CIS: Carbohydrate intolerance syndrome

Carbohydrate intolerance comes in many shades and colors, shapes and sizes.

I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)

At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.

An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.

This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.

Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.

How about Kevin?

Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:

HDL 36 mg/dl
Triglycerides 333 mg/dl

BP 132/78
Waist circumference 34 inches
Blood sugar 98 mg/dl

Kevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis.

Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.

But take a look at his underlying lipoprotein patterns (NMR):

LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)
Small LDL 1811 nmol/l
Large HDL 0.0 mg/dl


In other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.

Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.

We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar.

CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come.

The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)

The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.

Comments (28) -

  • Sarah

    1/28/2009 2:45:00 PM |

    What's a "fake grape"?

  • Anonymous

    1/28/2009 4:19:00 PM |

    Do you think instant oats, or rolled oats, are ok?

    How about grits?  

    A Southerner trying to find something to replace cheerios or bagel for breakfast!  Already gave up eggs and bacon!

  • Anonymous

    1/28/2009 6:19:00 PM |

    "green fake grapes"
    - can you expand on this or provide a link to another blog entry that explains what is wrong with these? Thanks.

  • Diana Hsieh

    1/29/2009 1:09:00 AM |

    Anonymous -- Why give up eggs and bacon?  Reducing carbs requires increasing fat intake -- and contrary to the conventional wisdom, that's a good thing for your health.  (See Gary Taubes' _Good Calories, Bad Calories_.)

  • Anonymous

    1/29/2009 1:43:00 AM |

    Green grapes:  negligible amounts of reversatol.

    AJL

  • Anonymous

    1/29/2009 2:30:00 AM |

    Yes, I'd like to know if carbs like whole, cooked oat groats and/or wild rice are okay on TYP?  These are the only grains my cardiologist allows on his program.

    Also, what about oat bran, both cooked and uncooked?

    And lastly, ground flax seed?

    madcook

  • Anne

    1/29/2009 3:06:00 AM |

    Anonymous ~ bring back the eggs. add some veges and cheese and that makes a great breakfast. When I eat bacon I buy the stuff without the nitrites. My breakfast often looks like my dinner - lots of low carb veges and protein.

    I am a Southerner and grits are too high carb for me - shoots my blood sugar up to 200. Yup, I have CIS or maybe it is T2DM. Whatever I have, keeping my carbs low seems to be working well.

  • Anonymous

    1/29/2009 4:05:00 AM |

    what's a fake grape?

  • Anna

    1/29/2009 7:59:00 AM |

    Salmon is great for breakfast, either leftover from dinner or cured salmon (gravlax).  So is a salami and cheese plate now and then, for variety.  Breakfast doesn't have to be sweet or  grainy, if one can get out of that mindset.  

    Avocado omelet, sausage (make 2-3 days worth at one time and reheat), baked custard, smoothies.  There are all sorts of great non-grain breakfasts.

  • Grapes of wrath

    1/29/2009 12:22:00 PM |

    Can't say I have heard of fake grapes, well maybe the plastic ones.

  • keith

    1/29/2009 1:17:00 PM |

    fake grapes are seedless green grapes that are effectively candy. fruit with seeds that are close to the way they occurred in nature before we mass produced them are healthier.

  • Dr. William Davis

    1/29/2009 2:19:00 PM |

    Madcook--

    All are fine, with little rise in blood sugar except for the oat products, which can raise blood sugar in very carb-sensitive people.

    Ground flaxseed is the very best, with pure protein, oils (including linolenic acid), and fiber but with no digestible starches.

  • Anonymous

    1/29/2009 3:37:00 PM |

    This blog is great, that's why I added it to my top ten health blogs. www.mydailywellnesstip.com

    Jean-Luc Boissonneault

  • Frederick

    1/29/2009 7:01:00 PM |

    Dr. Davis,

    I recently received some curious results on my blood panels and am curious for your feedback. I am sorry to trouble you with my personal story but am not sure where else to go for info. I appreciate any help you can provide, in addition to what you have already done with this blog, which is a terrific resource.

