What to eat: Part I

6. April 2010 William Davis (0)
I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

4. April 2010 William Davis (16)
There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

4. April 2010 William Davis (0)
Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

3. April 2010 William Davis (1)
It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

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.
Red flags for lipoprotein(a)

Red flags for lipoprotein(a)

17. January 2008 William Davis (24)


Lipoprotein(a), Lp(a), is an important cause for heart disease, heart attack, and coronary atherosclerotic plaque.

How do you know you have it?

Of course, it could be as simple as checking a blood level. But there are also a number of red flags for the presence of Lp(a), tell-tale signs that suggest it is present and contributing to the growth of coronary plaque.

I've seen so much of this pattern over the years that it's gotten so that I can pretty much pick out most of the people with Lp(a) just by either looking at them or by hearing their story. I do this simply by knowing what hints to look for.

Some of the red flags for Lp(a) include:

--High blood pressure in a slender person. Overweight is the overwhelmingly common reason for high blood pressure. However, inappropriate high blood pressure in a slender person can serve to tip you off that Lp(a) is present.

--HIgh LDL cholesterol poorly responsive to statin drugs. For instance, someone's LDL cholesterol of 190 mg/dl will be treated with Lipitor 40 mg, but drops to only 165 mg/dl, a very poor response. This can sometimes point towards Lp(a).

--Family clustering of heart disease in people before age 60. For instance, father with heart attack age 53, uncle with heart attack at age 55, aunt with heart attack age 59, etc. This clustering of risk, more often than not, signals Lp(a).

--Coronary disease or high heart scan score in the presence of relatively bland appearing lipids. For instance, LDL cholesterol 130 mg/dl, HDL 55 mg/dl, triglycerides 70 mg/dl on no medications or other efforts--figures ordinarily not associated with high likelihood of heart disease--yet heart disease is indeed present. This can mean that Lp(a) is the concealed culprit behind coronary atherosclerosis.

These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

Once Lp(a) is identified, then the battle begins to gain control over this somewhat troublesome genetic pattern. Resourcesfulness and some ingenuity may be required. However, knowing that you have it shows you where to concentrate your efforts.
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Comments (24) -

  • Anonymous

    1/17/2008 1:03:00 AM |

    I wish I knew more about exactly what Lp(a) will do that will cause me problems.  I have high Lp(a)(22 on my VAP test).

    I am 5'2" and weight 110.  I am a fitness professional -  healthy blood pressure level.

    My TC at it's worse was 226 with low Trig, high HDL, and high LDL (144).  My Dr wanted me to get the LDL down with drugs.  I chose the supplement path, and increased my fiber intake.

    My TC is now around 224, but my HDL is 86, and LDL 118.  My real LDL size pattern is A/B.  My HDL 2 & 3, and VLDL 3 are all in the desireable range.

    Oh - I do have a family history of heart disease (mother had strokes in her 60s).

    I had a heart scan - no measurable plaque found.  I'm 55 years old.

    That darn LpInnocent.  Should I be worried it's going to do something I'm not aware of?

    Bonnie

  • Dr. Davis

    1/17/2008 1:41:00 AM |

    Yes. You might have a Lp(a) variant that accounts more for carotid disease than coronary disease, judging from your mom's history. Also, you are still young. Some women will not fully express Lp(a) characteristics until their late 50s.

    All the principles we talk about for Lp(a) on the Track Your Plaque website still apply. Also, please see our upcoming report that summarizes unique strategies for Lp(a) treatment to be released in the next two weeks.

  • Anonymous

    1/17/2008 5:32:00 AM |

    If Bonnie thinks her LP(a) at 22 is high, I guess mine is high also at 24, but at least its a whole lot better than it was 18 months ago when it was 52.   I attribute the reduction to DMAE and NAC,thanks to your recomendations, Dr. Davis.

    Your list of possible examples of high LP(a) just doesn't include me.

    My BMI is 21.  I have relatively low blood pressure,95-110 over 70.  My age is 65.   Total Chol=190; LDL=110  HDL>65 and sometimes as high as 100.  Low Trigs < 70.

    No family history (mother still kicking at 95). Father died in hi 70's from pancreatic cancer with a very strong heart and lung system.  And yet I have had a really high LP(a)!!!

