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

2. April 2010 William Davis (12)
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

1. April 2010 William Davis (11)
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

28. March 2010 William Davis (16)
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?

26. March 2010 William Davis (20)
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

23. March 2010 William Davis (24)
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?

21. March 2010 William Davis (19)
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

19. March 2010 William Davis (0)
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

19. March 2010 William Davis (83)
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

18. March 2010 William Davis (0)
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

18. March 2010 William Davis (74)
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.
Why small LDL particles are the #1 cause of heart disease in the US

Why small LDL particles are the #1 cause of heart disease in the US

15. September 2011 William Davis (77)
Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet
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Comments (77) -

  • Bill

    9/15/2011 1:13:26 PM |

    But is there any real evidence that small LDL is a *cause* of heart disease? Correlation alone isn't sufficient, of course, and Chris Masterjohn has said that even the correlation largely disappears when traditional "risk factors" such as HDL, LDL, and triglycerides are added to the model.

    I ask in part because I am about to arm wrestle with my primary care doctor about my recent cholesterol panel:

    Total: 382
    HDL: 157
    LDL: 217 (calculated)
    Triglycerides: 39

    He's upset about the LDL, of course, especially since it's progressively risen over time (coinciding with dietary changes pretty compatible with TYP and including quite a bit of sat fat after years as a low-fat vegetarian). Naturally, he wants me to reduce my fat consumption and retest in four months, and I'm sure a statin drug recommendation will follow just as the sunset inevitably follows the sunrise.

    I am thinking of asking for a full lipoprotein panel, with the expectation that it will calm him down by showing 1) much lower real, measured LDL with my rock bottom triglycerides and 2) strong Pattern A LDL with my sky high HDL and low triglycerides.

    But I'm not certain if I can really make a convincing empirical case to him that Pattern A is benign with a high LDL. (I'm also hesitating after hearing Chris Masterjohn say that LDL particle size measurements are hugely dependent on the type of assay used and that as a result it's not clear what, biologically, any given result means until these methodological discrepancies are sorted out.)

  • Peter Silverman

    9/15/2011 2:41:59 PM |

    The article you cite says the number of LDL particles may be more important than the size.  Is that your experience?

  • Howard

    9/15/2011 3:02:31 PM |

    @Bill : Chris Masterjohn also mentioned in a recent podcast that the current measurement technology for LDL particle size is just not sufficiently accurate to be useful.

  • chuck

    9/15/2011 3:48:18 PM |

    what is your feeling on oxidized ldl?

  • chuck

    9/15/2011 3:52:16 PM |

    @howard
    yes, based on the hour to hour, day to day, week to week, and month to month natural fluctuations of lipids in the blood it is difficult to make any real judgements about cholesterol readings without doing multiple panels over a period of time.  the whole medical community seems to be screwed up in this respect.

  • Kathy

    9/15/2011 4:13:20 PM |

    I have no idea what Dr. Davis' response will be, but if you're interested in getting an NMR profile done on your own dime (and if there is a convenient location near you), check out directlabs.com for their September special.  An NMR profile will only set you back $79 (reg $127).  I've been waiting for this "sale" and am getting it done to show my own doctor.  Your health is ultimately in your hands - keep up the good fight!
    Best,
    Kathy

  • edward white

    9/15/2011 5:02:18 PM |

    Dr D,
    I totally agree small LDL is driven by excess carbohydrate intake and postprandial
    triglycerides. However there is a substantial subset of people whose small LDL
    is genetically driven. I believe you are aware of this phenomena.
    Please let these folks know what their options are to address this important issue!
    There can be a good deal of frustration when carbs and triglycerides are addressed but
    with little lowering of small LDL.
    Please help this substantial number of people out by outlining their options...
    Gib

  • Unix-Jedi

    9/15/2011 5:22:13 PM |

    Thanks for that information, Kathy.

  • cancerclasses

    9/15/2011 5:57:26 PM |

    It ain't good,  just ask Wikipedia.   From the Wiki page re 'Chronic endothelial injury hypothesis':
    "Once LDL accumulates in the subendothelial space, it tends to become modified or oxidized.[5] This oxidized LDL plays several key roles in furthering the course of the inflammatory process. It is chemotactic to monocytes; oxidized LDL causes endothelial cells to secrete molecules that cause monocytes to penetrate between the endothelial cells and accumulate in the intima.[6]

    Oxidized LDL promotes death of endothelial cells by augmenting apoptosis. Also, through the activation of collagenases, ox-LDL contributes to a process which may lead to the rupture of the fibrous plaque[7] Oxidized LDL decreases the availability of endothelial nitric oxide (NO), which, in turn, increases the adhesion of monocytes to the endothelium.[8] Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis."

