Pre-diabetes: An explanation for explosive coronary plaque growth

Art's first CT heart scan in March, 2006 yielded a concerning score of 1336. He felt fine--no chest discomfort, no breathlessness, etc.

Art agreed to take the statin cholesterol drug his primary care doctor prescribed. He also agreed to take the fish oil, niacin, and some of the nutritional supplements that we advised. But Art just couldn't bring himself to make the commitment to lose weight.

At the start of his program, Art--at 5 ft. 8 inches--was 40 lbs overweight (212 lb). This was important since his blood sugar wavered in the pre-diabetic range, going as high as 130 mg. (The American Diabetes Assn. defines diabetes as a blood glucose of 126 mg or greater.)

One year later, Art's lipid and lipoprotein values were corrected to perfection. But he still weighed in at a hefty 209 lbs--essentially no change. His blood sugar likewise hovered in the 120's.

I felt Art need to be prodded, so I asked him to undergo another heart scan. His score: 1935--a 600 point increase, or 45%!

Only now has Art begun to comprehend to power of diabetes and pre-diabetes to fan the flames of plaque growth. Recent published data, in fact, show that the majority of recently diagnosed diabetics already have well-established coronary artery disease.

Don't let this happen to you. Do not dismiss diabetic patterns as they will catch up to you. If Art can lose the 30-40 lbs in the abdominal weight that is creating the diabetic pattern, he will likely succeed in stopping plaque growth. Otherwise, it's just a matter of time before his heart attack, stent, or bypass.

Who cares if you're pre-diabetic?

Marta is a smart lady. She's worked in hospital laboratories for the last 23 years and knows many of the ins and outs of lab tests and their implications.

After years of being told that her cholesterol was acceptable, she needed to undergo urgent bypass surgery after experiencing severe breathlessness that proved to be a small warning heart attack at age 57. But this made Marta skeptical of relying on cholesterol to identify heart disease risk.

I met Marta two years after her bypass surgery when she was seeking better answers. And, indeed, she proved to have several concealed sources of heart disease: small LDL particles, Lipoprotein(a), intermediate-density lipoprotein (IDL--a very important abnormality that means she is unable to clear dietary fats from her blood), among others. But she was also mildly diabetic with a blood sugar of 131 mg (normal < or = 100 mg). This had not been previously recognized.

As I'm a cardiologist and our program focuses on reversal and control of coronary plaque, I asked Marta to return to her primary care doctor to continue the conversation about diabetes. She was a bit frightened but followed through.

"Well, you're not urinating excessively. And your long-term measure of blood sugar, hemoglobin A1C, is still normal. I wouldn't worry about it. We'll just watch it."

I guess I should know better. What the poor primary care doctor doesn't know is that pre-diabetes and mild diabetes are potent risks for heart disease. In fact, some of the most explosive rates of plaque growth occur when these patterns are present. It's well established that risk for heart attack in a diabetic is the same as that of someone who's already suffered a prior heart attack--very high risk, in other words.

Marta's primary care doctor's advice would be like inquiring about cancer and the doctor says "Let's just wait until it's metastatic--then we'll start to worry." Of course, this is insane.

Pre-diabetes and mild diabetes should not be ignored or just "watched". Even though the blood sugar itself may not be high enough to endanger you, the hidden patterns underlying your body's unresponsiveness to insulin creates a torrent of hidden coronary risk.

For better answers, Track Your Plaque members can read "Shutting Off Metabolic Syndrome" at http://www.cureality.com/library/fl_dp001metabolic.asp on the www.cureality.com website. ("Metabolic syndrome" is the name commonly given to the constellation of abnormalities associated with pre-diabetes and diabetes.)

Don't get smug!

It may sound silly, but after someone succeeds in stopping their heart scan score from increasing or reduces their score, I warn them to not get smug. Let me explain.

