Go the distance!

How long should it take to stop or reverse coronary plaque growth? How long will it require to stop your heart scan score of, say, 350, from increasing at the expected rate of 30% per year, slow it down (we say "decelerate") to less than 30%, or stop it altogether? Or, actually reduce your score?

It can vary widely. Several simple patterns do seem to emerge, however. Our experience is that lower scores, particularly less than 100 at the start, are easier to gain control over. Scores of 50 or less, in fact, commonly can return to zero.

Higher scores, particularly those >1000, are more difficult to slow or reduce, though we've done it many times. You'll generally have to try harder and it may take longer. It's not uncommon to not stop plaque growth with a starting score this high until your 2nd or 3rd year of effort.

Sometimes it may take even longer. An occasional person requires four or five years to gain control. And there are, unfortunately, some people who never really gain complete control. They slow plaque growth compared to what it would have been with conventional efforts, but never completely halt growth. Why? Sometimes it's a matter of less than full commitment. Other times, we just don't know. Thankfully, these especially difficult cases are few and the majority enjoy substantial slowing or reversal.

Since, in some people, success may take time, you've got to stick it out. Have you ever gotten lost in a strange city only to find out later that the place you were looking for was right around the corner? It can be the same way with stopping coronary plaque growth. If you start with a score of 1000 and, after two years of effort, you've only slowed growth to 11% per year and then give up in frustration, you may have missed the opportunity to have stopped growth entirely in your third year.

All we can do is tip the scales heavily in your favor. We provide you with the best tools known. You've got to provide the commitment, the consistent effort of taking your supplements or medication, making the lifestyle changes, choosing the right foods and avoiding the wrong ones. But you've got to go the distance and not give up too easily.

What you need is an expert in health!

Where can you find an expert in health?

In my experience, they're hard--very hard--to find.

Your hospital? Certainly not the hospitals I know. The hospitals I know are experts in disease, but not in health. Hospitals are helpful when you're sick. But if you're well and would like to stay that way, there's no reason to hang around a hospital. Prevent cancer, prevent heart disease, stay well? There's no place for this conversation in a hospital.

In fact, hospital staff are among the most unhealthy people I come across. Obesity is a nationwide problem affecting millions of Americans. But it's especially a problem among people who work in hospitals. I shudder in horror when I go to a hospital cafeteria and witness the sorts of food they serve in hospitals and see what the staff eat. Should they be regarded as experts in health?

How about doctors? If you associate with physicians like the ones I know, most have lots of knowledge about disease, but little understanding of health. A rare one has insight and interest in health.

I went to a recent meeting with my cardiology colleagues. Food served: pizza, Coca-Cola, spaghetti, fried onion rings, white bread with butter. They all dug in without hesitation. Over half were miserably overweight. Several were, in fact, diabetic; several more, pre-diabetic. I know that at least several are smokers. Experts in health?

Drug companies? Well, they're interested in health only as far as it provides profits. But health for its own sake? Ask anybody from a drug manufacturer about their views on the nutritional supplement movement and watch them sneer.

Food manufacturers? You mean like Coca-Cola, Pepsi-Cola, Nabisco, and General Mills? How about fast-food operations like McDonald's, Pizza Hut, and KFC?

The message: Know where to look for genuine information on health. You won't get it from hospitals. You won't get it from drug company marketing. For the most part, you can't even get it from your physician.

Instead, you're going to witness a broad movement towards self-empowerment in health, fueled by the internet and services like ours (Track Your Plaque). These are information resources that are not driven by profit, intent on providing truth, and not afraid to reject prevailing views.

It does not mean that hospitals are unnecessary, or that food manufacturers are evil, or that fast food should be legislated out of existence. We live in a capitalistic society, driven by supply and demand. Hopefully, demand is borne from educated choices from informed consumers. That's where information that's reliable, credible, and not profit driven come in.

