Heart attack guaranteed

What if you knew for a fact that your risk for heart attack was 100% by, say, age 58? This is indeed true for many people, though at age 60, 65, 70--or 45.

In other words, unless something were done about the causes of heart disease, you would inevitably suffer a heart attack at 58.

What sort of action could you take at age 45?

Obviously, not smoking is an absolute requirement. Continue and you may as well start getting your affairs together.

How about exercising and eating a generally healthy diet? Will your risk be reduced to zero? No. It might be reduced 20-30%, depending on genetic factors.

How about a statin drug? Watch TV ads during Oprah, and you might think it's a cure. But in reality, while it is a financial bonanza for the drug manufacturers, it will reduce risk for heart attack by 30%.

(Note that risk reduction by following multiple strategies is not necessarily additive. In other words, if you have a healthy lifestyle and take a statin agent, is risk reduced 60% (30 + 30)? No, because the effects may overlap.)

So, eating healthy, exercising, and taking a statin drug might reduce risk 35-40%, maybe 50% in the best case scenario. Would you be satisfied? Most would not.

Add fish oil at a truly therapeutic dose. Risk reduction by itself: 28%.

Add niacin or other strategies for correction of your individual, specific causes of heart disease: Now we're up to 90% reduction.

Throw in a tracking process to prove whether or not atherosclerotic plaque has progressed or reversed. Now we're approaching 100% if plaque reverses. The only way I know how to track plaque is through CT heart scans. What other test is readily available to you with low radiation exposure, yet is relatively inexpensive and precise? It certainly is not stress testing, heart catheterization, CT angiograms, or other techniques. Cholesterol won't tell you. Besides CT heart scans, there's nothing else I know of.

Let's fact it: For many people, uncorrected risk for heart attack is truly 100% at some age. Take action while you can.

That, in a nutshell, is the Track Your Plaque program.

Heart scan curiosities 3



This is a sample image from the heart scan of a 54-year old, 212 lb, 5 ft 2 inch woman. The heart is the whitish-gray in the center; lungs are the dark (air-filled) areas on either side of the heart. Note the massive amount of surrounding gray tissues that encircles the heart and lungs. This is fat. At this weight, the diameter of total fat exceeds the combined diameter of the heart and lungs. If we were to show the abdomen, there would be even more fat. (The image shows the body not well centered because the technologist centers the heart, since this is, after all, a heart scan.)





This is a 55-year old, 151 lb, 5 ft 4 inch woman. Note the contrast in the quantity of fat tissue surrounding the chest, a much more normal appearance. Note that this woman is still around 25 lb over ideal weight, but not to the extreme degree of the woman above.

Another curious observation: Note the more whitish streaking in the heavier woman's lungs. Heart scans are performed while holding a deep inspiration (a deep breath inwards), mostly to eliminate lung respiratory motion during image acquisition. Nonetheless, the heavier woman's lungs are not as fully expanded as the more slender woman. In other words, the heavier woman cannot inflate her lungs as effectively as the thinner woman. Ever notice how breathless heavy people are? Some of this effect is just being out of shape. But there's also the added effect of the abdominal fat exerting upwards compression on the lung tissues, and the constrictive effect of the encircling fat mass. At the beginning of inspiration, the chest fat exerts the resistance of inertia to inspiration that is absent, or less, in a slender person. With each breath, the heavy woman must move 50 lbs or so of surrounding fat mass just to inhale.

The heavier woman is, in effect, suffocating herself in fat.

The distortions to the human body incurred by extreme weight gain are both fascinating and shocking. I hope you're breathing easily.

The shameful "standard of care"

John's initial heart scan four years ago showed a score of 329. His physician prescribed Zocor for a somewhat high LDL cholesterol.

One year later, John asked for another scan. His score: 385, a 17% increase. John exercised harder and cut his fat intake.

This past fall--3 years after his last scan--John had yet another heart scan. Score: 641, a 66% increase over the last scan, all the while on Zocor.

John sought an opinion from a reputable cardiologist. He concurred with the prescription of Zocor and advised annual stress tests. That's it.

Followers of the Track Your Plaque approach know that the expected uncorrected rate of increase in heart scan score is 30% per year. On Zocor or other cholesterol reducing statin agent, a common rate of growth is between 18-24% per year--better but not great. Plaque growth is certainly not stopped.