    I can't afford a CT scan, as much as I would like to get one, but I did have a lipoprotein breakdown which showed
    VLDL=25; LDL particle number 789 dense LDL IV=101 HDL Total=9066 and Buoyant HDL 2b=2528.  All  measured in (nmol/L).  My density was neither A nor B, but in an intermediate zone near the A border.

    My homocysteine is raised (12.26) probably because of the 750mg of Slo-Niacin I take, but I'm trading niacin's lipid enhancements for it.

    When my LP(a) was at 52, all blood work was similar to now, weight was the same, exercise, diet, everything was the same.   I don't understand why it was so high.   I was hoping your list would give me a clue, but I'm just not on it!!!

    Noreen

  • Anonymous

    1/17/2008 6:44:00 AM |

    Thanks.  My mom unfortunately led an extremely sedentary lifestyle, and didn't eat well or take care of herself.  I always assumed her strokes were a result of that.  I guess it was probably part of it, but not all of it.

    I did not know about Carotid disease - seems all I ever hear about is Heart Disease these days.

    I look forward to finding out more about the new approaches to dealing with Lp(a)!

    Bonnie

  • Dr. Davis

    1/17/2008 1:36:00 PM |

    Hi, Noreen-
    I'm curious about the DMAE. I've used it (unsuccessfully) for memory enhancement, but not to reduce Lp(a). What is the basis for this?

  • Anonymous

    1/17/2008 3:45:00 PM |

    Big Goof, Dr. D!!!  I was tired and didn't get up to check my supplements.  I'm taking 50mg of DHEA for lowering the LP(a)!!!

    Sorry, thats what I get for getting into this stuff so late at night!!!

    I'm still at a loss as why mine went so high (52)!!!   Especially with no family history of heart disease.

    Noreen

  • Anonymous

    1/17/2008 4:11:00 PM |

    Noreen - your post reminded me of something that I find curious.

    When I first had my Lp(a) tested it wsa a separate test from my Cholesterol test.  Results came back 59 wih a reference range of  0-29.  

    Next time it was measured it was part of a VAP test, and when I saw it at 22 I thought it had dropped (by some miracle Smile.  Then I noticed the reference range was different, and that the high end of the range was 10.  

    Different tests maybe?

    Bonnie

  • Anonymous

    1/17/2008 6:00:00 PM |

    Thanks Bonnie -- Yes, it was different labs, but the reference range was less than 30 on each one.   I did read somewhere that some labs use less than 20 as the normal range, but these two labs used < 30.

    This lab also did a nutrient profile and found that I was deficient in pantothenate, glutamine and glutathione.   I was already taking 500mg NAC, but they recommended 1000mg, so I'm now taking 1200mg of Jarrow Sustain NAC in hopes it will satisfy the glutathione deficiency and lower that LP(a) further.  

    I also started taking pantothenate to satisfy that and read that it can reduce LDL, so I'm hopefull there.   I upped the glutamine that I was already taking and switched to a powder form.

    Thanks,
    Noreen

  • Dr. Davis

    1/17/2008 7:41:00 PM |

    Hi, Noreen-
    Somebody, Mom or Dad, had to give you Lp(a), though the expression and consequences of Lp(a) can vary.

  • Anonymous

    1/17/2008 8:25:00 PM |

    Is it a dominant characteristic from just one parent or can it be a recessive one from both with neither having it?   I don't think my mom has ever been tested, but her doctor said her heart is still very strong at 95.    My paternal grandfather died of a massive heart attack at 78.  Before that he was hospitalized several times with fluid in his chest (cardio-myapthy) maybe?

    I was under the impression that if it were genetic that nothing will reduce it.  Is this wrong?   Mine did come down to 24 after taking the NAC and DHEA.   I'm really looking forward to reading that paper on lowering it too.  Thanks so much,
    Noreen

  • Bad_CRC

    1/17/2008 9:09:00 PM |

    Dr. Davis, just to clarify:

    1. Lp(a) is not like IDL, where having any measurable amount is abnormal, right?  Mine was 7 mg/dL, and I took this to mean that I don't "have Lp(a)."

    2. Also unlike IDL, small LDL, etc., it's purely hereditary and not a symptom of metabolic syndrome or similar, correct?  So if I don't have it at 30, I don't need to worry about developing it by 50?