Lipoprotein(a) and small LDL

It's been my suspicion for some time that the combination of lipoprotein(a), or Lp(a), in combination with small LDL particles is a really bad risk for heart disease. People with this combination seem to have much higher heart scan scores for age than others. This seems to be a pattern that we'll see in the occasional woman less than 50 years old who already has a high heaert scan score. (It's unusual for women to have detectable coronary plaque before age 50.)

Very little data exists to support this idea and we are in the process of performing a small study to see whether it's true or not. My gut sense: it's among the most potent causes of coronary plaque around.

Case in point: Even though I spend a great deal of my time and energy advocating heart disease prevention, I still maintain my hospital privileges and skills. I had to cover one of the emergency rooms in town this past weekend (a requirement to maintain my hospital privileges).

One of the patients I saw was a 40-year old man--we'll call him Roland-- suffering a very large heart attack, a so-called "anterior myocardial infarction", or a heart attack involving the most important front portion of the heart. Thankfully, he came to the ER within 45 minutes after his chest pain started. The situation was immediately obvious and I was called to the ER. We quickly took him to the cardiac catheterization laboratory and put a stent in the left anterior descending artery and flow was restored. His chest pain dissipated over the next few minutes.

Nonetheless, Roland was left with a large area of reduced contraction of his heart muscle. Only time will tell how much recovery he'll have.

Roland was extremely lucky. The majority of people with closure of the artery that he'd experienced die within minutes. He did, in fact, "arrest" briefly, i.e., his heart became electrically unstable, though he recovered promptly.

Along with the multiple tubes of blood we required to run tests for his heart attack management, we had Roland's lipids and other measures sent off, as well. Wouldn't you know: Lp(a) and small LDL. This may have accounted for a heart attack at age 40.

Keep a lookout for this when you have lipoprotein testing. Conveniently, niacin can be used to treat both patterns, though higher doses are generally required for the Lp(a) part of the pattern. It's also my belief that the sort of Lp(a) measurement performed by the Liposcience laboratory (www.liposcience.com) is superior. They use a particle number based measure, not a weight-based measure. It is therefore independent of particle size, which can vary. Further work will, I believe, reveal some very important insights into the dreaded Lp(a).

"Please don't tell my doctor I had a heart scan!"

I overheard this recent conversation between a CT technologist and a 53-year old woman (who I'll call Joan) who just had a scan at a heart scan center:


CT Tech: It appears to me that you have a moderate quantity of coronary plaque. But you should know that this is a lot of plaque for a woman in your age group. A cardiologist will review your scan after it's been put through a software program that allows us to score your images.

Joan: (Sighing) I guess now I know. I've always suspected that I would have some plaque because of my mother. I just don't want to go through what she had to.

CT Tech: Then it's really important that you discuss these results with your doctor. If you wrote your doctor's name on the information sheet, we'll send him the results.

Joan: Oh, no! Don't send my doctor the results! I already asked him if I should get a scan and he said there was no reason to. He said he already knew that my cholesterol was kind of high and that was everything he needed to know. He actually got kind of irritated when I asked. So I think it's best that he doesn't get involved.


This is a conversation that I've overheard many times. (I'm not intentionally an eavesdropper; the physician reading station at the scan center where I interpret scans--Milwaukee Heart Scan--is situated so that I easily overhear conversations between the technologists and patients as they review images immediately after undergoing a scan.)

If Joan feels uncomfortable discussing her heart scan results with her doctor, where can she turn? Get another opinion? Rely on family and friends? Keep it a secret? Read up about heart disease on the internet? Ignore her heart scan?

I've seen people do all of these things. Ideally, people like Joan would simply tell their doctor about their scan and review the results. He/she would then 1) Discuss the implications of the scan, 2) Identify all concealed causes of plaque, and then 3) Help construct an effective program to gain control of plaque to halt or reverse its growth. Well, in my experience, fat chance. 98% of the time it won't happen.