  • Bob

    9/15/2011 6:12:21 PM |

    Test reply

  • cancerclasses

    9/15/2011 6:13:54 PM |

    Yes, French cardiologist Guy-Andre Pelouze MD. at the recent Ancestral Health Symposium said in his presentation "Paleodiet and atheroma: A Cardiovascular Surgeon’s Perspective" that:

    1. Native (the reduced form of) LDL cholesterol is NOT atherogenic, only the oxidized form leads to atheroma, atherogenesis & arterial plaque formation.

    2. Without oxidized cholesterol it's very difficult to have arterial plaque formation

    3. Anti-oxidants are ineffective in preventing atheroma.

    4. SDLDL easily enter the subendothelial space because SDLDL are less than 25 nm in diameter and the subendothelial space is 26 nm.

    5. Subendothelial space in humans is very different in humans than other mammals due to the large amount of smooth muscle in the arterial media below the the intima layer.

    And there's much more.  To see a video of Dr. Pelouze's presentation hosted on the Ancestral Health page at Vimeo just google 'vimeo, paleodiet and atheroma', then scroll to video number 33 in the right side box.

  • cancerclasses

    9/15/2011 6:42:38 PM |

    Do you REALLY believe that? We have the ability to measure the distance between the earth and the moon almost down to the millimeter, and certainly down to the centimeter. We have the ability to measure individual atoms with electron and other types of microscopy used in materials engineering and computer chip manufacturing.  Medical, biochemical & physiological textbooks are full of descriptions of the sizes of white and red blood cells, bacteria and viruses, etc. ad infinitum.  Do you REALLY think we lack the ability to measure SDLDL?  Don't be so ready to believe something just because somebody says something about it.  Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion.  

    Furthermore, what's the point of a statement like that?  Should we just give up measuring and trying to understand how SDLDL causes atheroma just because ONE guy says we can't measure them to his degree of satisfaction?  Should we just give up worrying about what we eat, and what we are being sold as foods that are arbitrarily declared to be safe to eat by some anonymous bureaucrat at the FDA?  Should we just ignore the ever increasing incidence rates of cancer, heart disease and atherosclerosis that by all applications of observation and simple logic are known to be entirely due to the modern industrial foods diet in every society and the peoples that subsist on them?  

    I don't think so.  Homey don't play that anymore, at least this one doesn't.

  • cancerclasses

    9/15/2011 6:55:16 PM |

    @Bill,  Google and see this study: 'Detection of low density lipoprotein particle fusion by proton nuclear magnetic resonance spectroscopy'.    
    "Abstract: Recent evidence suggests that fusion of low density lipoprotein (LDL) particles is a key process in the initial accumulation of lipid in the arterial intima. In order to gain a better understanding of this early event in the development of atherosclerosis, it would thus be necessary to characterize the process of LDL fusion in detail. Such studies, however, pose severe methodological difficulties, such as differentiation of particle fusion from aggregation. In this paper we describe the use of novel methodology, based on 1H NMR spectroscopy, to study lipoprotein particle fusion."

  • Don

    9/15/2011 7:24:04 PM |

    Bill,
    You have no worry since your triglycerides are quite low and therefore your LDL particles are of healthy size.  Your correctly calculated LDL is only 161 using the Iranian formula (used if triglycerides low).  See LDL calculator here:
    http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm

    And never use statins, just cut carbs.
    Don

  • cancerclasses

    9/15/2011 7:34:54 PM |

    "About 80% of cholesterol is composed of fats and oils (Current Atherosclerosis Reports 2004). The
    majority of an arterial clog, 55%, comes from defective cooking oils, containing mainly damaged omega 6. Most of us unknowingly purchase these oils in the cooking oil section of the supermarket. These are the oils we fry with and the oils added to most packaged foods; both fresh and frozen.

    Here’s another shocker. It’s not the saturated fat —it’s the adulterated omega-6 from food processing that clogs arteries! Contrary to what we have heard for decades, it is not the saturated fat you eat that clogs your arteries! How do we know this? A 1994 Lancet article reported investigating the components of arterial plaques. In an aortic artery clog, they found that there are over ten different compounds in arterial plaque, but NO saturated fat. This means the bacon, eggs, cheese, steak, whipped cream, etc. isn’t the reason for a clogged artery. These natural saturated fats are actually good for you. You need them for body structure.

    With the consumption and transport of defective processed oils, LDL cholesterol acts like a “poison delivery system,” bringing deadly transfats and other ruined oils  into the cells. It is primarily the oxidized (adulterated) omega-6 that clogs the arteries, NOT saturated fat!"  