    In May 2007 my blood panel looked like this:

    Total cholesterol 155
    Trigylcerides 65
    HDL 50
    LDL (calc) 92

    In Jan 2009 I received the following:

    Total cholesterol 311!
    Trigylcerides 43
    HDL 88
    LDL (calc) 214!

    I am currently 41, athletic, do high intensity short duration exercise 3-4 times/wk, low body fat, fairly good health. I changed my diet in Jan 2008 from a standard "healthy" diet to paleo style after reading Cordain's book. I followed Cordain's recommendations fairly closely for about six months, eating lots of fruits and veggies, lean meat (trimming the fat), very few starches, and nuts seeds avocados, olive oil, etc. In summer I began reading some blogs and books which recommended a diet higher in sat fats, lower in protein and lower in PUFAs, so I made some changes by severely limiting PUFAs (no more nuts, less fatty chicken and pork) and eating fattier red meat, coconut oil. I also cut down on veggies and fruits and added starches and white rice.

    While I would consider myself a little skeptical about the meaning of cholesterol tests, I am by no means an expert and was amazed by the increase in cholesterol and am very curious what this means and why. I understand that some of the numbers here (e.g. total cholesterol) don't mean much, that some of the numbers (e.g. hdl/tris ratio) are good, that LDL calc is often inaccurate, and that based on my low tris, my LDL is likely to be large and fluffy instead of small and dense. But I am still amazed by the rise and curious what it means. Should I be concerned? Why did this happen so fast? Thanks again for any guidance you can provide.

  • Dr. William Davis

    1/29/2009 10:33:00 PM |

    Frederick--

    While I don't make a habit out of responding to personal questions (because they would overwhelm time demands), your changes are quite profound.

    However, there are a number of underlying processes that could account for such a change. One solution would be to obtain lipoprotein analysis to see what the true, underlying patterns are, e.g., what is measured LDL?

    Also, consider thyroid issues.

    Also consider consulting the Track Your Plaque program, in which these discussions are conducted in detail every day.

  • Anna

    1/29/2009 11:13:00 PM |

    Frederick,

    While my numbers are not exactly the same as yours (past and present), they show a similar trend since I have adopted a more paleo-oriented diet, starting about 5 years ago.  The main difference is that I am female, 47 yo (not menopausal yet, and I wouldn't call myself athletic.  I really haven't been worried about the lab numbers, though they raise my endocrinologists eyebrows.  I had my first coronary calcium scan in Dec '08 and my score was 0, no evidence of coronary artery plaque.

    Have you had a coronary calcium scan yet?  That should tell you if your coronary arteries are building plaque or not.  And of course, the detailed analysis of your lipoproteins needs to be done, too, as Dr.Davis mentioned.  

    Keep in mind, the vast majority of the studies and references for  "good" or "bad" lab results in "Westernized" people come from people who *don't* eat paleo.  So there really isn't much of a comparison data base for those Westerners who eat paleo.  Peter at Hyperlipid blog has some discussion of this "lack of comparison data issue".

  • Anonymous

    1/30/2009 4:49:00 AM |

    Frederick,

    Please join us over on the Track Your Plaque membership website.  We routinely discuss issues such as yours, there is a wealth of information there beyond Dr. Davis' book, and we are a friendly, supportive, and well informed group.

    That aside, it appears you have gotten standard blood testing.  Please get an NMR lipoprofile, Berkeley or VAP test done... you will learn so much more.

    You were eating Paleo, but then you've cut out nuts and I see this little kicker: " I also cut down on veggies and fruits and added starches and white rice."  Hummmm... that is definitely not Paleo anymore, and if you are indeed carb sensitive, those additions could completely tip the cart and put you where you appear to be now.

    And I see that Dr. Davis has mentioned thyroid issues... get your doctor to test for those.  You are now "of an age" where these issues begin to express themselves.

    If you have not had one, go get a heart scan.  You will then know where you stand with regard to plaque formation.  BTW, I am talking about a simple heart scan, not the whiz bang 64-slice thing with the big dose of radiation.  Knowledge is power in this regard.