I think it will happen in 10-20 years as public dissatisfaction with the limited answers provided through conventional routes grows and compels physicians to sit up and take notice that people are dying around them every day because of ignorance, misinformation, and greed.

But in 2006, if you're in a situation like Joan--your doctor is giving you lame answers to your questions or dismissing your concerns as neurotic--then PLEASE, PLEASE, PLEASE take advantage of the universe of tools in the Track Your Plaque program.

People tell me sometimes that our program is not that easy--it requires reading, thinking, follow-through, and often asking (persuading?) your doctor that some extra steps (like blood work) need to be performed. The alternative? Take Lipitor and keep your mouth shut? Just accept your fate, grin and bear it, hoping luck will hold out? To me, there's no rational choice here.

Doctor, why do I have heart disease?

I see a great many people in my practice who come for a 2nd opinion regarding their coronary disease.

When I ask patients whether they ever asked their primary doctor or cardiologist why they have heart disease in the first place, I get one of several responses:

1) My doctor said it from high cholesterol.

2) My doctor said it was "genetic" or "part of your family history" and so unidentifiable and uncorrectable. Tough luck.

3) I didn't ask and they didn't tell me.


Let's talk about each of these.

Can heart disease be only from high cholesterol and, if so, can taking a statin cholesterol drug be a "cure"? In the vast majority of cases, in my experience, cholesterol by itself is rarely the only identifiable cause of coronary disease.

Most people have a multitude of causes (e.g., small LDL, low HDL, vitamin D deficiency, concealed pre-diabetic patterns, etc.). This explains why many people with high LDL don't have heart disease and why others with low HDL do have heart disease. High LDL cholesterol is only part of the cause.

Does "genetic" or being part of your family's history also mean unidentifiable and uncorrectable? Absolutely not.

What your doctor is really saying is "I don't know enough to diagnose the causes because I haven't kept up with the scientific literature", or "I don't want to be bothered with this because it takes a lot of time and pays me very little money; I'd rather wait until you need a stent ", or "The drug representatives haven't told me about any new drugs". This is ignorance and laziness at best, greed and profiteering at worst. Don't fall for it. I hope that by now you recognize that the great majority of causes of heart disease are identifiable and correctable.

If you didn't think to ask, now you know that you should. If you and your doctor don't think about why you have coronary plaque in the first place, how can you develop a program to control it?

You need to ask. And you need to get confident answers. "I don't know" or "It's genetic" and the like are unacceptable.

Pill pushers

Have you read the latest cover story from Forbes magazine? It's entitled "Pill Pushers: How the drug industry abandoned science for salesmanship".

It's great reading. (A condensed version is available at the www.forbes.com website: http://www.forbes.com/business/forbes/2006/0508/094a.html. They require you to provide your e-mail address though it's free.)

Drug industry advertising has raised consciousness of all the prescription therapies available for us--that's good. However, they've gone so far overboard trying to squeeze more and more revenues out of drugs that they've cost this country a huge amount in increased health care costs and even lost lives. (Forbes does a great job of summarizing some of these instances.)

Drugs like Lipitor, Crestor, Zocor; diabetes agents; anti-hypertensive agents, etc., that is, medications taken chronically, a huge financial bonanzas for drug companies. Not only do they get $100-200 per month, but they get it month after month after month. That's per drug.

Now not all medications are bad or unnecessary. There are times when they can be truly necessary and beneficial. But don't rely on drug company advertising to tell us when.

Heart disease reversal is getting easier and easier

I've recently observed that more and more of our patients on the Track Your Plaque program seem to be stopping or reducing their heart scan scores. And they're doing it faster, in less time, and with larger drops in score.

I'm not entirely sure why the sudden surge in success. However, I do wonder if adding therapeutic levels of vitamin D--at least in our generally sun-deprived Wisconsin participants--is responsible. However, we've also gotten a lot smarter on how to correct the parameters that seems to have outsized effects on plaque growth, especially small LDL.

