuring wonderful wheat products in every meal. We could measure blood sugar, triglycerides, LDL, small LDL, weight, etc.


Any predictions?

Why bananas increase cholesterol

Anything that increases postprandial (after-eating) blood sugar will increase the number of LDL particles in the blood.

An increase in LDL particles is an important factor in causing heart disease: The greater the number of LDL particles, the more opportunity they have to interact with the walls of arteries, contributing to atherosclerosis.

Carbohydrates increase small LDL, especially if postprandial sugar is increased. Here's another way carbohydrates increase LDL particles: The duration of time LDL particles hang around in the blood stream is doubled.

When blood sugar increases, such as after the 30 grams carbohydrates in a medium-sized banana, glycation of LDL particles occurs. This means that a gglucose (sugar) molecule reacts with a lysine residue in the apoprotein B of the LDL particle. This induces a change in conformation that makes it less readily recognized by the LDL receptor. Thus, the glycated LDL particle persists for a longer period of time in the blood stream.

LDL particles are therefore cleared less efficiently, numbers of LDL particles increase.

Plant-based or animal-based?

The ideal diet for heart and overall health restricts carbohydrate intake. I say this because carbohydrates:

Make you fat--Carbohydrates increase visceral fat, in particular.
Increase triglycerides
Reduce HDL
Increase small LDL particles
Increase glycation of LDL
Increase blood pressure
Increase c-reactive protein


Reducing carbohydrates reverses all the above.

But here's a common mistake many people make when following a low-carbohydrate diet: Converting to a low-carb, high-animal product diet.

It accounts for a breakfast of a 3-egg omelette with cheese and butter, 4 strips of bacon, 2 sausages, cream in coffee. Low-carb? It certainly is. But it is a purely high-animal product, no-plant-based meal.

I believe a strong argument can be made that a low-carbohydrate but plant-based diet with animal products as the side dish is a better way to go.

Consider that:

1) Animal products have little to no fiber, while plant-based products like spinach, avocado, and walnuts and other raw nuts have substantial quantities.

2) Plant products are a source of polyphenols and flavonoids--This encompasses a large universe of nutrients, from epigallocatechins in tea, polymeric procyanidins from cocoa, to hydroxytyrosol from olives, and anthocyanins from red wine and eggplant. The inflow of these beneficial compounds needs to be frequent and generous, not piddly amounts taken infrequently.

3) Vitamin C--While it's easy to obtain, the fact that you and I need to obtain vitamin C from frequent ingestion of plant sources suggests that humans were meant to eat lots of plants. While it may require a few months of deficiency before your teeth fall out, imagine what low-grade deficiency can do over a long period.

4) Vitamin K1--Rich in green vegetables, vitamin K1 is virtually absent in animal products.

5) Tocotrienols--I've been watching the data on this fascinating family of powerful oil-soluble antioxidants unfold for 20 years. Tocotrienols come only from plants. (I recently had an extended conversation with the brilliant biochemist, Dr. Barrie Tan, who is incredibly knowledgeable about tocotrienols, having developed several methods of extraction from plants, including his discovery of the highly concentrated source, annatto. Be sure to watch for future conversations about tocotrienols.)

6) Meats and dairy yield a net acid load--While plant foods are net basic. At the very least, this yields risk for osteoporosis, since acids are ultimately buffered by basic calcium salts from the bones. Tissue and blood pH is a tightly regulated system; veering off just a teensy-weensy bit from the normal pH of 7.4 to an acidic pH of, say, 7.2, leads to . . . death. In short, pH control is very important. A net acid challenge from animal products is a lot like drinking carbonated soda, a huge acid challenge that leads to osteoporosis and other health issues.

Conversely, a pure plant-based diet has its own set of problems. Eating a pure plant-based diet can lead to deficiencies of vitamin B12, omega-3 fatty acids (no, linolenic acid from flaxseed will NOT cut it), vitamin K2, carnitine, and coenzyme Q10.