    Thanks

  • Dr. Davis

    1/17/2008 10:26:00 PM |

    Lp(a) is genetic but blood levels are manipulable. But Mom or Dad HAD to give it to you, they just may not have fully expressed its consequences (which does happen occassionally, for not entirely clear reasons).

  • Dr. Davis

    1/17/2008 10:28:00 PM |

    Hi, Bad--
    Yes, correct on both counts.

  • Anonymous

    1/17/2008 10:33:00 PM |

    But Mom or Dad HAD to give it to you, they just may not have fully expressed its consequences (which does happen occassionally, for not entirely clear reasons).

    So Dr. Davis, are you saying that if you have this genetic marker, that it is inevitable that at some point down the line it will do bad things - no matter how good all of the rest of your risk factors are? (assuming there continues to be no reliable way to reduce it).

    Bonnie

  • Dr. Davis

    1/17/2008 10:54:00 PM |

    No, not inevitable, but darn close. It could be expressed as hearet disease, carotid disease, aneurysms, or just hypertension.

  • Anonymous

    1/18/2008 2:29:00 AM |

    Are there any major differences between  Lp(a) testing via a VAP test as compared to NMR?

    VAP seems to use a lower test range (over 10 being considered high). Does this mean their test is different than others, or simply they use a lower marker to differentiate between high and low? And would a Lp(a) test via VAP be as accurate as one from NMR, etc,?

    My VAP numbers for Lp(a) was pretty low, around 4-5, if I remember right. I just want to make sure this was an accurate test.

  • Dr. Davis

    1/18/2008 1:19:00 PM |

    There are several methodological differences among the various Lp(a) measures. For this reason, I advise everyone to always stick with the same laboratory. There may also be differences in the validity or accuracy. This is detailed in a full Special Report on the Track Your Plaque website.

  • Joan

    1/18/2008 8:54:00 PM |

    My Lp(a) score came back at 160--that's right--160!  I have a stent in one artery, obviously I have CAD.  I presently take Zocor 20 mg. and an Ace Inhibitor drug.  I can not take Niacin---what can I do?


       Joan

  • Anonymous

    1/19/2008 2:35:00 AM |

    Dr Davis,
    My Cardiologist has me on 1500mg Niacin which reduces LP(a)to around 30 and that seems to be about the lowest I can get it, as more Niacin gives me a rash. So He says we need to reduce LDL as low as possible by diet,exercise and possibly a low Statin dose. Reducing the amount of carriers, He says, will negate to a large degree, the risk of my high LP(a). Does this sound like sound treatment?   Thanks.....

  • Dr. Davis

    1/19/2008 5:06:00 AM |

    That sounds like a very solid approach to Lp(a). Congratulations to your doctor for being up to date in his thinking about Lp(a).

    Also, watch for an upcoming report on our Track Your Plaque website for a review of unique therapies for Lp(a).

  • Dr. Davis

    1/19/2008 5:13:00 AM |

    I'm afraid that's a bit too much to handle in a blog post.

    You are invited to read our Track Your Plaque Special Reports on Lp(a), including an upcoming review of unique therapies to be posted within the next two weeks.

  • Anonymous

    1/19/2008 5:40:00 AM |

    Also, watch for an upcoming report on our Track Your Plaque website for a review of unique therapies for Lp(a)

    Can you see me tapping my foot..... impatiently.....  

    Smile  
    (Just kidding)


    I hesitate to take Niacin because I have a tendency toward slightly high liver enzymes for some reason (possibly mild NAFLD since all other tests came back negative), and I've read Niacin can raise liver enzymes.  I look forward to hearing about other possibilities.

    Bonnie

  • Anonymous

    2/20/2008 6:50:00 PM |

    SO after all is said and done should a LP(a) redaing of 12 be of any concern? It is noted as "high" on my VAP test but it certainly is close to normal. All of my other readings on the VAP are normal.

    John

  • buy jeans

    11/3/2010 2:26:48 PM |

    These red flags are not perfect. If you lack any of them, it doesn't necessarily rule out the possbility of having Lp(a). They simply serve as signs to suggest that Lp(a) may be lurking.

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