Yesterday alone, we had two people we added to our list of successes. One, an attorney, stopped his score in one year, with no change (compared to the expected increase of 30%). Another, a woman from the northeast, dropped her score 10% in one year. Her story is remarkable for beginning at a score >1000. In general, the higher your starting score, the longer it takes to stop or reduce it.

These are just two examples. It seems to be happening at an accelerating pace.

I can only hope that our surge in success (not 100%--yet!) will continue. But, every week, we're adding more and more people to our list of success stories.

A used car lot on every street corner

Imagine that, every day, a parade of used-car salesmen knock on your front door to sell you a special "deal". Day in, day out they knock, expecting you to hear about their offers openly.

Is there any doubt about their intentions or motives? Of course not. They're just trying to profit from selling you a car.

That's how it is in a medical office nowadays. Drug representatives, 5, 6, or more each and every day, promoting drugs. Except that the profits from drugs are far greater than a used automobile, and there's a third party involved in the transaction: you.

Today, a pushy representative came to my office. My staff and I tried to tell him that I was not interested in speaking to him. But he proved such a nuisance that I finally came out to tell him that I objected to the idea of drug reps just hanging around trying to hawk their wares.

He blurted, "Doctor, do you have patients with angina? Our new drug, ranolazine, is perfect. Forget about nitroglycerin, beta blockers, and all that. Here's the latest study proving it's better." He tried to shove a reprint of the study at me.

Getting to the bottom line, I asked, "What does it cost the patient?"

"Well, the co-pay is between $40 and $60. We're not yet well covered by insurance, so it'll cost patients around $200 a month."

Need I say more? Here's a drug that does little more than help relieve anginal chest pains. It doesn't reverse coronary plaque. It won't avoid heart attack, death, or procedures. It just modestly cuts back on the frequency of chest pain. And all for the cost of a single heart scan--a heart scan that could have prevented the entire cascade of symptoms/procedures/medication/hospitalization etc.

Hospitals, drug companies, medical device manufacturers. They're all businesses that thrive on your doctor's failure to detect and control your coronary plaque. Sometimes, even your doctor is part of this conspiracy to squeeze dollars out of human disease. Don't fall for it.

Heart disease reversal at age 77

I met Agnes 18 months ago after she underwent a heart scan that revealed a scary score of over 1100. Although in her mid-70s, this was still a very high score. (Recall that a score this high carries a risk for heart attack and death of 25% per year.) Poor Agnes was a wreck over this unexpected result. "I can't sleep, I can't stop thinking about it!"

She'd undergone the scan because her 44-year old son had a heart scan score of 2200! Unfortunately, he ended up with a bypass operation for very severe disease.

Despite having been seeing a cardiologist in Boston for the last 8 years for a murmur, we uncovered multiple hidden lipoprotein patterns, many of which she shared with her son. Her most notable abnormalities were a low HDL and small LDL. Nearly 100% of all LDL particles were, in fact, small. This pattern also caused her LDL cholesterol to be underestimated by over 40%.

18 months on the Track Your Plaque program and Agnes came into town to get a repeat scan. Her score was 10.2% lower. She'd learned to live with the idea that she had hidden heart disease missed by her doctor and cardiologist for many years. But knowledge of the substantial reversal she'd achieved in the 18 months on the program gave Agnes tremendous peace of mind.

Agnes left the office with a big smile.

If you need a reason to quit smoking...

If you've read Track Your Plaque, you already know my feelings about smoking and coronary plaque. Smoke, and you will lose the battle for control over coronary plaque growth--it will grow and grow until catastrophe strikes.

Nonetheless, this is not sufficiently motivating for some people.

If you need more motivation to quit smoking, just take a look at your heart scan sometime, accompanied by either one of the doctors or technicians at the scan center you choose. After you've had an opportunity to look at your coronary arteries, take a look at the lungs. The heart is in the middle and the lungs are the two large black areas on either side of the heart. (They're not really black; that's just the way the images are color-coded.)