So, rather than a breakfast of 3-egg omelet with bacon, sausage, cream, and cheese, how about a handful of pecans, some blueberries, and a 2-egg omelet made with basil-olive oil pesto? Or a spinach salad with walnuts, feta cheese, and lots of olive oil?

Fat is not the demon

So my patient, Dane, generously volunteered to be on the Dr. Oz show, as I discussed previously.

What we didn't know, nor did the producer who contacted us mention, that Dane would be counseled by low-fat guru Dr. Dean Ornish on a strict low-fat diet. The teaser introduction essentially tells the entire story.

Ironically, that is the exact opposite of the dietary program that I advocate. I rejected the 10% fat diet long ago after I became a type II diabetic, gained 30 lbs, and suffered miserable deterioration of my cholesterol values on this diet. I also witnessed similar results in many hundreds of people, all following a strict low-fat diet. In fact, elimination of wheat--whole, white, or otherwise--along with limitation or elimination of all other grains has been among the most powerful health strategies I have ever witnessed.

I now regret having subjected my patient to this theatrical misinformation. Dane is a smart cookie--That's probably why he was not allowed more than a "yes" or "no" during Dr. Oz's monologue, else Dane might have pitched in about some ideas that would have tripped Oz and Ornish up.

In their defense, if we took 100 Americans all following a typical 21st century diet of fast food, white bread buns, Coca Cola and other soft drinks, chips, barbecue sauce, and French fries, converting to a plant-based, high-carbohydrate, grain-rich diet is indeed an improvement. People will, at first, lose weight and enjoy an initial response. (The occasional person with the Apo E4 genetic pattern, heterozygote or homozygote, may even enjoy long-term benefits, a topic for another day.)

But the majority of people, in my experience, after an initial positive response to an Ornish-like low-fat, high-carbohydrate diet will either plateau (stay overweight, have low HDL, high triglycerides, plenty of small LDL, and high blood sugars) or deteriorate, much as I did.

Thankfully, Dane has been a good sport about this, understanding that this is essentially show business. I believe he understands that the information was all well-intended and, after all, we are all working towards the same goal: reduction of heart disease risk.

By the way, regardless of which diet you follow, it is, in my view, absurd to believe that diet alone will do it. What about vitamin D normalization, thyroid normalization (thyroid disease is incredibly common), omega-3 fatty acids from fish oil, identification of hidden sources of risk (something that is unlikely in Ornish, since small LDL particles skyrocket on a low-fat diet), postprandial glucoses, etc., all the pieces we focus on to gain control over coronary plaque? Eating green peppers and barley soup alone is not going to do it.
Lipoprotein(a) Research Foundation

Lipoprotein(a) Research Foundation

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies


Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.


Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.



Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.




From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

Comments (18) -

  • Keyheart

    4/16/2008 1:02:00 PM |

    I am in favor of such a foundation and would be a donor.

  • Anonymous

    4/16/2008 2:21:00 PM |

    I would be more than willing to donate for such a good cause.

  • Anonymous

    4/16/2008 4:28:00 PM |

    As one with high Lp(a), I too, would support this effort.

    Does anyone know anything about an Ultra sound stroke screening test done by a company called Lifeline Screening. They offer 4 tests, one which checks the Carotid artery for blockage, for $139.00.  They have mobile units that travel around and perform these tests and others.

    I had a Heart Scan last year that showed no measurable plaque, but wondered if this type of test was useful for checking other locations of potential plaque?  Or is it hype?  They are going to be in my area in June.

    http://www.lifelinescreening.com/Services/Pages/Index.aspx

    Bonnie

  • Vivian

    4/16/2008 6:20:00 PM |

    I second that

  • Anna

    4/16/2008 9:07:00 PM |

    There is an extra http:/ in the link to HeartHawk's blog.

  • Warren

    4/17/2008 4:16:00 AM |

    I'm a TYP member and would be happy to donate services to set up the organization and obtain 501(c)(3) approval so contributions would be tax deductible.

