What's that in your mouth?




Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

De Novo Lipo-what?

Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):





From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.


Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

Gretchen's postprandial diet experiment II

I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A wheat-free 2010

A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:


Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.


Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.



Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase and you

Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

If you take niacin, you must exercise

We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

To track small LDL, track blood sugar

Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Blood glucose 160

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

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

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

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

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

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

Comments (28) -

  • Pater_Fortunatos

    2/25/2011 8:20:12 PM |

    There are lot of unusual and interesting formulations you are using, but I really can't understand the meaning of this one:

    "Glycation and of LDL particles."

    Maybe my english is not the best (I am no native english speaker).Maybe you could enlighten me?

    About the article. Now I realize that during 35 years of life, I had lots of such glycemic  values and not having any idea about effects.
    Do you have any ideea about glycemic index if I eat quite a lot of fruits? (can't control it lately).

    Thank you!

  • Might-o'chondri-AL

    2/25/2011 8:50:30 PM |

    Hi Pater_F.,
    I just read this post too, so see your quote shows a word to edit out. Remove the word "and", then it reads correctly "Glycation of LDL ...."

  • Flavia

    2/25/2011 9:05:59 PM |

    Hi Dr. Davis,

    What do you think is a safe amount of carbs to eat in one sitting? No more than 50 maybe? What really gets me is the aging!! I do not want wrinkles!

    For a 5'4, 125lb woman, what would you recommend is the top limit of carbs to have per meal to avoid this?

  • susan

    2/25/2011 10:54:14 PM |

    Thanks for the info about how the body handles high glucose levels. Funny you should mention a glucose of 160…

    I generally stay with the low carb lifestyle. I’ve been checking my glucose on a fairly regular basis and it generally runs in the high 80s to high 90s. Exercise can bring it down to mid 70s. Fasting levels are creeping up into the low 100s.

    Late yesterday afternoon, however -- after a good low carb day -- I succumbed to my baser urges and consumed several handfuls of mini Reese’s PB cups. Pretty dumb, I know.  

    2 hours later, BG = 161  -- whoa, I guess that was even dumber than I thought
    After a good low carb dinner, BG = 99  -- respectable, considering  
    This morning’s AM Fasting BG = 150 – what the heck??  (it’s been running a little high, but not that high
    Large coffee w/ cream on the way to work, BG = 118  -- getting there, slowly  
    Low carb breakfast and lunch, BG = 113  -- wow! Never dreamed it would take this long  

    Well, I knew it was a stupid thing to do. Now I know how stupid it really was. I’m sure my BG will continue to come back down to a reasonable level. I’ve been toying with the idea of rejoining the gym and starting the Slow Burn program. Guess it’s time.

  • Dr. William Davis

    2/26/2011 12:41:00 AM |

    Thanks for catching the typo, Pater and Might.

    HI, Flavia--

    It is truly an individual thing. For some, it's 20, 30, or 50 grams. For others, it's zero.

    Body size, age, genetics, recent exercise, et. all enter into the equation. This is why I am a fan of checking postprandial blood glucoses.


    Hi, Susan--

    It can really be a sobering experience. When this happens to me, I feel awful for several hours, sometimes all day. I've learned that it's not worth the momentary indulgence.

  • belly fat exercises

    2/26/2011 7:22:01 AM |

    Yes insulin lowers blood sugar levels by converting glucose to glycogen which is stored in the liver and by increasing cell permeability to glucose.

  • Might-o'chondri-AL

    2/26/2011 8:41:02 AM |

    Individual liver condition may influence how dangerous the blood sugar reaction actually is.

    "Fasting, overnight, trigs (triglycerides) are mostly bound to VLDL. But once eat there are trigs complexed to chylomicrons (from the intestine), IDL (intermediate density  lipo-protein, a VLDL spin off), in standard VLDL and even HDL.

    HDL, "good" lipo-protein, is the returner of cholesterol from the peripheral regions of the body back to the liver; it too carries trigs. In the liver hepatic trig lipase enzymes hydrolize (cleave) off the HDL's trig load; and those trigs can then get complexed to both IDL and chylomicrons.