Smokers will see large cavities in their lungs--literally, half-inch to one-inch wide holes that contain only air. Many of them. These represent remnants of lung tissue, digested away and now useless from the damage incurred through smoking.

Non-smokers should see uniform lung tissue without such cavities.

What surprised me early on in my heart scan experience was how little smoking exposure was required to generate these cavities. A 40-year old, for instance, who smoked a half-pack per day for 10 years would have them. Heavier smokers, of course, showed far more extensive cavities.

Officially, these cavities are called "emphysematous blebs", meaning the scars of the lung disease, emphysema.

When I've pointed out these cavities or emphysematous blebs to patients, 9 out of 10 times they immediately become non-smokers. Commonly, they'd exclaim, "I had no idea I was really damaging my lungs!" Most admitted that they were awaiting some bona fide evidence that they were truly doing some harm to their bodies. Well, that's it.

Give it a try if you're struggling.
Why haven't you heard about lipoprotein(a)?

Why haven't you heard about lipoprotein(a)?

Lipoprotein(a), or Lp(a), is the combined product of a low-density lipoprotein (LDL) particle joined with the liver-produced protein, apoprotein(a).

Apoprotein(a)'s characteristics are genetically-determined: If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. You will also share her risk for heart disease and stroke.

When apoprotein(a) joins with LDL, the combined Lp(a) particle is among the most aggressive known causes for coronary and carotid plaque. If apoprotein(a) joins with a small LDL, the Lp(a) particle that results is especially aggressive. This is the pattern I see, for instance, in people who have heart attacks or have high heart scan scores in their 40s or 50s.

Lp(a) is not rare. Estimates of incidence vary from population to population. In the population I see, who often come to me because they have positive heart scan scores or existing coronary disease (in other words, a "skewed" or "selected" population), approximately 30% express substantial blood levels of Lp(a).

Then why haven't you heard about Lp(a)? If it is an aggressive, perhaps the MOST aggressive known cause for heart disease and stroke, why isn't Lp(a)featured in news reports, Oprah, or The Health Channel?

Easy: Because the treatments are nutritional and inexpensive.

The expression of Lp(a), despite being a genetically-programmed characteristic, can be modified; it can be reduced. In fact, of the five people who have reduced their coronary calcium (heart scan) score the most in the Track Your Plaque program, four have Lp(a). While sometimes difficult to gain control over, people with Lp(a) represent some of the biggest success stories in the Track Your Plaque program.

Treatments for Lp(a) include (in order of my current preference):

1) High-dose fish oil--We currently use 6000 mg EPA + DHA per day
2) Niacin
3) DHEA
4) Thyroid normalization--especially T3

Hormonal strategies beyond DHEA can exert a small Lp(a)-reducing effect: testosterone for men, estrogens (human, no horse!) for women.

In other words, there is no high-ticket pharmaceutical treatment for Lp(a). All the treatments are either nutritional, like high-dose fish oil, or low-cost generic drugs, like liothyronine (T3) or Armour thyroid.

That is the sad state of affairs in healthcare today: If there is no money to be made by the pharmaceutical industry, then there are no sexy sales representatives to promote a new drug to the gullible practicing physician. Because most education for physicians is provided by the drug industry today, no drug marketing means no awareness of this aggressive cause for heart disease and stroke called Lp(a). (When a drug manufacturer finally releases a prescription agent effective for reducing Lp(a), such as eprotirome, then you'll see TV ads, magazine stories, and TV talk show discussions about the importance of Lp(a). That's how the world works.)

Now you know better.