  • Bad_CRC

    4/17/2008 6:36:00 PM |

    Bonnie,

    Dr. D has said that carotid plaque correlates about 70% with coronary plaque.  CIMT gives you another quantitative measure to track, but one that is a distant second to CAC for longitudinal use (a lot of variation in scores, plus it's deceptively easy to regress).  Still, with the carotid US they can see non-calcified plaque.  I'd think of it not so much as specific for stroke risk as another measure of subclinical, systemic atherosclerosis.  I got one because I'm too young to have calcified plaque; I'm hoping to track that IMT number and thereby avoid ever getting calcification in the first place.  In your situation I'd definitely do it; if I already had scorable coronary plaque then I'd think there's less utility in the CIMT.  Also, it's totally non-invasive -- no radiation.

  • Anonymous

    5/8/2008 7:30:00 PM |

    Just an idea on a cloudy afternoon - TYP might look at coming out with a product line of supplements and apparel to raise funds.  Profits would be dedicated toward a heart health research foundation.  I'm sure TYP followers would appreciate buying supplements that have a TYP quality stamp of approval along with the knowledge that funds generated would be dedicated toward research that helps them. And I've thought it would be fun to show up at a heart walkathon wearing a Track Your Plaque shirt.  A shirt could have a TYP logo on it saying something along the lines of "I trust Track Your Plaque" and then list the  different items that make the program successful.

  • Anonymous

    8/8/2009 7:24:51 PM |

    As a 61 year old women with 7 coronary artery stents, I would be very interested in aiding research and participating in  any studies anywhere. My daughter,a physician just had her Lp(a) tested twice and both times it was 90.My cardiologist has always said my problem was genetic and I am going to ask her to test my Lp(a.Thanks for this site.

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Normal fasting glucose with high HbA1c

Normal fasting glucose with high HbA1c

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.  

Comments (24) -

  • Mark

    3/23/2010 5:56:04 PM |

    So what is the basic recommendation here?
    Eat meat, nuts, vegetables, no starch, no fruit? A ketogenic diet?

    It looks like the recommendation is to avoid blood sugar spikes primarily. I would think that insulin is less of a worry because insulin doesn't necessarily mean that sugar is in the system (dairy for example).

    Some clarification would be greatly appreciated. Thanks

  • Anonymous

    3/23/2010 6:44:31 PM |

    Dr. Davis, my husband has the opposite problem, can you (or anyone else) explain it?  His 1-hour postprandial glucose never exceeds 90 and yet he has an HBA1C of 5.9.  We have checked his glucose at different times and it never goes over 100.  He is on a very low carb diet.  

    His HBA1C indicates an average blood glucose of 123, but we never see readings this high.  Is there something else that can glycating hemoglobin and thus show an elevated HBA1C reading?

  • Anonymous

    3/23/2010 7:03:19 PM |

    What would be considered an optimal (or at least good) HbA1c level? And same for fasting glucose?

    I have noticed my fasting glucose tends to vary, between 80-95, with my HbA1c at 4.6.

    Curious also if there is any data on HbA1c correlating directly with triglyceride levels.

    My own trig values are higher than I like, around 125-150, yet I limit carbs, use fish oil, and think my HbA1c number is relatively decent.  So wondering if carbs/glucose isn't my problem, what else raises triglycerides?

  • Jake P.

    3/23/2010 10:30:18 PM |

    Dr Davis, do you have any recommendations on blood glucose test meters, as far as brand/model? Also, I'd prefer something that doesn't require a prescription, if possible.

  • Dr. William Davis

    3/24/2010 1:41:43 AM |

    Anon--

    The only two causes I am aware of are 1) iron deficiency anemia, and 2) hemoglobin variants.

    Also, are you confident of the accuracy of your blood glucose meter? You can check it by running side-by-side glucoses with a blood draw.

  • Dr. William Davis

    3/24/2010 1:42:31 AM |

    I've had good experiences with One Touch Ultramini, Aviva, Relion, and Accuchek meters. All are available without prescription.

  • Anonymous

    3/24/2010 5:26:17 AM |

    This is exactly why everybody should have a blood glucose meter, and know their numbers.