    For more just google 'Brian Peskin saturated fat' and read the day away to your heart's content.

  • Jack Kronk

    9/15/2011 8:37:50 PM |

    "just because somebody says something about it. Use your own brain, put together everything you know and can learn on your own and connect ALL the dots before drawing a conclusion. "

    lol. you must not know who CMast is.

  • cancerclasses

    9/15/2011 10:27:09 PM |

    Yeah, I do, and that's why I said that.

  • Dr. William Davis

    9/16/2011 2:40:13 AM |

    Hi, Gib--

    The strategies that reduce small LDL are the same whether it's genetically-driven or acquired. However, when (presumptively) genetically-driven, it's just harder and requires a more meticulous effort.

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern.

  • Dr. William Davis

    9/16/2011 2:42:32 AM |

    Big issue. Note that the real culprit in causing plaque may be glycated oxidized LDL.

  • Dr. William Davis

    9/16/2011 2:43:51 AM |

    Hi, Peter--

    No, I think that is wrong. It might be correct if small LDL is regarded in a dichotomous way, i.e., pattern A vs. pattern B. But, when viewed quantitatively, I believe the real culprit is quantity of small LDL.

  • Dr. William Davis

    9/16/2011 2:46:58 AM |

    No question: The various lipoprotein testing companies need to talk and standardize their definitions. But this does not invalidate the concepts.

    Chris Masterjohn is a very bright guy. But on this I disagree. I believe it is wrong to assume that triglycerides and HDL behave in perfect tandem with small LDL. While they do indeed correlate, they do not correlate perfectly and demonstrate independent behavior depending on postprandial phenomena and genetic factors like apo E and apo C.

  • Joyce

    9/16/2011 5:17:54 PM |

    This has nothing to do with LDL, but I don't know where else to ask this, so I'll dive right in.

    I am reading and enjoying your book Wheat Belly, but don't understand why you lump chia seed in with other non-gluten grains to avoid or minimize. .  In my mind it is closer to flax.  Chia is truly an oil-seed and not a grain according to Dr. Coates, the "father" of chia seed research.  I have used it generously, and feel it aids in weight loss.  Chia seed is high in protein and fiber and low in carbs.  Why are you telling us to avoid or limit it?  I feel it is healthier than flax even.

    Please, can you clarify your stance on chia?  I was very disappointed to read that in your book.  Other than that, I really enjoyed Wheat Belly, having avoided gluten for a few years now.

  • Joyce

    9/16/2011 5:33:17 PM |

    P.S.  According to calorieking.com website, 1 oz. raw chia contains 0 carbs and 1 oz. dried chia contains only 1 gram of useable carb.

  • Adriana

    9/17/2011 10:16:37 AM |

    Not everybody who has good HDL, good TG and eats a low carb paleo diet will have low small particle LDL numbers which is why an NMR LipoProfile is important.  People with gut issues, yeast issues,  H. Pylori or an otherwise compromised liver can have unhealthy LDL despite doing everything right on the diet front.  Getting to the root of these issues is critical to resolving it.

  • Dr. William Davis

    9/17/2011 1:23:49 PM |

    Thanks, Joyce. But I don't remember lumping chia with the bad stuff.

    In fact, as you point out, chia belongs with flaxseed as one of the few truly healthy, low-carb foods.

  • Joyce

    9/17/2011 1:45:31 PM |

    Dr. Davies, on p. 212 of your book, chia is lumped in with other non gluten grains.  Maybe in future editions, the publisher can remove that?

    Although I have been gluten free for years, my husband is finally going gluten free..ALL BECAUSE OF YOUR BOOK!  He has some health issues, so for that I humbly thank you.

    Also, his next Toastmasters speech will be on "Wheat Belly"...how about that!

    Thank you so much for a wonderful book.  Your recipes are awesome.  I look forward to a Wheat Belly cookbook!!!!

  • Linda

    9/17/2011 2:57:40 PM |

    There are so many well read and brilliant posters here that I am going to jump in and ask a question totally off topic. This is not Dr. Davis' area of expertise, so I hope others may help.
    I do believe I am dealing with a bone/heel spur. Too much treadmilling, trying to increase speed, etc. I have done research on the condition and I read that turmeric, taken 2-3 times a day, is helpful. I just recently began taking D3 as well, 5000 IU a day. Will the Vit D3 help as well?
    Any thoughts? No, I am choosing not to visit a doctor for a cortisone shot. I am using NSAIDS for the pain and that works very well.

  • nina

    9/17/2011 4:48:56 PM |

    I've just spotted this post.  Never tried chia and wonder what you thought.  Have your patients reported similar effects?