But that is the full extent of interest and responsibility of your cardiologist. Prescribe a statin drug, perform a stress test, and the full extent of his obligation has been fulfilled. In legal terms, your physician has met the prevailing
"standard of care". No more, no less.

In other words, the prevailing standard of care falls shamefully short of what is truly possible. For the majority of the motivated and interested, coronary plaque reversal--reduction of your heart scan score--should be the standard aimed for. It's not always achievable, but it is so vastly superior to the prescribe statin, wait for heart attack approach endorsed by most cardiologists.

Heart scan curiosities 2



This is an example of a so-called "hiatal hernia", meaning the stomach has migrated through the diaphragmatic hiatus into the chest--the stomach is literally in the chest. This example is an unusually large one. Hiatal hernias can cause chest pain, indigestion, and a variety of other gastrointestinal complaints. Heart scans are reasonably useful to screen for this disorder, though very small ones could escape detection by this method.

Sometimes, you can actually hear the gurgling of stomach contents (the common "growling" stomach) by listening to the chest. Large ones like this actually crowd your heart (the gray structure above the circled hernia), irritating it and even causing abnormal rhythm disorders. The dense dark material within the hernia represents lunch.

I would not advocate CT heart scans as a principal method to make a diagnosis, but sometimes it just pops up during a heart scan and we pass it on to the person scanned.

Vitamin D: New Miracle Drug

At the meetings of the American Society of Bone and Mineral Research, Dr. Bruce Troen of the University of Miami detailed his views on the extraordinary benefits of vitamin D replacement. He also talked about the enormous problem of unrecognized vitamin deficiency.

“There’s a huge epidemic of hypovitaminosis D, and the real key here is not just that it’ll benefit you from a bone and neuromuscular standpoint, but if you correct hypovitaminosis D and the corresponding secondary hyperparathyroidism, then you’re going to decrease prostate cancer, colon cancer—actually “up to 17 different cancers, breast cancer included.”

Unfortunately, Dr. Troen did not talk much about the heart benefits of vitamin D, likely since the data is scant, nearly non-existent. However, if the Track Your Plaque experience means anything, I predict that vitamin D replacement will become among the most powerful tools you can use to gain control over coronary plaque.

Read the text of a report from the Internal Medicine World Report to read more of Dr. Troen's comments.


http://www.imwr.com/article.php?s=IMWR/2006/11&p=40

Heart disease "reversal" by stress test


Here's an interesting example of a 71-year old man who achieved "reversal" of an abnormality by a nuclear stress test.

This man underwent bypass surgery around 10 years ago, two stents three years ago. A nuclear stress test in April, 2005 showed an area of poor blood flow in the front of the heart. On the images, normal blood flow is shown by the yellow/orange areas. poor or absent blood flow is shown by the blue/purple areas within the white outline.

Now, I can tell you that this man is no paragon of health. He's only accepted limited changes in his otherwise conventional program--in other words, someone who I'd be shocked achieved true reversal of his heart disease. (I didn't have him undergo any CT heart scans because of the difficulties in scoring someone who has undergone bypass surgery and stents, and because of limited motivation. True plaque reversal is for the motivated.)This patient did, however, accept adding fish oil and niacin to his program.

Nonetheless, stress testing can be helpful as a "safety check". Here's the follow-up stress test:
You'll notice that the blue/purple areas of poor blood flow have just about disappeared. This occurred without procedures.

Does this represent "reversal"? No, it does not. It does represent reversal of this phenomenon of poor flow. It does not represent reversal of the plaque lining the artery wall. That's because improvement of flow, as in this man, can be achieved with relatively easy efforts, e.g., improvement in diet, statin drugs, blood pressure control, etc. True reversal or reduction of coronary plaque, however, is tougher.

If blood flow is improved, who cares whether plaque shrinks? Does it still matter? It does. That's because the "event" that gets us in trouble is not progressive reduction in blood flow, but "rupture" of a plaque. A reduction in plaque--genuine reversal--is what slashes risk of plaque rupture.

Calcium reflects total plaque





People frequently ask, "Why measure coronary artery calcium? My doctor said that calcium only tells you if there's hard plaque, and that hard plaque is stable. He/she says that calcium doesn't tell you anything about soft plaque."