    While I have not been diagnosed as having type 2 diabetes, I was darned close.  My meter, and the information found here and in the blogs that link to and from it, have helped me to lose about 3 pounds per week for the past 6 months, and not be hungry or feel deprived.

    I was like Jonathan.  Until 6 months ago my fasting glucose was always under 100.  Now that I am managing to keep my average BG reading, including post prandial readings, under 95, I have stopped suffering from the inflammatory symptoms I've had for a decade.

    My meter and initial 100 test strips was the best under $50 purchase I've ever made.

    Thanks for the USEFUL information I get at The Heart Scan Blog.

  • Alfredo E.

    3/24/2010 2:52:07 PM |

    Hi All. I eat a low carbs diet and I have the a high fasting glucose, 95-105, but a low postprandial, 85-100.

    I also exercise everyday and do Intermittent Fasting.

    What could be the mechanism working here?

    Thanks for your ideas.

    Alfredo E.

  • Anonymous

    3/24/2010 3:20:00 PM |

    David Mendosa has a good blog/site/comments... on diabeties for many things A1C, food, low carb, etc. Check him out at www.mendosa.com
    Look under "health central" or

    http://www.healthcentral.com/diabetes/c/17/75106/david-guide-a1c-6-0

    For A1C guidance.

    He seems to lean away from strict AHA, ADA, and government things that do not work for him.

    His meter data is getting a little dated, and he does not specify exact things like he states vitamin D, as opposed to stating: D3. And he seems to be a little soft about major statements, possible law suit shy.

  • Anonymous

    3/24/2010 4:01:15 PM |

    I'm curious why you believe that gaining control over postprandial glucose will result in lower *fasting* glucose.  Is there a mechanism for this?  I've found that my fasting glucose hasn't fallen since I started the TYP diet 3 months ago; it's still in the mid to high 90s -- even though my one hour glucose is rarely much higher than that.

  • Anonymous

    3/24/2010 6:40:34 PM |

    Responding to Dr. Davis' comment:
    "The only two causes I am aware of are 1) iron deficiency anemia, and 2) hemoglobin variants.

    Also, are you confident of the accuracy of your blood glucose meter? You can check it by running side-by-side glucoses with a blood draw."

    I don't think he has iron deficiency anemia unless high ferritin level indicates that?  His ferritin level was 320 at the time he got the HBA1C of 5.9.  What are hemoglobin variants?

    We have the Accuchek meter and have also had fasting and post-prandial lab tests done and the meter seems to be in the ballpark.

    Thank you very much for your reply.

  • Anne

    3/24/2010 9:28:20 PM |

    My fasting was below 100. My A1C was 6.5. A OGTT spiked at 202. My doctors told me as long as my fasting BG was good, I did not have to worry as I only had insulin resistance not diabetes. That was 10 yrs ago.

    A year ago I bought a glucometer and started eliminating foods that spike my BG. My last A1C was 5.5.

    I wish I could get a hold of the results of my OGTT from 40 yrs ago. I was told it was slightly abnormal but I did not have diabetes. How much damage has been done from elevated postprandial blood sugars?

  • Anonymous

    3/25/2010 12:20:28 AM |

    Dr. Davis,

    Would you anticipate that a healthy 25 year old would obtains similarly high postprandial sugars to those meals?  Or do young, healthly, slim people have high glucose tolerance, and hence low postprandial responses to sugar?  I've seen many articles featuring sports stars who subsist on high carb, low fat diets, such as rafael nadal, roger federer, tiger woods... I find it hard to believe they exceed 120 mg/dl postprandially...

    David

  • mikyy748

    3/27/2010 5:31:11 AM |

    Please help with an explanation ! My last meal of the day (with NO carbs) is around 4PM. At 9-10PM, my glucose test shows about 100-105. But... in the morning the test shows 125-130. How is it possible?!

  • Anonymous

    4/10/2010 4:37:12 AM |

    Veeerrrrry interesting!