    The re-circulated trigs add to the new trigs certain foods generate. When we look specificly at LDL bound trigs those trigs were passed on over from VLDL trigs, whether if were freshly tagged onto VLDL or from overnight fasting VLDL trigs.

    In the case of chylomicron trigs and IDL trigs the lipase enzymes in the adipose (fat) tissue and
    intestine, as well as triglyceride lipase enzymes in the liver, cleave those trigs into component free fatty acids and glycerol. In practical terms that's when we get fat in a form we can "get fat" from.

    Fat in the liver tissue also causes extra fatty acids to go out into the blood stream and, among other tissue, into skeletal muscles. The muscles of course do have the potential to use fat as fuel.

    Only problem is when insulin resistance starts to develop progressively in the liver, when fat in there messes with our trig balancing act. The back log concentration of intra-hepatic trigs is one of the conditions
    when post meal hyper-insulinism is dangerous.

    Then there is a further complication. When insulin resistance starts to go on outside the liver those peripheral tissues keep performing lypolysis. They are
    trying to burn fat while waiting on blood glucose stuck outside their cells. So even more freed up fatty acids go back in the blood to burden the liver.

    At this stage the liver
    can't re-esterfy (break back down) the burden of free fatty acids into trigs. So more gets built into fat inside the liver and eventually can lead to blockages (steatosis). It is a vicious cycle looping trigs and free fatty acids in a double "whammy" on the liver.

    To recap the immediately preceeding. A new/young/healthy liver takes in a meal, produces some extra trigs and sends it out tagged to VLDL. Once liver damaged/old/fat there are high levels of free fatty acids in circulation, the liver response to insulin drops (liver insulin resistance), the liver passes along meals glucose but the skeletal muscles are full of trig derivatives (di-acyl-glycerides, to be precise), so the muscles don't pick up the glucose either.

    Once an individual's liver fat is interfering with things to an even worse degree there are further complications. Namely the trigs complexed to VLDL get out of the liver less and it is mostly chylomicron trig and IDL trig complexes circulating in the blood.

    In fact, a measurement where total trigs keeps dropping can
    indicate chronic liver disease. And in hepatitis the physical synthesis of VLDL is
    progressively reduced; the virus inhibits protein movement in the liver microsome needed for VLDL production.

    Remember there is a liver triglyceride lipase enzyme. It has several functions and can act as a binder for many other lipoproteins, including LDL.

    Individuals who geneticly, or due to pathology (like in hepatitis), produce too little of this enzyme have another problem. This enzyme insufficiency makes the blood
    level of HDL complexed trigs keep rising (trig can't be cleaved off HDL who brought it back to liver)so HDL can't do it's "good" cholesterol job.

    The same enzyme insufficiency also lets trigs complexed to LDL, IDL and chylomircrons become elevated in the blood stream.

  • Might-o'chondri-AL

    2/26/2011 9:04:46 AM |

    Cut off my post's theory, too long.

    If individual has no fat in the liver (or minimal liver fat that is not enough to mess up trig metabolism), then blood sugar spike generated trigs not a problem. This can be genetic propensity, liver circadian rhythm co-incidence &/or life style.

    Those laying down liver fat, geneticly impinged &/or life style disadvantaged seem to be getting good advice from Doc.

  • Anne

    2/26/2011 1:14:56 PM |

    Watch out if you are in intensive care. The American College of Physicians now recommends that blood sugar be maintained between 140-200mg/dL. Their main concern is blood sugar going too low. In Hospital Blood Sugar Levels Should be Higher

    They will also feed you an ADA approved high carbohydrate diet to guarantee those highs.

  • Nigel Kinbrum

    2/26/2011 3:05:29 PM |

    @Dr. Davis: Are those your own BG readings after eating oatmeal? If low-carb/keto adapted, eating a pile of carbs is a bad idea as glycolytic pathways are down-regulated.

    @Anne: How about wearing a bracelet with important medical information on it in the event of becoming unconscious?

  • Anonymous

    2/26/2011 3:09:43 PM |

    These recent blog entries regarding blood sugar are extremely simple even to the point of being vague.