Is that true? Is calcium only a reflection of "hard" plaque? Is hard plaque also more stable, less prone to rupture and causes heart attack?

Actually, calcium is a means of measuring total plaque, both soft and hard. That's because calcium comprises 20% of total plaque volume. Within plaque, there may be areas that are soft (labeled "lipid pool" in the diagram). There are also areas made of calcium (shown in white arcs within the plaque). Even though this is just a graphic, it's representative of what is seen when we perform intracoronary ultrasound of a live human being's coronary artery. In other words, this cross section contains both "soft" (lipid pool) as well as "hard" (calcium) elements.

Is this artery "soft" or "hard"? It's both, of course. The artery compostion can vary millimeter by millimeter, having more soft or hard elements. The artery can also change over time in either direction. Thus, "soft" plaque may indeed be soft today, only to be "hard" in 6 months, and vice versa.

The essential point is that measuring just "soft" plaque provides limited information. What the CT heart scan does is provide a gauge of total plaque, soft and hard, and it does so easily, safely, precisely. If your score increases, the lengthwise volume of total plaque has also grown. If your score decreases, the total amount of plaque has also decreased.

Don't mistake marketing for truth

We're all so inundated with marketing messages for food. Unfortunately, many people confuse the messages delivered through marketing with the truth.

For instance:

Pork: "The other white meat." Pork is a high-saturated fat food.

"Bananas: A great source of potassium." Bananas are a high glycemic index (rapid sugar release), low fiber food.

"Pretzels: A low-fat snack." A high glycemic index food made from white wheat flour. It makes you fat and skyrockets blood sugar.

Jif peanut butter: "Choosy moms choose Jif." Do they also choose hydrogenated fats?

Hi-C: Upbeat jingles like "Who put the straw in my Hi-C fruit drink, a new cool straw that wriggles and bends? Who put the straw in my Hi-C fruit drink, with Vitamin C for me and my friends? Who was that man, I'd like to shake his hand, he made my Hi-C cooler than before!" What about the 25 grams of sugar per 4 oz serving? And the high fructose corn syrup that creates an insatiable sweet tooth, raises triglycrides 30%, and exagerates pre-diabetes?


Marketing is not reliable, unbiased information. If Ford boasts that their cars are superior to GM, do you say "Well then, I need to buy a Ford?" Of course not. Take marketing for what it is: A method of persuading people to buy. It may or may not contain the truth. It's a big part of the reason Americans are the fattest people on earth and are experiencing an explosion of chronic diseases of excess.

Tattered Red Dress

"Are you taking your health to heart? Perhaps you understand the importance of eating a diet low in cholesterol or getting 30 minutes of exercise a day. But do you know your own risk of developing cardiovascular disease?


It’s time to take your heart health personally. Heart disease is the No. 1 killer of American women — and that means it is not “someone else’s problem.” As a woman, it’s your problem.

That’s where the Go Red Heart Checkup comes in. This comprehensive evaluation of your overall heart health can help you now and in the future. By knowing your numbers and assessing your risks now, you can work with your doctor to significantly reduce your chances of getting heart disease tomorrow, next year, or 30 years from now!"



So reads some of the materials promoted by the American Heart Association Red Dress campaign to increase awareness of heart disease in women. The effort is well-intended. There is no doubt that most women are unaware of just how common coronary disease is in females.

But I've got a problem with the solutions offered. "Know your numbers"? Eat healthy, don't be overweight, be active, don't smoke. That's the gist of the program's message--nothing new. In 2006, why would some sort of screening effort for detectin of heart disease not be part of the message? Why isn't there any message about the real, truly effective means to detect hidden heart disease in women--namely, heart scanning?

Does a 58-year old woman with normal blood pressure, LDL 144, HDL 51, 20 lbs overweight have hidden heart disease? I've said it before and I'll say it again: You can't tell from the numbers. She could die of a heart attack tomorrow without warning, or maybe she'll be dancing on our graves when she's 95 and never have experienced any manifestation of heart disease. The numbers will not tell you this.

I'm glad the American Heart Association has seen fit to invest its sponsors' money in a campaign to promote prevention. I wish they hadn't fallen so far short of a truly helpful message. Perhaps the sponsors (like Pfizer, maker of Lipitor) will benefit, anyway.