    Nina

  • steve

    9/17/2011 7:26:34 PM |

    We are now seeing more and more people achieve zero or near-zero small LDL with strict carb reduction. The big exception is apo E4 people, who can still struggle because of the peculiar physiologic effects of this pattern

    Could you go in to more depth as to what strict carb reduction menas?  Is it no more than 50grams of starchy carbs such as rice or potatoes, or 100Grams?  I am guessing it is individualized, but some range of restricitons with those who have been successful would be helpful.  
    I have always had a low level of Trigs- never higher tnah 75 even on a hi carb diet, and was surprised to find the NMR showing all small particles!  So Dr. Davis is right to say low Trgs not always indicative of having large LDL.  Switched to elimination of most carbs and totally changed the profile.  Only issue that is while i produced lots of particles with carb diet, i also produce lots of LDL particles with carb restriction.  Genetics i guess!  I am an ApoE 3/3, which was a surprise.  
    Thanks for the good work Dr. D.  Have gotten several to buy Wheat Belly.  It will have an impact!

  • Joyce

    9/17/2011 7:30:40 PM |

    Nina, I am not Dr. Davis (wish I had his knowlege!), and I hope he doesn't mind me jumping in here, but I leaned about chia a few years ago when I read a book by Dr. Wayne Coates on the subject.  Chia has definitely helped me lose weight.  It is very filling.  When mixed with fluids, the chia seeds expand, and they really help to fill you up.  I've found all sorts of wonderful chia recipes on the web - from Chia "Tapioca" to beverages, etc.  I mix  it into many foods.  I think it enhances their taste.  I feel the chia seeds help with weight loss because of their appetite suppressant potential.  I hope this helped, and my apology to the good doctor for hogging the thread.

  • PeteKl

    9/17/2011 10:24:07 PM |

    Your post doesn't provide a lot of info, but if I were to guess I would say your problem is more likely related to walking/running incorrectly than nutritional (assuming you are in reasonable physical condition).  The human foot wasn't designed to be encased in the heavily cushioned shoes we typically wear today.   As a result many of us don't know how to walk or run correctly.

    Some of the better shoe stores will video tape you on a treadmill.  Just seeing the tape may be enough for you to realize what you are doing wrong.  If that doesn't help, there are professionals who should be able to figure out what might be happening.  

    Also consider reading "Born to Run" if you haven't already (it's a good read even for non-runners).  It probably won't give you a direct solution, but it may give you some ideas on where to look.  Good luck.

  • Louise

    9/18/2011 2:10:34 AM |

    Dr. Davis,
       I am 56 and have a strong history of heart disease in my family. I have been eating low carb for a couple of years... ( around 60 gms carb per day average..no pasta, no potato, almost no grain)  My most recent lipid panel showed LDL of 140. HDL 81, Triglycerides 43, CRP 0.2. .  I requested a test to show size of LDL. My doctor declined to order this, saying all LDL is bad.  Instead I was sent for a heart scan  ( paid out of pocket) and my calcium score was 0.  
      So now I'm trying to lower my LDL by lowering saturated fat.  Hard to do when you eat low carb. I wonder if I might be one of those Apo E 4 types that you mention, so thought I should try,.
      Here are my questions:
         Can I test my LDL size myself, through a home test? Or should I try to find out if I have Apo E 4?
          Do I really need to lower LDL if my calcium score is 0?
    Louise

  • Bob Goldstein

    9/18/2011 4:02:36 AM |

    For the last year I have eaten zero fruit, zero grains, zero sugar. Have mostly eaten beef, occasionally eggs cooked in butter. Have done two VAP tests the last year. When I started a year ago, trigs were 115, now 142. HDL was 50, now 46. My LDL did show a change of going from pattern A/B to pattern A.
    Any ideas why a diet for a year devoid of fruit, sugar, grains, would show an increase in trigs, and a slight decrease in HDL. If I have Apo E4 would my ldl go from A/B to A.
    I have lost 25 lbs. in the past year. Could this be a reason my numbers seem to be off?
    Thanks,
    Bob

  • Dr. William Davis

    9/18/2011 3:44:29 PM |

    Hi, Bob--

    Yes, blood drawn in the midst of weight loss can be very misleading.

    Transient effects include increased triglycerides, reduced HDL, even much higher blood sugar. Thankfully, it all gets much better once weight plateaus for a couple of months.

  • Dr. William Davis

    9/18/2011 3:47:39 PM |

    Hi, Louise--

    Sad that you have to educate your doctor.