    I have been on an extremely resrricted carb diet for several months.  My One Touch (and my wife's, she's T1 on a pump) my glucose levels never vary from 100-120 with the vast majority right around 110-113. Tests are run about once a day at various times including 1-2 hours post prandial.

    At my PCP's office (she's also an endocrinologist) today, her office machine complained of an HbA1C of 20+ and wouldn't give a reading, while it did report my other lipid levels, most moderately elevated as usual.

    Tubes were drawn for processing by a lab.  Of course it's the weekend and I'm obsessing about it... sigh.
    I worry that my low carb lifestyle might be masking what would be high glucose readings which is not very logical, or if something is wrong with my blood such as anemia.  A quick google and here I am.

    I wonder if this is common for extremely low-carber diabetics?

    Am on low doses of Diovan, HCTZ and colchicine...

    Thanks to all for any thoughts.
    -Ron

  • Anonymous

    4/13/2010 2:26:58 PM |

    Thanks to all who commented ;)

    Lab work came back with an HbA1C of 5.9, so the office machine was just being stupid as hoped/mostly expected.

    Good luck to everyone else.

  • mongander

    4/27/2010 11:22:25 PM |

    This MedScape article doesn't make sense.  It claims that <6 may be too low...That >7 has a better all cause mortality.
    http://www.medscape.com/viewarticle/720391

  • William A. Ryan

    7/15/2010 1:32:59 PM |

    FYI, another possible cause of abnormally high HbA1c is Vitamin B12 and/or folate deficiency.  This causes anemia with low red blood cell turnover, so any given Hb molecule is floating around longer, and thus has a higher probability of glycation.

  • Helena

    9/29/2010 11:01:56 PM |

    So.. I just started testing my blood sugar again today... first reading was 90
    Then I had lunch. Rice and curry with coconut milk (probably loaded with sugar) and it went from 156 to 258 to 124 in 2.5 hours after that meal... I am a little concerned.

    Think I will go back on my low carb diet ASAP!

  • Helena

    9/30/2010 3:22:01 PM |

    Let me correct my numbers... I didn't have them in front of me when I wrote the previous post so here they are:

    Lunch was Rice, shrimp, coconut milk based curry pot

    Blood levels:
    60 min after - 193
    90 min after - 217
    130 min after - 258
    2.5 hrs after - 140

    This morning I had a reading of 89 and after having my protein shake with cream and water it was 106...

    Def going to go back to my low carb diet asap!
    Thanks for a great blog full of valuable information and help to get back on track.

  • Anonymous

    10/15/2010 2:05:41 PM |

    This is a recent day of testing. 90 minutes after eating 50 grams of processed brown flax, my BG was about 117, but it also depends on what I eat the night before. 2 hrs after eating 8 oz hummus with tahini, my BG was 101. 1 hr after eating a 143 gram (quick rolled) oat cake with 95 grams chocolate syrup with a lot of sugar and water, my BG was 120. Next day fasting BG was 120. Carbs do a good job of BG stabilization, although I'm trying to decrease some carbs and lower my fasting BG. I will try soymilk, and less carbs.

  • H Saleem

    11/22/2010 9:04:14 PM |

    Hi, Let me add my 2Cs. The objectives for diabetics and pre-diabetics are poles apart and confusing the two can  lead to irreparable loss for the pre-diabetics and those with insulin resistance.  

    For diabetics, when the disease is well established, the focus is on minimizing the harm i.e. to minimize the blood sugar level. Elevated blood sugar does so much harm in the long run that it should be kept under control through any means possible: diet, exercise, medicine, weight loss etc. When one plan and/or drug regimen fails to control the blood glucose level, it is replaced by another, all the time focusing on maintaining optimum blood glucose levels resulting in normal (for diabetics) readings on fasting glucose, HbA1C etc. I am not fully aware but possibly there is no mainstream healthcare regimen or drug that focuses on  reversing the disease or trying to minimize diabetes damages (other than those caused by high blood glucose) like destruction of pancreatic cells.