Panic in the streets

Several days ago, I wrote about a local prominent judge in my neighborhood who was unexpectedly found dead in bed of a heart attack at age 49.

As expected, I've received multiple calls from patients and physicians who want heart catheterizations. For instance, an internist I know called me in a panic. He asked that I perform a heart catheterization in a patient with a heart scan score of 768. I've been seeing this patient for about a year. He's without symptoms, even with strenuous exercise; stress tests (i.e., tests of coronary bloow flow) have been normal.

I remind patients and colleagues every day, day in day out: Having a heart scan score revealing some measure of coronary plaque is not a sufficient reason by itself to proceed with procedures. Fear of suffering a fate like the unfortunate judge is also not a reason to proceed with procedures.

Increased awareness of the gravity of heart disease is a good thing. Some good can come out of a needless tragedy like this. The lesson from the judge's unfortunate experience: he needed a CT heart scan. I'm told that the judge's doctor advised him that a heart scan was a waste of time. I hope that appropriate legal action for negligence is taken by the judge's family against this physician.

Not doing a heart scan is wrong. That's the lesson to learn. The lesson is not that everybody with coronary plaque needs a procedure. Had the judge undergone a simple heart scan, intensified prevention could have been instituted and he'd still be alive with his wife and children today.

The indications for procedures are unchanged by your heart scan. If a stress test is abnormal and indicates poor flow to a part of the heart, that would be a reason. If symptoms like chest discomfort or breathlessness appear, that's an indication. If there's evidence of poor heart muscle contraction, that's a reason to proceed with a procedure. But just having coronary plaque is not a sufficient reason.
Is Lp(a) part of your legacy to your children?

Is Lp(a) part of your legacy to your children?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

Comments (21) -

  • craig&jan

    9/15/2009 4:59:09 AM |

    Finally switched to a new PCP who says she loves lipids!  Very interested in all facets of cardiac risk, thyroid, etc.

    My father is 88 and still very active. My mom passed away at 84 following her first health event which was a stroke.  
    I have been following this blog's recommendations for supplements, diet,etc. The new dr did a lipid panel and without any rx meds, my total was 199, HDL 61, Tri 68, LDL 124.  My Lp(a) was tested by my previous dr and was 34. I was told that was high and I probably had inherited my mother's pattern and she most likely had an Lp(a)problem. The new dr says I must go on Crestor 5mg a day to lower my LDL to 100. She says that will protect me from depositing more plaque in the coming years, in effect immobilizing the Lp(a). Would you say that was a fair assessment and reason to start on a statin?  She feels the lowest dose possible is enough to benefit by lowering the LDL.  Your post is exactly the situation I'm in and adding meds are my biggest question.  I will tell my children who are in their late 20's. I'm in my mid-50's with no other health issues.  I'd love your take on it.

    Thanks.

    Jan

  • craig&jan

    9/15/2009 4:59:09 AM |

    Finally switched to a new PCP who says she loves lipids!  Very interested in all facets of cardiac risk, thyroid, etc.

    My father is 88 and still very active. My mom passed away at 84 following her first health event which was a stroke.  
    I have been following this blog's recommendations for supplements, diet,etc. The new dr did a lipid panel and without any rx meds, my total was 199, HDL 61, Tri 68, LDL 124.  My Lp(a) was tested by my previous dr and was 34. I was told that was high and I probably had inherited my mother's pattern and she most likely had an Lp(a)problem. The new dr says I must go on Crestor 5mg a day to lower my LDL to 100. She says that will protect me from depositing more plaque in the coming years, in effect immobilizing the Lp(a). Would you say that was a fair assessment and reason to start on a statin?  She feels the lowest dose possible is enough to benefit by lowering the LDL.  Your post is exactly the situation I'm in and adding meds are my biggest question.  I will tell my children who are in their late 20's. I'm in my mid-50's with no other health issues.  I'd love your take on it.

    Thanks.

    Jan

  • Dr. William Davis

    9/15/2009 11:57:55 AM |

    Hi, Jan--

    Sadly, that is the typical primary care response, someone who has minimal to no insight into Lp(a).