I'll tell you about Jack. I met Jack a few years ago after he had a heart scan at age 39. His score: 1441! A score this high at his age obviously puts him in the 99th percentile. Also recall that a score >1000 carries a 25% annual risk for heart attack.

This captured Jack's attention. At the start, his lipoproteins were disastrous with numerous abnormal patterns. Jack committed to the program. After one year, his lipoproteins were around 80-90% corrected towards perfection. He'd lost 27 lbs, was exercising six days a week, and felt great.

Jack's repeat score one year later: 1107--over a 300 point drop! A huge success. He was ecstatic.

Unfortunately, work and life in general distracted him. Jack allowed himself to drift back to old habits, indulging in fast food 2 or 3 times a week, slacking on exercise such that it became sporadic, half-hearted efforts, and regained 15 lbs. He even failed to show up for appointments and we lost contact for two years.

One day, Jack simply decided to see where he stood, so he got himself another heart scan. The score: 2473--over a doubling from his reduced score.

The message: Long-term consistency is key, even after you've achieved control over your score. Stick with your program--and don't get smug!

Holidays are dangerous!

If you're on holiday from work today, make sure you're not on holiday from your health, too.

Too often, people come back to the office telling me that the holidays simply got out of hand--cookouts, picnics, family gatherings, etc.--and they simply couldn't avoid overeating, overdrinking, sitting around--and gaining 3-5 lbs in a weekend. (Our record is 10 lbs in a weekend!)

I don't want to harp on this issue and ruin your holiday, but I can't stress how important it is that you don't allow this to happen to you. Weight gained in a brief space of time has exceptionally destructive effects. Ever see the movie "Super Size Me"? It's an entertaining and well-done yet graphic portrayal of the damaging effects of rapid weight gain.

Enjoy your time off. Relax, enjoy your family and friends--but continue to pay attention to choosing the right foods, don't overeat, take time out to do something (or several things) physical. It'll pay off hugely in the long run.

More on carotid plaque...

Although not a perfect test, carotid ultrasound is an exceptionally easy and accessible test. Using high-frequency sound, clear images are available for most people.

I say it's not perfect because the way it's done in 2006 makes it a non-quantitative test. It is a qualitative test. In other words, you may find out that there's a 30% blockage ("stenosis"), at the far end of the common carotid artery on the right side. Unfortunately, this gives you an isolated measure of diameter of the plaque compared to the artery. What it does not tell you is what the volume of the entire plaque is. That's a far more accurate measure (and one that is incorporated into your heart scan score, by the way).

Nonetheless, carotid ultrasound is easy, very safe, and available in most hospitals and many clinics. One difficulty: most insurance companies will not allow you to go through a carotid ultrasound scan as a "screening" procedure, i.e., a test just to see if you have a carotid plaque. They will generally pay if you're having symptoms of a stroke or "mini-stroke" (transient ischemic attack, or "TIA"), have an abnormal sound in your carotid ultrasound detected by your doctor (a carotid "bruit"), or some other unusual indications. Sometimes, a resourceful physician will muster up a diagnosis based on something in your history (e.g., left arm numbness, a common and often benign complaint that can also signal stroke).

Another option are the mobile scanners or some hospital services that offer carotid screening, usually for a very modest price. Drawback: Sporadic availability, difficulty in obtaining serial scans, and imprecise reporting since it's viewed as a screening test. But it's better than nothing.

My hope is that, as screening services using safe imaging techniques like ultrasound propagate and increase in direct availability to the public, you'll be able to circumvent the obstacles imposed by your insurance company and even, sometimes, your doctor. But try your doctor first.

Carotid plaque can be shrunk

Rose, a 64-year old woman, just had a 70% carotid blockage identified by a screening ultrasound. When the result was given to her doctor, he prescribed Lipitor and told Rose that an ultrasound would be required every year. She would need carotid surgery, an "endarterectomy", if the blockage worsened.

"Can't I reduce the amount of blockage I have?" asked Rose.

"No. Once you've got it, it doesn't get any better."