    For pre-diabetics and those with insulin resistance, the focus should NOT be on lowering blood glucose level DIRECTLY. For pre-diabetes, it is possible to keep on "travelling" towards diabetes in reality but assuming otherwise just because some "local" interference does not let the blood sugar rise. So if you start taking any alpha-glucidase, your postprandial reading will not rise much. But this does not mean that you have controlled pre-diabetes. The causes are all there like being over-weight, lack of exercise bla bla. And your body's normal ability to regulate blood sugar keeps on deteriorating ultimately leading to a point when the alpha-glucidase alone will not be sufficient. So when pre-diabetes is treated like diabetes, it can lead to actual diabetes. This is because here the focus should not be on lowering blood glucose levels or "treating" the condition but REVERSING it. In other words the goal should be to transform the body back to the point where it can naturally process the foods while keeping the blood glucose levels and HbA1C levels in normal range. All this without the help of any drugs or special diet or aids. And for this the usual solutions are already well known: weight-loss, exercise etc.

    The moral of the story is that if you are pre-diabetic, you can keep yourself happy by eating almonds, vinegar or psyllium with meals to "show" you that your post-prandial glucose levels are in range. This can be done by eating a low-carn diet or taking diabetes drugs. But if keep the same weight, continue the same eating habbits, and do no exercise then you are possibly doing nothing to prevent a preventable disease.

  • H Saleem

    11/22/2010 9:04:58 PM |

    Hi, Let me add my 2Cs. The objectives for diabetics and pre-diabetics are poles apart and confusing the two can  lead to irreparable loss for the pre-diabetics and those with insulin resistance.  

    For diabetics, when the disease is well established, the focus is on minimizing the harm i.e. to minimize the blood sugar level. Elevated blood sugar does so much harm in the long run that it should be kept under control through any means possible: diet, exercise, medicine, weight loss etc. When one plan and/or drug regimen fails to control the blood glucose level, it is replaced by another, all the time focusing on maintaining optimum blood glucose levels resulting in normal (for diabetics) readings on fasting glucose, HbA1C etc. I am not fully aware but possibly there is no mainstream healthcare regimen or drug that focuses on  reversing the disease or trying to minimize diabetes damages (other than those caused by high blood glucose) like destruction of pancreatic cells.

    For pre-diabetics and those with insulin resistance, the focus should NOT be on lowering blood glucose level DIRECTLY. For pre-diabetes, it is possible to keep on "travelling" towards diabetes in reality but assuming otherwise just because some "local" interference does not let the blood sugar rise. So if you start taking any alpha-glucidase, your postprandial reading will not rise much. But this does not mean that you have controlled pre-diabetes. The causes are all there like being over-weight, lack of exercise bla bla. And your body's normal ability to regulate blood sugar keeps on deteriorating ultimately leading to a point when the alpha-glucidase alone will not be sufficient. So when pre-diabetes is treated like diabetes, it can lead to actual diabetes. This is because here the focus should not be on lowering blood glucose levels or "treating" the condition but REVERSING it. In other words the goal should be to transform the body back to the point where it can naturally process the foods while keeping the blood glucose levels and HbA1C levels in normal range. All this without the help of any drugs or special diet or aids. And for this the usual solutions are already well known: weight-loss, exercise etc.

    The moral of the story is that if you are pre-diabetic, you can keep yourself happy by eating almonds, vinegar or psyllium with meals to "show" you that your post-prandial glucose levels are in range. This can be done by eating a low-carn diet or taking diabetes drugs. But if keep the same weight, continue the same eating habbits, and do no exercise then you are possibly doing nothing to prevent a preventable disease.

  • KDL

    12/12/2010 9:50:40 PM |

    I have a 16 year old daughter who HBA1c is 11.7 (yes very high).  I have been working with her especialist to bring it down.  The problem is her daily readings are normal for a type 1 diabetic. I know the monitors can be cheated however I am pretty confident that most of the time she does the right thing.  I also know that sometimes she does not.  However I am wondering if there are any other things that can cause this annomoly?

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