    I find it unacceptable that a nice person engaged in health is refused a simple, helpful test. Tell your doctor goodbye and find one willing to act as your partner and advocate in health, not an obstruction.

    Yes, you can test it yourself through services like PrivateMDLabs.com. My view is to 1) identify how much, if any small LDL there is, then 2) reduce small LDL with diet. If you have only large LDL, you will absolutely need an LDL particle number by NMR or an apoprotein B to know what the REAL value is.

  • Dr. William Davis

    9/18/2011 3:49:52 PM |

    Thanks, Steve.

    There are a number of posts on this blog that detail how to gauge individual carbohydrate sensitivity. The best way is to check 1-hour after-eating blood sugars. Second best: count carb with the cutoff being determined individually. Just go back over the past 6 months and you will find several discussions.

  • Dr. William Davis

    9/18/2011 3:51:17 PM |

    Hi, Joyce--

    Thank you!

    If chia is listed as among undesirable non-gluten grains, that was my error. Remember what Mark Twain said: "Don't read about health, else you might die of a typo."

  • nina

    9/18/2011 5:13:58 PM |

    Thanks for your response Joyce.  

    The part that fascinated me was the idea that chia triggers a drop in blood sugars without a pre-spike.  I can't find anything on the net about that and wondered if other people had similar experiences.

    Nina

  • Bob Goldstein

    9/18/2011 7:08:22 PM |

    Thanks for the reply Dr. Davis. I have a blood test scheduled six months from now, and hopefully I will see better numbers. My LDL shows pattern A so at least I did see one positive change.
    Love your blog. Have learned a lot and it was the reason I gave up grains and sugar. 1 full year, no cheats.

  • Annlee

    9/18/2011 10:41:56 PM |

    Consider also going barefoot as much as possible - around the house, etc. You don't necessarily have to run barefoot (unless you work into it *gradually* and choose to continue it). I've recovered from heel spurs with stretching my achilles, with emphasis on stretching the soleus, and letting my feet bear my weight without any props underneath. For stretches, Anderson & Anderson have a very good book - Stretching - available on amazon.com. You didn't develop the spurs overnight, and they won't clear that quickly, either. Be patient and work with your body.

    You may also wish to consider vitamin K2, very good for ensuring calcium deposition occurs in the correct locations.

  • Kira

    9/19/2011 6:52:43 AM |

    Hi Doctor Davis, I talked to your about a year ago and you were kind enough then to comment on my blood results saying there was nothing to worry about - according to the Iranian formula.  I would greatly appreciate if you looked at my new results, they scared my whole family, I certainly am not going to show to the family physician, and I don't even want to think about changing from paleo style of eating to some kind of low fat cholesterol lowering diet, and taking any drugs/supplements. But may be I have to? I am 36 y.o., 5'4 and weigh 104lb.
    Glucose 85
    VAP TEST:
    Lipids
    LDL Cholesterol 149!
    HDL 130
    VLDL 14
    CHOLESTEROL, Total 293!
    Triglycerides 48
    Non HDL Col (LDL+VLDL) 163!
    apoB100-calc 96
    IDL Cholest 4
    Remnant Lipo. (IDL+VLDL3) 12
    Sub-Class Information:
    HDL-2  35
    HDL-3  95
    VLDL-3  8
    LDL1 Pattern A 3.1
    LDL2 Pattern A 26.0
    LDL3 Pattern B  71.0
    LDL 4 Pattern B  31.4

    The ordinary, non-VAP Lipid panel shows:
    Cholest TOTAL 279 !
    Triglycerides 48
    HDL Cholest 144
    VLDL Cholest Cal 10
    LDL Cholest Calc 125 !

    Also, I can't understand how my vit. D can be so low - 29.0, when I have been sun tanning all summer here in Orange County, California, at peak hours. Is there anything that you know of that may inhibit the vit. D conversion from the sun?
    Again, I greatly appreciate any insight that you can give me on this situation...

  • Louise

    9/19/2011 4:52:38 PM |

    Dr Davis,
      Thank you for your reply.  For now, I found a lab I can go to and get myself tested. Two hours away.. (Oddly, I must leave NY state to get this done due to billing law.). I'm going to do this! Do you agree that my best choice is the NMR?

  • otterotter

    9/19/2011 5:43:51 PM |

    Hi Gib,

    Option 1 will be cutting the saturated fat and cholesterol from the diet in addition to cutting the carbs. I tried eliminating eggs and cheese and my total cholesterol down from 400 to 260. By adding back "one egg a day", it went back to 320 (that's the impact of the dietary cholesterol on me, confirmed twice). I am currrently trying to replacing all saturated fat with mono unsaturated fat (olive+canola), just want to see how big the impact is. I am also going to test coconut oil separately, it is a cholesterol-free plant based medium-chain saturated fat, there is a chance I might respond to it differently.