Is this true? Once you've got carotid plaque, you can only expect it to get worse and it can't be reduced?

This is absolutely not true. In fact, compared to coronary plaque, carotid plaque is easier to reduce!

Of course, the Track Your Plaque program is designed to help you control or reduce coronary plaque. But, in our experience, people who have both coronary and carotid plaque will show far greater and faster reduction of carotid plaque. Dramatic reductions are sometimes seen. I've personally seen 50-70% blockages reduced to <30% on many occasions.

The requirements to achieve reduction of carotid plaque are very similar to the approach we use to reduce coronary plaque. One difference is that hypertension may play a more important role with carotid plaque and needs to be reduced confidently to the normal range before carotid plaque is controlled.

I find it shocking that the attitude like the one provided by this physician continue to prevail. Unlike coronary plaque, which has a relatively small body of scientific literature documenting how it can be reduced, carotid plaque actually enjoys a substantial clinical literature. Part of the reason is that the carotids are more easily imaged using ultrasound. (Heart structures can be seen with ultrasound, but not the coronary arteries.)

Numerous agents have been shown to contribute to reduction of carotid plaque: statin drugs, niacin, fish oil, the anti-diabetic "TZD" drugs (Actos, Avandia), several anti-hypertensive drugs, vitamin E, pomegranate juice, and several others.

It outrages me to hear stories like this. Rose is not the only one.

Don't accept the flip dismissals or the over-enthusiastic referral for carotid procedures. Insist on a conversation about plaque regression.


Note: Although I am a vigorous advocate of atherosclerotic plaque regression, this does not mean that if you have a severe (70% blockage or greater), or if there are symptoms from your carotid disease, that you should engage in a program of reversal. You must always take the advice of your doctor if your safety is in question.

Vitamin D--A coronary risk factor

Look up "coronary risk factors" in any text and you'll find high cholesterol, smoking, diabetes, and high blood pressure listed. You won't find deficiency of vitamin D listed.

Ask 99% of physicians if a deficiency of vitamin D is a coronary risk factor and you'll get rolling eyes and a sigh.

Yet, in the Track Your Plaque experience, vitamin D is emerging as a very important factor in coronary plaque development. We have observed that there are a substantial number of people whose lipids and lipoproteins are not abnormal enough to fully explain their heart scan score. In other words, there seems to be something else necessary to satisfactorily explain the magnitude of coronary plaque.

I believe that severe vitamin D deficiency is at least one of the most important factors. We've seen many people with blood levels of vitamin in the range of severe deficiency (<20 ng/ml of 25-OH-Vitamin D3) yet bland lipids and lipoproteins.

Correcting vitamin D blood levels to 50 ng/ml also seems to be among the required factors in stopping coronary plaque growth, or stopping your heart scan score from increasing.

Keep your eye on this extremely important and exciting issue. Sadly, it won't be propelled into the media like the conversation about cholesterol or high-tech procedures, since no company stands to profit from it. But you and I don't have to play that game.

Cholesterol is dead!

I saw a patient in the office yesterday. He came to me for an opinion regarding his high heart scan score of 525, putting him in the 90th percentile (5% annual risk of heart attack).

His doctor had been puzzled because his LDL cholesterols had ranged from 110 to 131 mg--actually below average. (The average LDL for the U.S. is 132 mg.) Likewise, HDL was a favorable 63 mg.

Lipoprotein analysis told the story loud and clear. His LDL particle number, a far more precise measure of LDL, was 2448 nmol/l. This means that his true LDL was more like 240-250 mg! (You can get a sense for what the true LDL is from LDL particle number by dropping the last digit: 2448 becomes 244.) Conventional LDL was therefore inaccurate by over 100 mg.

He also had a severe small LDL particle pattern. The cause of his coronary plaque was a large excess of small LDL particles. LDL cholesterol (and total cholesterol, likewise) didn't even hint at this pattern. Nor did his favorable HDL.