    I have no affiliation with Dr. Davis nor Track Your Plaque, other than as a very satisfied member/subscriber for the past several years.  I would feel alone and bewildered by such issues, were it not for TYP, which is IMO the most cutting edge program available.

    Good luck to you in finding answers to your personal situation.

    madcook

  • Nameless

    1/30/2009 9:25:00 PM |

    Frederick--

    Your rise in LDL... could it simply because you increased saturated fat intake? Your HDL also increased, which would make sense too. And trigs went down.

    Whether or not this is a good thing, I'm not sure. But increased animal fats usually equals higher LDL, higher HDL, lowered trigs (assuming fats replace carb intake).

    Have you measured your C-reactive protein before and after this diet change? I'm curious if saturated fats cause more inflammation, or less.

  • Dr. B G

    1/31/2009 2:12:00 AM |

    Frederick, Diana Hsieh:

    I don't worry about your LDL -- again it is a faulty inaccurate measure as Dr. D talked about in the 'Tale of Two LDL's post.

    Your TGs are Excellent!!

    Your HDLS totally ROCK and are the envy of anyone who knows anything about heart disease (or cancer).

    If you NMR'd or VAP'd your particles -- you would find that they are ALL Large, nice fluffy PHAT buoyant particles (just like Jimmy Moore's who has a similar diet/lifestyle as you two -- no grains, low carb, mod prot, mod-high fat and exercise).

    Likewise, you'll likely find that your HDL2b which are the regressive particles and necessary for optimal longevity and health will be stunning and awesome.

    Keep up the strong work and let us know if you get a particle count and density evaluated (~$99).

    -G

  • Dr. B G

    1/31/2009 2:12:00 AM |

    Frederick, Diana Hsieh:

    I don't worry about your LDL -- again it is a faulty inaccurate measure as Dr. D talked about in the 'Tale of Two LDL's post.

    Your TGs are Excellent!!

    Your HDLS totally ROCK and are the envy of anyone who knows anything about heart disease (or cancer).

    If you NMR'd or VAP'd your particles -- you would find that they are ALL Large, nice fluffy PHAT buoyant particles (just like Jimmy Moore's who has a similar diet/lifestyle as you two -- no grains, low carb, mod prot, mod-high fat and exercise).

    Likewise, you'll likely find that your HDL2b which are the regressive particles and necessary for optimal longevity and health will be stunning and awesome.

    Keep up the strong work and let us know if you get a particle count and density evaluated (~$99).

    -G

  • Anonymous

    1/31/2009 9:05:00 PM |

    Frederick-

    I think your changes are a simple result of "added starches and white rice".
    As you can see from this post from Dr. Davis just days ago, lipid levels can change dramatically and quickly with the added starches.


    http://heartscanblog.blogspot.com/2009/01/making-sense-out-of-lipid-changes.html

  • Trinkwasser

    2/2/2009 6:57:00 PM |

    Here's a big amen! to this post. My FBG is usually under 90 and never over 100. My GTT came back at 193 so "not diabetic" (I've since managed "truly" diabetic numbers by eating on top of a liver dump, but they are unofficial, measured on my own meter.)

    BMI about 22 so not overweight. Fit and active.

    So the ADA calculator still tells me I am at "low risk of diabetes" and that's what doctors have told me all my life despite the most horrendous lipids, including gallstones in my twenties, rising BP, episodes going back 50 years of what I now know to be reactive hypoglycemia (they knock my A1c right down)including ferocious night sweats in childhood. And of course all the other symptoms of diabetes, nocturia, chronic skin infections etc. all blown off because I didn't show that magic FBG rise.

    Curiously all these "neurotic" "hypochondriac" "anxiety" "depression" "pretending to be ill for sympathy" "personality disorder" symptoms have normalised by doing one thing: eating the exact opposite of the "Heart Healthy" diet - so long as I keep carbs to about 60g with the odd excursion to 100g or so I produce better numbers than a lot of "normies".