    I have found a site that goes into great detail regarding blood sugar, its control, and the problems associated with both high and low blood sugar levels. The blogs entries are so successful that they were edited and published as a book.

    The author continues to blog weekly and includes practical detail, as well as references to current medical science. Don't let the label "diabetes" throw you. There is a tremendous amount of information regarding how to avoid T2DM with improved blood sugar control. How and when to check your blood sugar, using your meter to determine the impact of what you eat on blood sugar, the deleterious effects of higher than normal blood sugars, even what is normal sugar are all addressed and in useful detail...there are even discussions regarding low carb and paleolithic diets. If you want 5-10 quickly and poorly written sentences on a topic, read the HeartScan blog. If you are interested in reading entire well written intelligent essays visit these sites below. I think that the "MD" label misleads many readers. Don't let the fact that the writer of the Blood Sugar 101 sites is not an "MD" throw you. She is a diabetic and has lived with it for several years. Her approach to medical treatment is that it should be "evidence-based" which seems often missing from other sites.

    Take a few minutes to review,

    Blood sugar 101 (general information site)
    http://www.phlaunt.com/diabetes/

    Associated blog site
    http://diabetesupdate.blogspot.com/

  • Anonymous

    2/26/2011 4:59:13 PM |

    What happened to the post about the Blood Sugar site? It seems to have been deleted. I am sute that I saw it here earlier. Does anyone know the url for the site. it looked interesting.

  • Anonymous

    2/26/2011 6:45:18 PM |

    yeah i saw it too. seems poster was a bit critical of Dr. Davis last several postings. sorry don't have the web sites mentioned. didn't know that you could delete a post that you don't like.

  • Anonymous

    2/27/2011 2:30:17 AM |

    @ Anne,

    In the ICU, there is risk with both too high and too low a blood sugar.  Perhaps 140-200 is an unhappy medium where risks are balanced.

    'Recent research, including a study in the Feb. 15 issue of the Annals of Internal Medicine, has found that the use of intensive insulin therapy comes with an increased risk of low blood sugar (hypoglycemia) which can be deadly. The study also concluded that using intensive insulin therapy to significantly lower blood sugar levels isn't associated with greater improvements in health outcomes.'

    Many ICU patients aren't eating anything anyway.  It isn't until after they are on the general medical floor that the ADA diet is given, and their sugars chased down to a lower range with insulin and/or drugs!

    Teresa

  • Might-o'chondri-AL

    2/27/2011 2:32:27 AM |

    11,000 Koreans studied by Stamford's Sun Kim, M.D. published in Journal Clinical Endocrinology (2011):

    27% had fatty liver (ultrasound diagnosis); 47% of those with fatty liver had high fasting insulin vs. only 17% of those without fatty liver having high fasting insulin. All subjects with fatty liver also had high blood sugar, high trigs and low HDL.

    Participants followed for 5 years; and data correlated on those with, and those without fatty liver who became clinically diabetic. Study conclusion is that fatty liver in participants preceeds Type 2 Diabetes by +/- 5 years in a statistically significant number (ie: no fatty liver = less risk of developing adult onset diabetes).

    Doc undoubtably has new patients and blog readers who have mildly fatty livers that don't think he's right. He should make them hire Revelo to put them through their paces instead.(Joke attempt there Revelo, not a personal digg.)

  • Anonymous

    2/27/2011 5:07:52 PM |

    I am familiar with the web sites that were mentioned in the deleted post. I did not think the post was very critical at all. It only said that these sites provided more detailed information regarding the recent blood-sugar related topics being discussed here. By the way, these sites contain a good deal information that you will only see around here at the Doctor’s pay-to-join blog.

  • revelo

    2/27/2011 7:59:44 PM |

    The martinet in me would be happy to whip anyone into shape who needs it. Seriously though, even the most extreme exercise program is child's play compared to what happens when you get sick. Imagine someone saying to you: "First I'm going to saw through your ribcage, and then I'm going to slice through your arteries..." It's like something out of a horror movie. And yet that is what happens during open heart surgery. And then there are those ailments for which there is no medical relief, surgical or otherwise. Be afraid of getting sick, be very afraid. Be willing to endure any sort of diet and exercise regime to avoid getting sick.