    So, no, I would not agree with this approach that was first popularized by a single substudy performed by Dr. Greg Brown at the University of Washington.

    I take a very different view of Lp(a) that varies depending on age. However, this is a lengthy topic either for a future post or refer to the detailed discussions in the Track Your Plaque website.

  • ABick

    9/15/2009 3:47:10 PM |

    Dr. Davis - Is any amount of Lp(a) a significant risk factor for CVD?  Or is there a relatively safe threshold that if one is below there should be limited risk?

  • steve

    9/15/2009 4:42:52 PM |

    Dr Davis:  what would you say is a high Lp(a)? The NMR range is <75nmol, and the other measurement i think is <32or 40dl.  Would a 30-40 be high on NMR, or 15-20 per dl?
    Thanks,

  • Scott Miller

    9/15/2009 8:01:37 PM |

    Dr. Davis,

    I read all of your posts, greatly admire your practice, open-mindedness, and vast knowledge.

    I have measured my Lp(a) for several years, and have kept it at a bare minimum, usually below 8, most recent a reading of 3. I do this through a paleo-like diet:

    o High-fat (avoiding polyunsaturated fats, but high in saturated fats, mono unsaturated fats, and marine omega-3's)
    o Moderate protein (mostly from animal sources)
    o Low-carb (no grains, no added sugars, absolutely no processed fructose, and eating mostly high-water-volume vegetables, which are naturally very low in actual glucose polymers)

    My primary goals:
    o Maintain ultra low inflammation
    o Maintain low insulin usage (thru maintaining low-normal blood glucose, in the 80's)

    I'm 48, in supremely great health, and look around 35-yrs-old.

    My question: I've thoroughly looked for studies linking Lp(a) to gluten consumption, but I've come up empty. Are you aware of any studies?

  • Dr. William Davis

    9/15/2009 9:17:14 PM |

    AB and Steve--

    Because there are several different methods to measure Lp(a) for which the "reference ranges" differ, it is best to consult the range offered by the lab used, which are pretty good indicators of normal vs. abnormal.

    Scott--

    I know of no data specifically relating gluten to Lp(a). Anecdotally, there may be an effect, but it is likely relatively small.

  • Scott Miller

    9/16/2009 2:14:38 AM |

    Dr. Davis, I thought you had found in your practice a link between gluten and Lp(a). Or, at least, wheat and Lp(a)?

  • Dr. William Davis

    9/16/2009 2:30:01 AM |

    Hi, Scott-

    It's difficult to separate out the effects of wheat elimination vs. carbohydrate reduction, increased fat/oil intake. So I cannot say with absolute confidence that gluten specifically affects Lp(a).

    It's an interesting concept, but I don't believe that we have an answer.

  • David

    9/16/2009 4:41:08 AM |

    Dr. Davis- Have you ever seen Lp(a) cause heart disease in the very young? Under 35 or even under 30? I know that even children can have high Lp(a), and it makes me wonder if plaque growth is going on throughout childhood in these cases or if it is rather somehow "activated" once a certain point is reached and accelerates in a very short time toward the kind of events we see in the 40s and 50s age groups.

  • Lou

    9/16/2009 4:16:09 PM |

    Dr Davis

    I found a lab in Europe that will do an Lp(a) test and also Apolipoprotein A. I want to do the Lp(a) test as you suggest.

    The lab also offers an Apolipoprotein B test. Is the Apolipoprotein B of any use value? I couldn't see much info about it on your blog/book.

    Thanks
    Lou

  • Kent

    9/16/2009 4:54:47 PM |

    I see various thoughts and studies on the effects of monounsaturated fats on LP(a). I see Scotts example of using lots of saturated and monounsaturated fats and lowering his LP(a). I see other studies where they say monounsaturateds can raise LP(a) by 10-12%. What gives?

  • Dr. William Davis

    9/17/2009 1:45:11 AM |

    Hi, David--

    Rarely will Lp(a) cause heart disease before age 35. There are always exceptions, but they are exceptionally rare.


    Lou--

    Apo B is an improvement over calculated LDL. Yes, it is worth the few extra bucks. My personal favorite, however, is NMR LDL particle number, the best measure of LDl by a long stretch. Apo B is a second best.