Think of LDL particle number as an actual count of LDL particles per volume, e.g., number of particles per cc of blood. This makes it easier to conceptualize. LDL particle number is the measure you get when you have an NMR lipoprotein profile, our preferred method of lipoprotein testing. If this is unavailable to you, apoprotein B is a reasonable second choice, though not as accurate in my view. More info on NMR is available at their website, www.lipoprofile.com.

How to make a $1 million in cardiology

Want to make a $1,000,000 as a cardiologist in the next year? It's easy. All you have to do is:

1) Perform heart catheterizations or other procedures on anybody you can, even if it's not necessary. Perform them even if the patient has no symptoms and the stress test is normal.

2) Perform heart catheterizations if the patient is too timid or ill-informed to object.

3) Insert coronary stents in blockages, even when they're minor and it's not necessary.

4) Turn every heart procedure into a revenue-producing stream by looking for other profit opportunties, such as minor kidney artery blockages.

5) Heart disease is frightening. Scare the heck out of patients by exagerrating the dangers so they'll go through testing and procedures gratefully.


Sound absurd? Well, it would be if these weren't all true.

These are real examples, as awful as it sounds. I've witnessed all these behaviors. Not just occasionally, but with regularity.

Just today, I encountered a colleague who performs heart catheterizations routinely (up to several per day) when any symptom is present and the stress test is entirely normal. This is grossly inappropriate.

Your protection is being better-informed and avoid being sucked into the vast and frightening cardiovascular machine of revenue-yielding procedures. Part of your protection is to get a CT heart scan, then engage in a program of heart disease prevention.

Doctor, do I have lipoprotein (a)?

I met Joyce today for a 2nd opinion. She told me about this conversation she'd had with her cardiologist:

"Doctor, do you think I could have lipoprotein (a)? I read about how it can cause heart attacks even when cholesterol is controlled."

"What does it matter? Even if you have it, there's nothing we can do about it. There's no treatment for it."

Joyce was understandably groping for some means to prevent her coronary disease from causing more danger. At 56, she'd already survived a heart attack that resulted in two stents to her left anterior descending. Around 9 months later, she received a 3rd stent to another artery.

Her doctor had put her on Pravachol and said that was enough. "We know that cholesterol causes heart disease and the Pravachol reduces it. Why do we need to know anything more?"

So Joyce came to me for another view. I explained to her that there are, in fact, several ways to deal with lipoprotein(a). It is, without a doubt, among the more difficult patterns to manage--but not impossible. In fact, we have a growing list of participants in the Track Your Plaque program who have stopped or reduced their heart scan scores.

I continue to be horrified at the level of ignorance that prevails among my colleagues, the cardiologists, and the primary care community. If your doctor gives you advice like this, get a new doctor.
One hour blood sugar: Key to carbohydrate control and reversing diabetes

One hour blood sugar: Key to carbohydrate control and reversing diabetes

Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Comments (27) -

  • Might-o'chonri-AL

    8/2/2011 6:11:40 AM |

    Glyco-sylation occurs inside a cell's endoplasmic reticulum lumen when certain  carbohydrates  (in the form of N-linked oligo-saccharides) meld with a newly folded protein that gets translated into  a glyco-protein.  There are different rates of activation and de-activation  between glyco-sylated and un-glycosylated proteins; this affects how that protein migrates as it tries to perform it's job and how  glycation can induce degenerative states.  Tissue cells with endoplasmic reticulum stress can exasperate certain disease progression because such "stress" there promotes more glycosylation.

  • Annabel

    8/2/2011 12:40:42 PM |

    I couldn't agree more with the advice to test every 15 minutes as a means of discovering your own "sugar curve." When I tried this, I found that my own peak falls pretty consistently at 75 minutes after beginning a meal. Testing at 2 hours completely overlooks my highest blood glucose levels.

    It's a particularly good technique for those folks whose A1c levels are higher than their fingersticks would predict...it's almost surely because they're doing their sticks way past their glucose peak.