    Option 2 will be taking Statin drugs. I know it has side effects, but that's better than small dense LDL. Based on Dr Davis's previous response, for apoE, sometimes we have to go to Statin for the rescue. (My doc was pushing statin really hard on me, and I have been resisting that for the last year)

    otter

  • Joyce

    9/19/2011 5:50:45 PM |

    Dr. Davis, you are so funny.  We'll take your book....typos and all!  Now...how about a cookbook to compliment Wheat Belly/  PLEASE????

  • nina

    9/19/2011 7:41:34 PM |

    Sorry I missed the link:

    http://suzanneloomscreativity.blogspot.com/2011/09/lowering-blood-sugar.html

    Nina

  • PeteKl

    9/19/2011 9:24:31 PM |

    Hi Kira,

    Just out of curiosity, could you summarize your "paleo style of eating".  I have a good friend of mine who has similar numbers (low trigs, high HDL, high LDL).  I would describe her diet as "low-carb (no sugar, no grains), low-veggie (under 15%), high meat, high sat-fat (particularly cheese, eggs and coconut)".  Is your diet somewhat similar?  I would be interested to know how the two of you compare.

  • Dr. William Davis

    9/20/2011 12:36:46 PM |

    NMR is my preferred method, since it yields the LDL particle number, what I believe should be the gold standard.

  • Dr. William Davis

    9/20/2011 12:38:12 PM |

    Thanks for asking, Joyce! I've had very preliminary conversations with my editor, but nothing firm yet.

    In the meantime, in addition to the discussion on this blog, see the Wheat Belly Blog, where I will publish recipes one by one.

  • Dr. William Davis

    9/20/2011 12:41:39 PM |

    Hi, Kira--

    You have a surprising dominance of small LDL particles, despite your slender build and lifestyle (LDL 3+4 divided by "real" LDL). This is likely genetically-determined. The means of correcting this is beyond the scope of this blog, unfortunately. You might consider joining the discussion in the Track Your Plaque website.

    The vitamin D issue is common, an impaired or lost ability to activate vit D in the skin. It means doing it orally.

  • Adam

    9/20/2011 6:40:19 PM |

    Dr. Davis. I'm a type 1 diabetic who is on a low carb diet (mostly primal-esque) with only meat and veg. No fruit, no grains, no legumes. I lost 14 kgs in the first three months, then stabalized at around 89 kgs. Granted my fat is going down a wee bit as muscle mass increases (doing the slow burn exercises, plus HIIT training and martial arts). That is the background.

    The reason I'm posting here is confusion about cholesterol. I just got my latest results back from the lab, and they are the same. While my HbA1C is 5.3 (not bad), my cholesterol numbers don't look hot. Tryglicerides are fine (as I've stopped losing weight quickly), but HDL is low at 39, and LDL (doctor forgot to put in particle size check, but it cna't be that good as I'm a diabetic) was 150 on the spot. This was measured, not calculated.

    I take ~7k miligrams (or whatever the measurement is) of fish oil a day. Well, 7k of EHA/DHA, more in total quanity including inert substances. With my exercise, low carb diet, and fish oil supplements, how is it that my HDL are still so low? Any advice?

    Thanks!

  • Dr. William Davis

    9/20/2011 11:08:46 PM |

    Hi, Adam--

    How timely! See the next post after the one you responded to in which I discuss the transient effects of weight loss, including drops in HDL that rebound over time.

    Also, have you address vitamin D normalization? I aim for 60-70 ng/ml, which usually requires around 6000 units per day (gelcaps or drops only); the HDL-raising effect develops over a year or longer.

  • Adam

    9/21/2011 1:01:18 PM |

    Dr Davis,

    A pleasure to make your (virtual) acquaintance! My vitamin D, according to my last test (results came in yesterday, as I mentioned) levels are 59. A wee bit low, but not too bad, I think.

    I've been consistently 88/89kg for three months (I've been low carb/primal for 6 months total), so haven't lost any weight in the past three months, but still my HDL levels are very low. Do you have any suggestions?

    Cheers,

    Adam

  • Adam

    9/21/2011 1:03:52 PM |

    P.S. I'm pretty sure I've stabalized, as my triglycerides were at 29 or 39 (can't remember off hand, but pretty low). But still I had the low HDL and high LDL?

  • Dr. William Davis

    9/21/2011 9:37:43 PM |

    Hi, Adam--

    Of course, you are wheat-free, low-carb in addition to your vitamin D? Omega-3 fatty acids?