  • Dr. William Davis

    2/27/2011 8:08:44 PM |

    Ni, Nigel--

    No, not my personal blood sugars, but typical responses I've seen in many patients.


    Re: deleted comments
    I have no problem with criticisms. I do have problems with people saying things like "you're an asshole" or similar comments that add nothing to the conversation.

    I now have a zero-tolerance policy for rudeness, but NOT criticism.

  • Anne

    2/27/2011 9:16:04 PM |

    @ Nigel - I like MediAlert bracelets.

    @ Teresa - IMHO, the ADA meal plan is much too high in carbohydrates. It does not make sense to me to cause an elevated blood sugar and then use a medication to bring it down. How about lower the carbohydrate load and use minimal medication? You can find this program in Dr. Richard K Bernstein's book "Diabetes Solution".

    I am T2 and am able to keep my blood sugars in a good range by diet alone by greatly limiting my carbohydrates.  

    I understand those in the ICU present with many challenges to obtaining optimal blood sugar control.

  • Anonymous

    2/28/2011 1:50:55 AM |

    @ Anne,

    I was concerned that anyone without medical training who didn't look at the article linked to in your post wouldn't realize that there are risks to both too low and too high blood sugars in the intensive care unit.

    The comment about the ADA diet and using insulin and drugs to control blood sugars, was meant to poke fun at the ADA.  I apologize.  

    Teresa

  • Helen

    2/28/2011 11:54:36 PM |

    I don't doubt that high blood sugars are harmful, but I do wonder if when they are very transient if the effect is so terrible.  I have always had poor glycemic control.  In terms of going to 200 on a glucose tolerance test, I have diabetes.  But my blood sugars have been lower on a low-fat diet than they were on a low-carb one.  It also now takes me three times as many carbs to get to 175 or so than when I was on a low-carb diet and they are disposed of very quickly - I get down to 75-90 within an hour and a half.  I do think I have a MODY-like form of diabetes - that I'm not particularly insulin resistant.  I'm still not sure what all is going on, but I've been checking my blood sugar rather compulsively for 10 months, and this is what I've found.  

    I'm nearly 45 years old, have great blood pressure, triglycerides of 44 (this may be part of my particular MODY diabetes profile - a few types have genetically low triglycerides), high HDL and low LDL.  I look young for my age.  I don't have any microvascular complications.  I'm still very concerned about my glucose levels, but whatever diet I'm on my BG goes up above 160 with nearly every meal (I can catch it if I test at just the right time), but transiently.  A high-carb diet makes my fasting glucose and between-meal readings much lower, so the overall average is lower.

    Perhaps M-Al is right, if you are  storing fat in your liver, or if you are insulin resistant, it's a different story.  Perhaps anti-oxidant status, overall diet quality, and other lifestyle factors have an impact that large-scale studies don't pick up, since the numbers and outcomes of those with a Dunkin Donuts diet are averaged in with those with a whole foods diet, one along the lines of what Stephan Guyenet suggests.  

    I do think I'm not normal, and a "normal" person with the blood sugars Dr. Davis cites is courting trouble.  But I'm worried about getting too obsessive about my normal, since there's only so much I can do to control it.  It might be that I can be healthy even given the givens.  

    I also think it's worth considering that someone on a low-carb diet often is going to have more trouble disposing of a sudden influx of carbs.  It takes about three days of consistently higher carbs before the body adjusts.  Some people clearly develop higher triglyerides and other trouble on a high-carb diet.  My point is just that the context of one's particular phenotype is important - and sometimes tough to figure out.

  • Might-o'chondri-AL

    3/1/2011 5:56:01 AM |

    Hi Helen,
    I don't want to over step blog protocol, so this is just feedback. The blood test for glycated hemoglobin shows how the blood glucose dynamic is playing out the last couple of months.

    HbA1c is that test and, I believe, Doc set a result over 5.5% is undesireable. Maybe it would give you some insight to how your ranges of blood sugar are playing out.