    When test strips cost up to a buck apiece, it may feel hard to justify using six or eight of them on a single meal--but what you learn may save tens of thousands in medical bills!

  • Curt

    8/2/2011 1:31:12 PM |

    Another great article - thank you! I'm curious about your thoughts on controlled 1 hour blood sugars (mine are rarely over 110) but baseline levels that aren't much lower. Typically in the 95-105 range. I will get something in the 80s occasionally, but 100 is more common. I never really spike - even a high carb meal will only get me to 130s or so and that never really happens as I don't eat much sugar/starch at all.

    Another quick question: You've mentioned a couple times recently about this way of eating being particularly good for VISCERAL fat. That is exactly what I've found. Tremendous benefits and I feel great. I have leveled out for a while (months) in fat loss, however, with a good amount of subcutaneous fat still present. Is there another protocol for getting after this type of fat? I'm already no wheat, low carb, paleo.

    Thanks again for your excellent articles! Always learning something new.......

  • ShottleBop

    8/2/2011 1:38:20 PM |

    Do you have citations to support your statement that glycation occurs at BGs of 100 or more?  This is one of the more-commonly discussed issues on diabetes discussion boards--but folks are wont to ask for backup.

  • Jeff C

    8/2/2011 1:47:11 PM |

    Regarding glycation specifically...

    1. Do you agree that fructose ("frucation") causes more AGE than glucose?
    2. What to you make of Ray Peat's assertion that poly-fats are much more glycalating than glucose?

    "The so-called "advanced glycation end products," that have been blamed on glucose excess, are mostly derived from the peroxidation of the "essential fatty acids." The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do." (Fu, et al., 1996)." - Ray Peat

  • Richard

    8/2/2011 3:21:55 PM |

    Thanks for the great article!
    I've just begun tracking blood sugars closely, changed my diet to one very low in carbs and no grains, and am determined to find ways to keep at it. I've started a blog just track my progress and keep me honest: http://transformation-transformative.blogspot.com/
    I'll also try the 15 minute testing to see where my personal peak in blood sugar occurs.
    Again, many thanks!

  • steve

    8/2/2011 3:31:08 PM |

    Hi Dr. Davis:  What is the relationship between fasting BG taken at the Dr's office and A!C?  My fasting BG level is 73.5 but my A1C is 5.4.  I would have expected the A1C to more correspond to the fasting measurement; in the case of my wife it does.  Is it related more to the red blood cells lingering around longer or lipoprotein particles which increases the chance of glycation?  Recently had a larger than normal amount of carbs in a meal- rice and blueberries and BG spiked to 119, not to bad, but will experiment with carb portion to keep under 100 as BG may be a contributing factor to my CAD.  I am also a hyperabsorber of fat despite being an ApoE 3/3.

    As an aside, i have sent around a link of one of your interviews regarding Wheat Belly and many eyes have been opened as well as many looking to buy the book.  Might not be a bad idea to have a link to any of your interviews on Wheat Belly posted to this site.
    Thanks for the enlightening good work!

  • Dr. William Davis

    8/3/2011 12:23:09 AM |

    Hi, Shottle--
    This will be the topic of an upcoming discussion. The documentation of this effect is quite extensive. It is no longer a matter of "if" but "how much."

  • Dr. William Davis

    8/3/2011 12:25:11 AM |

    Hi, Jeff--
    This is one of oranges and apples comparisons.
    Fructose does indeed induce flagrant glycation. Glucose induces glycation, though less vigorously.

    However, there is a separate but very poorly named process called exogenous glycation which has less to do with glycation than with oxidation of fats.

    This will be the topic of future discussions.

  • Dr. William Davis

    8/3/2011 12:26:22 AM |

    My first thought is that, if weight loss is ongoing, there is a temporary situation of insulin resistance that generally dissipates with weight stabilization.