    Genealogical research shows the family is riddled with "metabolic syndrome" in non-obese people along with other diabetics who were also skinny Type 2s. I don't know how many other families, let alone individuals, have these obvious but not diagnosed type patterns.

    Or how many of them could be so comparatively easily treated.

    Well OK I cheat a bit, an ARB and a statin helps with the BP and LDL but they might not have been necessary if the thing had been caught earlier, or its comparatively slow progression hadn't been speeded up courtesy of the dietician.

    Yes it doesn't take a CSI to diagnose CIS. Just someone who looks at the Big Picture.

    My worst carbohydrate is wheat, spikes my BG about as bad as sugar, I can manage small quantities in the evening though. Fruit is nearly as bad except for berries.

    I shudder at all that healthy muesli I used to shovel into my face for breakfast and swill down with orange juice. I shudder more when I see the dietician's smile of approval.

    I can handle small quantities of oatcakes at breakfast, I favour high protein moderate fat and especially fish and salad, with other meats as a change. I can do ryebread in small quantities by lunchtime. I'd eat eggs if I could stand the taste.

    Carb input goes up on a slope from 15g at breakfast to 30g and sometimes 50g by evening. Masses of veggies, fish, meat, nuts and cheese and the occasional 85% chocolate make up the rest of my diet (oh and the coffee, and red wine, so not entirely paleo).

    None of this came from Medical Professionals in real life, it all came from the interweb and was run past my BG meter. Maybe by the 22nd century it will be mainstream and the Heart Healthy High Carb Low Fat diet will be consigned to the history books as a failed experiment on an entire population.

  • Dr. William Davis

    2/2/2009 10:38:00 PM |

    Trinkwasser--

    Thanks for sharing your wonderfully insightful experience.

    Do I have your permission to feature your comment as the focus of a blog post?

  • Trinkwasser

    2/6/2009 9:07:00 PM |

    You're more than welcome! I like to get my story out as it is a direct opposite of the standard "you made yourself ill through sloth and gluttony" accusation. Big major thanks must go to my late Aunt who did a lot of the genealogical research which discovered the pattern (she was told at 80 she had the blood pressure of a 30 year old, I was the exact opposite!) and died at 88 of an aneurysm: this despite being slightly overweight. So the genes can be survivable so long as we are careful!

  • Small business web site design

    4/3/2009 12:29:00 PM |

    nice  collection

  • Timothy Murphy, MD

    4/18/2009 4:14:00 PM |

    The amazing story of the ascent of the Keys Hypothesis regarding the connection between dietary fat and heart disease is well documented in "Good Calories, Bad Calories", by Gary Taubes.

    As a pediatrician, I do not often counsel about heart disease. But I do deal with obesity in children, and as I am now in my 50's, I am caring more because of my own health.

    The bottom line is that virtually everything we learned about preventing heart disease in medical school is wrong or untested, and an alternative hypothesis has existed that has been largely untested - yet is simpler (and therefore better).

    The role of glucose and insulin in the evolution of obesity and the development of heart disease is finally becoming clear(er), and with the definition of the Metabolic Syndrome, is becoming more "main stream". But the primary drivers of policy (NIH/NHLBI, FDA and ASDA) will not change their recommendations regarding carbohydrate intake.

    It is time for individuals to take charge of their own diet, and the information I have found here is all to the good. I am glad I found this blog.

    TM, Pittsburgh

  • Kelvin

    9/4/2009 12:45:22 PM |

    I am a classic CSI class and after running 5km for 1 1/2 years my blood stayed CSI classic as well, I didn'y follow a good diet but kept my weight down due to excerise - so then it happened - ventricle fibrulation - down for 6 min not breathing while I was shocked and had CPR - had bypass surgery - 46 yrs - read my story google "A hug for his life savers". Following a low card diet now my email is kwillikj@gmail.com

  • buy jeans

    11/3/2010 2:41:40 PM |

    Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.

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

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

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

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?

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

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?

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

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

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

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

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.