    Someone here (thank you sir) recommended summitcountymedicalsociety.prepaidlab.com ; I recently used them. Credit card payment gets you an email prescription (to print out) for blood tests, they've cooperating independent
    blood drawing clinics nationwide and lab results are emailed to you. (I needed their 800 phone # help some and they resolved every issue promptly.)

    Charge = US$13 for HbA1c test plus +/- $16 for processing fee(one fee for unlimited tests, it seemed). Their prices were so much cheaper than other online options.

  • Helen

    3/1/2011 11:51:40 AM |

    Thanks, M-Al -

    At initial Dx, my A1C was 6.4.  After seven months on a strict low-carb diet (like 60 g carbs/day) and a 20 lb weight loss (I'd only been 10 lbs overweight at Dx, for the first time in my life, but I lost 20 during that time.  I've now lost nearly 30, not all for good reasons.) it was down to 6.0.  I'm monitored quarterly and am due for another A1c.  We'll see if my lower readings are borne out by the test.  I don't expect miracles, but I'm doing the best I can.  Some people's blood sugars only come down so much.  Metformin was ineffective for me and insulin would probably be dangerous, since my BG dips so far on its own post-prandially after peaking.

  • Anonymous

    4/16/2011 9:58:46 AM |

    DISCLAIMER, MY ENGLISH IS NOT VERY GOOD and this is loong SO BARE WITH ME ON THIS,I HAVE READ @ printed all this BLOG AND DROVE MY FAMILY(DOCTORS) and FRIENDS @  CARZY 1 ! THANKS!

    So i finally got my  glucometer:  OneTouch Ultra (ahh) + brand new strips (ouch) not cheap here where i live...  my old man  (doctor, lives on a diet of coffee, diet soda, bread pasta, cookies, candy etc, etc, etc + a few drugs... and is tall and "lean") thinks im completely crazy. ( im 33, 78kgr, also lean and muscular)

    so my pattern: OMP-day  fasting
    ( 23h, 24h, 27h, 30 hrs regular fasts) + 3 day wrkts
    (home, chin ups, push ups, squats) rest of the tm im mostly sedentary

    my readings so far...

    D1: 13-4

    10:00 >  71mg/dL >  FS@BS (prior that  day ate a bit of candies... pascuas)

    11:00 >  ERROR (didnt put the right code, got pissed @ didn't test)

    D2: 14-4  (no carb)

    3:07 > 70mg/dL >  FS@BS

    EAT: meat (+)yolks(+) cheese (+) butter (-) water

    4:05  > 81 mg/dL > AE@BS

    5:05  > 77 mg/dL > AE@BS

    D3 15-4 "workout" day (chin ups)  + carb
    ERROR, 2 little blood, !"·$%didn't test  (assumed 70mg/dL  FS@BS)



    11:00 >EAT: (pWRKOUT)

    meat(-) yolks (+) cheese(-) butter (-) tomato juice (+) 350CC Whole MILK+ 100G " 60% CHOCOLATE"  ( 37g carbs. aprox 20@30g sucrose + milk sugars )
    this baby

    http://www.chocolatesaguila.com.ar/uploads/info_nutricional/tabletas_rellenas_3344.pdf

    ( copy paste if u care)

    11:00 >EAT

    12:05 >  75 mg/dL > AE@BS

    12:20 > 72 mg/dL  > AE@BS

    1:06 >  82 mg/dL > AE@BS  
    ( waited 2 long there?)

    2:09  > 70 mg/dL > AE@BS

    6:12 > 67 mg/dL > AE@BS

    D3 16-4  
    ("rest day" upped the carbs anyway)

    "FS@BS"  (didn't bother to test. low as usual, i guess)

    1:00 > ??? mg/dL
    EAT: salted peanuts... roasted in vegetable oil... 100gr (could not find my chocolate...)

    2:00 > ??? mg/dL
    EAT:
    one lean, small cut of meat+ ham+ 6 yolks omelet fried in butter,  the usual 100g cheeses- Roquefort, sardo, pategras,cuartirolo,feta, 6tbs tomato juice, salt, peeper, (napolitanta)

    Dessert: -2-  ice cold glasses of 300CC WHOLE MILK + 2 TBS of Cheap sugary cocoa powder  (approx 20@30g sucrose total + milk sugars)

    3:05 > 107 mg/dL (!)