    It's also possible that your pancreas has inadequate baseline production of insulin. I'm hoping it's the first possibility.

  • Dr. William Davis

    8/3/2011 12:28:05 AM |

    Hi, Steve-

    You will find that, if you did frequent fingersticks around the clock, the highish A1c reflects the higher blood glucose values that occur after meals.

    Thanks for the feedback on the Wheat Belly project. I will indeed crosslink some of the more relevant discussions.

  • Might-o'chondri-AL

    8/3/2011 2:39:31 AM |

    Advanced glycation end products (AGE) involve some of haemoglobin's hydro-carbon Beta side chain valine residue linking up to non-polar "glucose" aldehyde compounds and certain non-"glucose" aldehydes. Various pathological kinds of AGEs can occur from distinct events; in one situation it is macrophage activity producing enzymatic myelo-peroxidase, which can activate hypochlorite favoring a serine amino acid wing to form up to make the AGE called glyco-aldehyde.

    Probably the AGE called methyl-glyoxal is the one most relevant to diabetes prevention; since Type 1 diabetics blood serum levels of methyl-glyoxal is +/- 6 times higher than normal. This AGE can be formed when the byproduct triose-phosphate (triose = subset of carbs) is generated from the glycolytic pathway called  Embden-Meyerhof; this  byproduct risks being made into methyl-glyoxal.

    Maybe the most well known AGEs are the non-enzymatic Amadori products formed via hydrolysis; one is called glyoxal coming from glucose oxidation. And the other Amadori type AGE is 3-deoxy-glucosone (3DG), which requires fructo-selysine and the fructos-amine 3 kinase cascade to shuffle together 3DG.

  • Might-o'chondri-AL

    8/3/2011 2:40:38 AM |

    Diabetes reveals the problem with AGEs; this is because diabetics risk incurring kidney nephro-pathy, One of the pathological results is oxidative kidney stress, which limits sodium (Na) excretion thereby fostering  hyper-tension . When AGEs like 3DG, glyoxal & methyl-glyoxal  (among others, like pentosidine ) circulate into the kidneys their carbonyl compounds  are hard to clear by the kidneys; the side effect is to engender  uric uremia problems and meanwhile levels of carbonyls build up in what is called "carbonyl stress".
    Japan research of the plant compound chamaemeloside found that in humans it lowered levels of the AGEs 3DG & pentosidne better than any other natural remedy; optimal response was reduction of down to 1/5 th of subject's starting levels.  Chamaemeloside is the active compound in chamomile (Anthemis noblis); the extraction formula was 1 Kg of chamomile flowers steeped covered in 20 Lt. water for 3 hours at 80* celcius ( a lab temperature probably not critical for home remedy preparation).

  • Peter Silverman

    8/3/2011 12:56:13 PM |

    Volek and Phinney in their new book about carbohydrate restriction think that as you increase  fat from 30% to 60% of your diet, insulin resistance increases, then it drops when you go above 60%.  It seems that among the most experienced researchers of carbohydrate restriction, there's little consensus about the optimal amount of fat or carbs.  Ron Krausse, for instance, thinks 35% to 45% is optimal.

  • steve

    8/3/2011 5:23:50 PM |

    Peter:
    When these researchers talk about carb levels are they considering vegetables to be carbs, or just fruits, grains, potatoes?

  • frank weir

    8/3/2011 6:41:32 PM |

    You must mean, "can exacerbate certain disease progression...." meaning: to increase the severity, violence, or bitterness of; aggravate

  • frank weir

    8/3/2011 6:59:22 PM |

    This is wonderful information BUT I wonder if it might be unfortunate if folks who routinely have post-prandials of 120 to 140 take your 100 level as a sign of "failure"...things are seldom so cut and dried, black and white. I don't know if I'm hitting 100 or less  after every meal, but my A1C has dropped from 7.5 to 5.8 since last November restricting carbs. And I've lost 30 pounds. I will begin to be more dogmatic about one-hour glucose checks but my rough sense is that I'm not at 100 or less a majority of the time. But I might be wrong about that. Do you see what I'm getting at? Glucose control is an ongoing process that includes lots of self education since most GP's are not keen AT ALL on restricting carbs, including mine. When I read your post, my initial feeling was, "Cripes, 100 after EVERY meal? Don't think I can do that...."