    Note that doing the diet and taking the vitamin D yield rises over 1-2 years. Patience is required.

    Consider a little red wine and dark chocolate, as well.

  • Adam

    9/22/2011 5:10:38 AM |

    Thanks for the response! Yes, I am completely wheat free (and was before I read your book, which was excellent). I am very low carb due to the diabetes. My HDL did go from 29 to 39 this last test (after 6 months), so I suppose, as long as maintaining this diet will continue to increase my HDL, I am ok. My concern isn't immediate gratification but more continuous improvement.

    I'll come bug you again in 3 months if my HDL doesn't continue to increase Smile

    Many thanks!
    ---Adam

    P.S. I've never been accused of not drinking enough red wine Smile While I've been beer free for 6 or 7 months now, I do go through ~2 bottles of red a week.

  • Adam

    9/23/2011 1:35:08 PM |

    Hah! Me too, because if my HDL doesn't start going up I'm gonna freak as I don't know what else to about my numbers. Diet is about as stripped down as it can be, and I'm exercising as much as is reasonable.

    --Adam

  • Kira

    9/24/2011 6:23:22 AM |

    HI Peter. I would say  that my diet could pretty similar, with the exception that I am still eating some low-glycmic fruit everyday (some cantaloup, grapefruits, berries) and eat lots of veggies.

  • Kira

    9/24/2011 6:29:11 AM |

    Dr. Davis, thnx for your reply. I understand this is a blog and it is hard to go into details here, but would you say that it is worth for me to try change this situation by changing the die to using less saturated fat? and would NMR test clarify anything?

    PS How do I further discuss this issue "by joining the discussion in the Track Your Plaque website"?

    Thnx AGAINSmile

  • ShottleBop

    9/25/2011 3:47:09 PM |

    My numbers are like Bill's.  I was diagnosed as pre-diabetic in February, 2008 (today, I'd have been diagnosed as Type 2; my A1c was 6.5, and my FBGs were 127 and 123).  Started low-carbing shortly after that:  cut out grains, starchy veggies, almost all fruit, all milk (still use heavy cream and eat cheese).   My most recent blood lipids (accounting for some variation, but roughly consistent in pattern over the past three years):

    TC:  381
    LDL (direct):  279 (291 calculated)
    HDL:  80 (was 40 at diagnosis)
    Trigs:  52

    (At diagnosis, my numbers were:
    TC: 281
    LDL (direct) 215
    HDL: 40
    Trig: 142)

    I lost 65 pounds in the first 9 months after diagnosis, and, since then, have regained approximately 25 pounds (mostly muscle).  Weight has been stable for months.  My doctor is talking statins, again--which I plan to continue resisting.  I have ordered an NMR test, and will see what it has to say about my particle size.

  • Dr. William Davis

    9/26/2011 12:39:56 PM |

    Hi, Shottle--

    Good plan. I wouldn't be surprised if NMR sheds an entirely different light on your values.

  • ShottleBop

    9/29/2011 4:23:57 PM |

    They drew the blood this morning.

  • Bob

    9/30/2011 11:14:10 PM |

    Dr. Davis, I had my NMR test and the doctor who looked at it suggests that I have familial hypercholesterolemia. My LDL-P 3158
    LDL-C 280 HDL-C 58, TGL 105, HDL-P 28.0 small LDL-P 1122,
    LDL 21.7, LP-IR-33. I have been on no carb, no sugar, no wheat, or fruit for the last 14 months. Have been eating fatty meat twice a day and also eggs. Before I started eating beef, I was eating low carb, very little sat. fat. I was eating a lot of skinless chicken breast, and canned salmon, veggies, nuts, fruit but almost no beef. My LDL according to the basic lipid test was a little high but not crazy high. My HDL was in mid 30's. and trigs were high. I changed to a high saturated fat diet to raise HDL and lower trigs. I have been taking 1 gram of fish oil 2X daily. Is it possible that the fish oil is having an effect on my LDL? Not sure what to do about my diet. Obviously I won't go back to sugar and wheat but what about all the meat I have been eating. Would it be better to go back to skinless chicken and egg beaters even if it means my HDL going down? Just not sure what to do. Doctor believes I am at high risk since my father died at age 62 of sudden death.
    Thanks,
    Bob

  • Dr. William Davis

    10/1/2011 1:48:14 PM |

    Hi, Bob--

    This is a tough situation that, unfortunately, cannot be remedied diet alone. I hate saying that.