  • Dr. B G

    9/17/2009 2:13:23 PM |

    Kent,

    Saturated fatty acids (SFA)indeed potently control Lp(a) in the clinical trials as well as anecdotally in our TYP membership. Why? SFA are actually hormonal in action, binders of receptors just like omega-3 fatty acids which lower inflammation and raise HDLs.

    There is a study that shows if Lp(a) is = or < than HDL2, Lp(a) is effectively 'neutralized'. Some of our members had HDL2 of > 40-50 mg/dl. In fact, Lp(a) and HDL track  together and  Dr. Davis' TYP program includes every facet and strategy that raises HDL to one's genetic potential:
    --thyroid and hormone replacement
    --wheat/gluten/carb elimination
    --vitamin D

    With every 10% increase in vit D, there is a ~1% increase in HDL. Did u know Crestor raises vit D by 159%?! Of course Crestor has NASTY side effects -- Crestor raises oxLDL + Lp(a)).

    -G

  • Dr. B G

    9/17/2009 2:13:23 PM |

    Kent,

    Saturated fatty acids (SFA)indeed potently control Lp(a) in the clinical trials as well as anecdotally in our TYP membership. Why? SFA are actually hormonal in action, binders of receptors just like omega-3 fatty acids which lower inflammation and raise HDLs.

    There is a study that shows if Lp(a) is = or < than HDL2, Lp(a) is effectively 'neutralized'. Some of our members had HDL2 of > 40-50 mg/dl. In fact, Lp(a) and HDL track  together and  Dr. Davis' TYP program includes every facet and strategy that raises HDL to one's genetic potential:
    --thyroid and hormone replacement
    --wheat/gluten/carb elimination
    --vitamin D

    With every 10% increase in vit D, there is a ~1% increase in HDL. Did u know Crestor raises vit D by 159%?! Of course Crestor has NASTY side effects -- Crestor raises oxLDL + Lp(a)).

    -G

  • Anonymous

    9/17/2009 6:32:59 PM |

    My brother had a MI right after he turned 29. My parents now in sixties, do not have cholesterol related heart disease yet although my mom has some issues now due to thyroid problems. She has also developed diabetes unfortunately.

    Would this be Lp(a) related incidence?

  • Kent

    9/18/2009 5:10:58 PM |

    Dr. BG, Thanks for your response on the subject of fats. I was aware that saturated fats could substatially lower LP(a), however my area of concern has more to do with the mono unsaturated fats. Scott mentioned how he had lowered his LP(a) with a diet that included high intake of the mono unsaturated fats. Yet, I have read elsewhere that the mono unsaturated fats can raise LP(a) by 10-12%. (Vessby B et al 2002).
    So I guess my question remains do monos raise or lower LP(a)

  • Florida Butterfly

    2/9/2010 2:07:29 AM |

    I am 22 and just found out that I inherited the elevated lp(a) levels. As of now my number his higher than my dads! He just avoided a heart attack, and had stents put in just before it reached that point. Needless to say I inherited it from him.  I am starting Niacin, only 100 mg.  I will say that it is a serious struggle for me to change my lifestyle as in diet and exercise so early.   My lp(a) # was 65

  • buy jeans

    11/4/2010 5:13:10 PM |

    (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

  • Anthony Cozzi

    11/24/2011 1:46:27 AM |

    Dear Dr. Davis
    I am 58 years old and have had three stents ( one in 2000 and two in 2008 ).  My Lp(a) is >200 according to my last Berkely Test in 2010.  I am soon having another Berkely Test and would like to know exactly what I should have tested besides my Lp(a) and particle size.  I have been taking Niaspan (1500mg daily) and Simcor 1000/20, Fish Oil and Vitamin D3 ( 6000 iu ) all daily.  Would you suggest me taking any DHEA ?  I would really appreciate hearing from you.  I live in Chicago and could visit your office. 708-925-3010.  Thank you.
    Anthony Cozzi

  • Dr. William Davis

    11/25/2011 2:12:20 PM |

    Hi, Anthony--

    Thyroid assessment is crucial in Lp(a): TSH, free T3, free T4. Also, a DHEA level. Both issues are very important.

    Sorry, but my practice is now closed to new patients, since we were booking 6 months in advance. However, much of this can be found in the Track Your Plaque website.

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