  • Might-o'chondri-AL

    8/4/2011 1:05:26 AM |

    From another commentator here, in an  earlier thread of Dr. Davis' here is how to use HbA1c to determine your average blood glucose level (note: this is not a morning "fasting" level) .
    1st: multiply your HbA1c by 28.7
    2nd: subtract 46.7 from 1st amount
    3rd: take last number as your average waking hours mg/dL blood glucose over last  few months  
    ex:  HbA1c of 5.4 x 28.7 = 159.98 minus 46.7 = 108.28 mg/dL of average blood glucose level

  • Peter Silverman

    8/4/2011 2:24:31 AM |

    They don't count non-starchy vegetable as carbs.

  • ShottleBop

    8/4/2011 3:15:11 AM |

    Thanks for the heads up!

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  • Stephanie

    8/4/2011 2:13:27 PM |

    Dr. Davis,
    I have found that if I take my carb level too low (below 50g per day) that my fasting blood glucose levels actually go up rather than down.  If my carb intake is closer to 70-80, my fasting glucose is lower.

    Have you had this experience with some of your patients?  Can you shed any light onto what might be happening?

    Thanks!
    Stephanie

  • Anne

    8/4/2011 2:34:11 PM |

    Non-starchy vegetables do have carbs and I do have to count them. A half cup of broccoli can have about 6 carbs and since I limit my carbs to no more than 15g/meal, that broccoli on my plate is significant.

    I found getting a scale that reads carbs too was an important tool for me. I found I was ofter overestimating how much of a low carb veggie I could eat. If my blood sugar starts to rise, I go back to measuring and that seems to get me back on track.

    Anne

  • majkinetor

    8/14/2011 1:25:56 PM |

    I think thats normal, its commonly encountered on paleo forums/blogs. It has something to do with physiological insulin resistance, Petro @ Hyperlipid talked about. Look here:

    http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html

  • majkinetor

    8/14/2011 1:38:24 PM |

    I wouldn't suggest that everybody blindly follow CHO < 50g / day. As always, its about the context. People usually forget that. We mostly extrapolate from results of people who already have metabolic problems.

    Anyway, I am currently perfectly healthy apart from some minor dermatology problems (eczema).
    When I have prolonged periods of reduced CHO input (around 50g / day), I eventually start having some mucus problems. Dry eyes particularly, but also joint pain. I am not 100% sure if its about low carb diet, but it looks like it. Now I target 75g < CHO < 100g per day by adding small potato and a bit more chocolate to my diet.

    I think overemphasizing carb reduction is not good thing for most people. Carbs should go down by pretty big amount for most people, but not to extreme. In anyway, its better to measure then to guess. My sugar is never above 110 after meal and fasting is always around 95.

  • John F

    8/13/2012 9:48:10 AM |

    I decided to take this advice and have been tracking my 60 mins postprandial blood glucose for the past two days to see if all the years I've been low carbing have been making any difference. Especially working my way through different foods to see how they affect me and I've ranged from 64 mg/dl to 97 mg/dl so I'm pretty hapy.

    However this evening 60 minutes after my dinner of panfried steak with a creamy cajun sauce I got a reading of just 55 mg/dl. A lot of websites say this is too low. I'm 32, healthy male, 5,9", weigh 160 lbs, not diabetic and I don't feel sick so I'm not sure what to make of this low reading. The only thing I did was finish a hard CrossFit workout about 30 mins before I had dinner... so a total of 90 minutes before the blood glucose test.

    Any advice on what this "low" reading means? I'm hoping it's normal and means I'm burning fat!

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