    Like people with apo E4, familial heterozygous hypercholesterolemia people are fat sensitive. First order of nutritional business remains carb-restriction to minimize small LDL particles, but you can still show large increases in large LDL with fat intake. If apo E4 is present, too, then even something as great as fish oil can increase LDL measures. However, the dose of fish oil you are using is very small and not a likely factor.

  • Bob

    10/1/2011 2:57:34 PM |

    Thanks for the reply Dr. Davis. I know I won't go back to carbs and sugar, but what about beef. I have eaten almost nothing but beef the last 14 months. Would I be better off going back to skinless chicken breast? Egg Beaters, instead of eggs? Olive oil instead of butter? I know in the past when I limited saturated fat my HDL dropped to mid 30's.
    Bob

  • Dr. William Davis

    10/2/2011 2:46:17 PM |

    Hi, Bob--

    I think we could make a strong argument in favor of variety in diet and that includes meat sources. Yes, I think a broader range of meats (if you eat them; I don't want to sound like a bloodthirsty carnivore; I don't even like meat, personally) is better--fish, shellfish, fowl, pork, as well as eggs.

  • ShottleBop

    10/3/2011 10:02:47 PM |

    Results came back today:
    TC:  373 mg/dL (ref <200)
    LDL-C:  282 mg/dL (ref = 40)
    Trigs:  47 mg/dL (ref < 150)
    Large VLDL:  <0.7 (ref <=2.7)
    LDL-P:  1793 nmol/L (ref = 30.5)
    Large HDL-P:  14.2 umol/L (ref >=4.8)
    Small LDL-P:  146 nmol/L (ref  20.5)
    HDL size:  10.0 nm (ref >=9.2)
    VLDL concentration was too low to determine a size
    According to the interpretive information:
    My HDL-P (total) of 39.1 places me in the lowest category of risk (it is beyone "high")
    My small LDL-P places me well below the 25th percentile (while slightly higher than the "low" level of 117), and is indicative of lower risk for CVD
    My LDL size places me well above the 75th percentile, and well into Pattern A territory (75th percentile level is 20.6), and is indicative of lower risk for CVD

  • ShottleBop

    10/3/2011 10:04:16 PM |

    Correction:  My LDL-C was 282, vs. a reference of " 40"

  • ShottleBop

    10/3/2011 10:06:37 PM |

    I give up.  I am typing things in correctly, and the comment system is dropping words (maybe it's interpreting my use of "greater than" and "less than" symbols as markup code?).  My HDL-C was 82.  The reference level is greater than 40.  My LDL-C was 282; the reference level is less than 100.

  • ShottleBop

    10/3/2011 10:09:37 PM |

    I see it dropped more information than I thought at first.  No matter, the conclusion stays the same: except for my LDL particle number and concentration, all of my lipid values indicate that I am at lower (or much lower) than average risk of CVD.  Now if only my body takes that to heart . . ..

  • ShottleBop

    10/3/2011 10:16:32 PM |

    LDL particle size was 22.1
    HDL-P was 39.1 umol/L

  • Dr. William Davis

    10/4/2011 2:41:25 AM |

    Hi, Shottle--

    Your values highlight this tremendous void we have in knowing just what to do about nearly "pure" large LDL particles.

    In other words, you have lots of LDL particles, but they are nearly all the more benign large variety. What level of large LDL particles are "allowable" before they contribute to atherosclerotic plaque formation? Not known. My preference would be, given the extreme abundance of large LDL, to reduce with statin drug. I hate to say this, but this is the occasional exception in which I believe that statins might indeed be beneficial. This is not to be confused with the general and absurd overuse of the drugs, but an application for a very specific genetic variant.

  • Louise

    12/5/2011 10:58:49 PM |

    At last I have had an NMR.  Thank you for the suggestion of PrivateMDlabs.com.  I can recommend this
    to others who find their doctor unwilling to order tests.
    I am pondering my results, trying to figure out if they are okay, or if I need to cut back on fat now, or go lower with carb reduction. What are your thoughts, Dr Davis?
       LDL Particle Number  1091  ( IS this too high??)
        Small LDL - P    129
          LDL size     21
        Large VLDL - P   < 0.7
           Large HDL - P        12.1
            HDL size           9.7
          LP - IR score    11
    Triglycerides are 32  ( lower since I"ve gone completely
    grain free since my last lipid panel)

  • Dr. William Davis

    12/6/2011 5:26:54 PM |

    These values are excellent, Louise! The only less than perfect value is the large HDL, but this tends to drift higher very slowly.

  • GoodStew

    5/11/2013 1:56:57 AM |

    Seems particle size doesn't matter as much as particle number. According to Dr. Peter Attia, a particle is a particle.  More than 1000 is a risk factor whether they're small, medium or large and fluffy.

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