    - moved my arse a bit and did 2  slow sets of dumbbell squats, (40 reps with16k w total, super slow and easy)

    3:36 > 83 mg/dL

    4:37 > 66 mg/dL

    ok, any comments ? are my number ok?  what makes more sense , eating chocolate ( fiber, slower absrs possible less sucrose, or drinking  milk?  (talking desert here) i do not  eat vegetables, ( just, pepers, tomato juice and mushrooms) do not  eat fruit, and of course do not even touch gluten nor refined crap, and always try to limit my PUFA, and fructose load.

    also im thinking i should test my BS levels differently?  maybe  eating one (large) H fat, H 2 moderate protein, meal per day changes things a bit?  so maybe waiting 1 hrs is not enough ( thats why i used milk x 2 today, and did not wrkout to speed things a bit)

  • Anonymous

    4/16/2011 10:19:41 AM |

    edit, im 68 kgr ( not 78) ... always do the same mistake, maybe i need to gain weight!

  • Anonymous

    4/16/2011 11:01:28 AM |

    OneTouch Ultra Meter
    Eating pattern: OMP-day  
    ( 23h, 24h, 27h, 30 hrs  fasts)


    D1 REST DAY

    3:07 > 70mg/dL >  FS@BS

    EAT: meat (+)  yolks (+) cheese (+) butter ( -)  water

    4:05  > 81 mg/dL > AE@BS

    5:05  > 77 mg/dL > AE@BS


    D2 WRK DAY

    11:00 >  71mg/dL  FS@BS

    EAT: meat (-) yolks (+) cheese(-) butter (-) tomato juice (+)  +  350CC Wf MILK + 100G " 60% dark chocolate"

    12:05 >  75 mg/dL > AE@BS

    12:20 > 72 mg/dL  > AE@BS

    1:06 >  82 mg/dL > AE@BS

    2:09  > 70 mg/dL > AE@BS

    6:12 > 67 mg/dL > AE@BS


    D3  REST DAY (upped the carbs, + added liquid sugar, wrst  case)


    1:00 > ??? mg/dL
    EAT: salted peanuts... roasted in vegetable oil... 100gr

    2:00 > ??? mg/dL
    EAT:one lean, small cut of meat+ ham+ 6 yolks omelet fried in butter, 140g cheese, 6tbs tomato juice,  (napolitanta) 2  ice cold glasses of 300CC W MILK WITH 2 TBS of Cheap sugary cocoa powder  (aprox 20@30g sucrose + milk sugars)

    3:05 > 107 mg/dL (!)

    -did 2   slow sets of dumbbell squats, (40 reps with16k w total, no effort)

    3:36 > 83 mg/dL

    4:37 >  66 mg/dL

    Hypoglycemia?
    any opinions about my numbers, (imm33) should i ditch the milk @dark chocolate and eat "healthy vegetables" and "fruit" (no)


    should i wait longer 2 test my BS? (slower digestion time, one meal and all)

  • Anonymous

    4/17/2011 8:50:49 AM |

    today


    17-4 > WRKT

    9:00 > 69 mg/dL

    10:58 > EAT (6 YOLKS, CHEESE, BUTTER, 1TBS TOMATO JUICE - OMELET + 400GR MINCED MEAT, 6 STRIPS BACON, 5TBS TOMATO JUICE, BUTTER)

    2:07 > END

    DISHWASHING

    2:16 > 350cc WHOLE MILK

    2:21 > 100G 60% chocolate

    2:34 > END

    2:40 > 300cc WHOLE MILK + 1 TBS SUGAR (nesquik)

    3:01 > 71mg/dL

    3:36 > 74mg/dL

    4:39 > 83mg/dL

    5:42 > 74mg/dL

    650cc milk + lots of  sucrose... where is the zomg 160 blood glucose doctor? (btw i had been eating sucrose @ and grains like crazy 90% of my life, now im eating waay less sugar and 0 grains)

  • Anonymous

    4/17/2011 11:57:29 AM |

    edit,

    1:58 > EAT  (not 10:58...)

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