Are there any alternatives to niacin?

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

Is flaxseed oil a substitute for fish oil?


This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

If you have coronary artery disease . . . do you know why?

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

Have you tried inulin yet?

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.


The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

Fish oil update on Life Extension

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

More on Vitamin D

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.

Why not just get "perfect" lipids and call it a day?

What if you achieved the Track Your Plaque lipid targets: LDL cholesterol 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl?

After all, these are pretty stringent standards. Compared to national guidelines (the ATP-III Guidelines of the National Cholesterol Educational Panel), the Track Your Plaque 60-60-60 goals are laughably ambitious. There's a lot of wisdom hidden in those numbers. The triglyceride level of 60, for instance, is a level at which triglycerides become essentially unavailable for formation of triglyceride-containing lipoprotein particles such as small LDL and VLDL.

If you get to the 60-60-60 target, isn't that good enough? What if you just held your values there and went about your business? Will coronary plaque stop growing and will your CT heart scan score stop increasing?

Sometimes it will. But, unfortunately, many times it will not. The experience generated through clinical trials bear this out. Studies like the St. Francis Heart Study and the BELLES Trial both showed that just reducing LDL cholesterol is insufficient to stop plaque growth. Beyond the Track Your Plaque experience, there's no clinical trial experience that shows whether the 60-60-60 approach does any better.

In our experience, achieving 60-60-60 is indeed better than just reducing LDL. That makes sense. Just raising HDL from the average of 42 mg/dl for a male, 52 mg/dl for a woman adds advantage. Compound this with triglyceride reduction from the plaque-creating equation, and you've doubled success.

But there's even more. What if you had hidden patterns not revealed by conventional lipids? How about lipoprotein(a)? Small LDL? Postprandial (after-eating) abnormalities? Hypertensive effects (more common than you think)!

In 2006, stopping the increase in your heart scan score is, for most of us, not just a matter of taking Lipitor or its equivalent and sitting back. For nearly all of us, stopping the progression of your score is a multi-faceted effort.

Hospitals: Then and Now

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.


Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.




Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.

The dreaded small LDL particle

Brian is a 59-year old landscape architect whose starting CT heart scan score was 276.

Brian's food choices at the start were deplorable: a pound of sausage per week, sometimes more; butter on anything and everything; up to two pounds of cheese per week; hot dogs; etc. His lipoproteins were accordingly just as miserable: low HDL, high triglycerides, excessive (postprandial, or after-eating) IDL. Small LDL was a particularly stand-out pattern, with 95% of all LDL particles in the small category.

Brian made a dramatic turnaround in lifestyle and corrected all of his patterns--except for small LDL. After one year, small LDL still occupied 95% of all LDL particles, even though the quantity of LDL had been reduced. In order to help convince Brian that correction of his small LDL was going to be necessary to achieve control oover coronary plaque, I suggested that he undergo another heart scan. His score: 435, or a 57% increase.

Each day that passes, I gain more and more respect for small LDL as a cause for coronary plaque growth. Conventional thought among lipid experts is that small LDL should no longer be a factor if total LDL (e.g., LDL particle number) is reduced. But our experience suggests otherwise: when small LDL persists, we tend to see continued, sometimes frightening, plaque growth.

I therefore asked Brian to intensify his efforts: additional weight loss off his somewhat prominent abdomen (since visceral fat increases small LDL), further reduce wheat products and processed carbohydrates, increase niacin (to 1500 mg per day), and use more raw almonds and oat bran.

Don't let small LDL get the best of you. It is a nasty, sometimes persistent abnormality that has impressive effects on plaque growth.

Winning Through Intimidation

Do you remember the book, Winning Through Intimidation by author Robert J. Ringer?



In his 1984 bestseller, author Ringer details how to succeed in business by overwhelming clients and competition by appearing hugely successful and powerful. Rather than a business card, he'd hand out an elegant book to represent himself. He'd show up in a limousine to a meeting, even when he could barely afford it. He used these tactics, even when he was a small-fry, in commercial real estate and built a successful business following such techniques.

This reminds me a lot of what happens in conventional medical practice: The large and successful hospitals, filled with trained staff and technology, exude legitimacy and success. How can they possibly be wrong? Such overwhelming know-how and multiple levels of expertise mustbe right!

Let's be grateful that we do have access to such high-tech, capable care. Unfortunately, just as Mr. Ringer used deceptive practices to appear something he wasn't, this is also true in hospitals. Not all physicians have your best interests in mind. Their principal concern is how profitable your care can be for them--can you be persuaded to have your stent, bypass, etc.. After all, look around you: Aren't all this equipment and personnel impressive? Aren't you intimidated?

The patient that most recently drove home this issue for me recently was a smart and capable executive who came in for consultation. He had been told by his internist that a surgery (to replace his aorta, a HUGE procedure) was probably necessary. In my view, it was not--his process was simply not that far progressed. The risks for danger over the next several years was virtually nil. Unfortunately, this man, now confused and worried, sought an opinion from the chief of thoracic surgery (in the usual white coat and with professorial demeanor, I'm sure) in a major metropolitan hospital (in Chicago), who promptly rushed him off to the operating room.

The pathology report, cleverly not mentioned in any other of the hospital documentation, showed what I had suspected: this man had mild disease that wasn't even close to requiring surgery. But, with all that technology, $100,000 or so of costs, chief of surgery who looked the part, etc.--they must be right!

Robert Ringer's concepts only ring too true for hospitals and some of the unscrupulous physicians in practice. Don't allow yourself to be intimidated.
Red flags for lipoprotein(a)

Red flags for lipoprotein(a)



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.

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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