Comments (26) -

  • Matt Stone

    7/1/2010 4:18:14 PM |

    Ah, thyroid normalization. My favorite. Of course, this has a trickle-down effect on DHEA, estrogen, and testosterone as well. Perhaps Lp(a) is one mechanism by which Broda Barnes was able to prevent heart attacks in his patients?  

    http://180degreehealth.com

  • Anonymous

    7/1/2010 4:39:21 PM |

    Aw darn it. Again health info to be confused about. From Taubes' GCBC I read it was apoB supposed to be the one associated with smaller and denser LDL, "the bad LDL", and I thought apoA was the "large and fluffy" or more benign LDL. I'm pretty sure Dr. Lustig says pretty much the same in his "Sugar, the bitter truth" video. There goes my newly acquired "understanding" out the window again.

  • Anonymous

    7/1/2010 4:42:40 PM |

    The last of the 4 treatments doesnt' seem very specific...

    is "T3" a supplement.. if not, how does one go about normalizing the Thyroid?

  • Mike

    7/1/2010 8:12:19 PM |

    That's a lot of fish oil. I take about 1/5 that amount and would find it irritating to have to increase my intake by a factor of 5.

  • Drs. Cynthia and David

    7/1/2010 9:52:19 PM |

    If the pharma industry could actually come up with drugs that work and don't just chase surrogate markers, I'm sure that would be helpful.  I'm all for nutritional and lifestyle fixes, but this won't work perfectly for everyone all the time, so useful drug therapies would be nice too.

    Anonymous, I think you're confusing LDL pattern A and B ("fluffy" vs dense) with apoA and ApoB (HDL associated vs LDL associated proteins).

    Cynthia

  • Anthony

    7/1/2010 10:20:10 PM |

    Dr. Davis,
    How low do you like to see Lp(a)? I've seen recommendations of below 30mg/dl, below 20, and below 10. Mine is 19. Thanks,

    Anthony

  • Dr. William Davis

    7/2/2010 1:12:23 AM |

    Anthony-

    Excellent question . . . for which there's no solid answer.

    Despite all we know about Lp(a), no endpoint data have been generated. However, I can tell you that using particle count measurements in nmol/L a level of 60 nmol/L works very well. In mg/dl, a measure of weight per volume, it depends on the method of measurement used. If the "normal" range is 30 mg/dl or less, then aiming for around 20 mg/dl has worked well.

  • Anonymous

    7/2/2010 1:32:33 AM |

    I asked my cardiologist about it (heads up preventive cardiology at a major research institution in Texas) and he said:

    "Well, there's not anything we can do about it, so why test it?"

  • Anonymous

    7/2/2010 1:55:40 AM |

    My cardiologist and PCP have never ever discussed this with me even though I brought it up for discussion. I think my PCP didn't know much and ignored it. I desperately need a new cardiologist (I live in the SF bay area). Anybody here love their cardiologist and like to share some details? I will be forever thankful Smile

    TIA

  • Paul

    7/2/2010 6:09:32 AM |

    I found this to be a very interesting post over at the Animal Pharm blog concerning this very subject:
    Auto-Tuning Lp(a): Value of Low Carb, High Sat Fat


    They basically come to a very simple conclusion in controlling Lp(a); eat some damn saturated fat! And stay away from the damn carbs!

    Now, let me get back to making my LDL the plain and fluffy kind... someone pass me the ghee please...

  • Harry

    7/2/2010 2:41:24 PM |

    Anonymous and Drs. Cynthia and David, there are several "A" designated particles that frequently get confused. Dr. Davis is talking about lipoprotein(a), with a lower case "a", which consists of an LDL particle with a particle of apolipoprotein(a) attached to it. This apolipoprotein is also designated by a lower case "a". Lp(a) is very atherogenic, and should be minimized.

    Apolipoprotein A, with an upper case "A", on the other hand, is an atheroprotective particle that is a component of HDL. It comes in several varieties. The most plentiful one is designated Apolipoprotein A-I, or Apo A-I, which is the main particle that participates in reverse cholesterol transport, which is the principal way that HDL protects against atherosclerosis, by removing cholesterol from plaque and transporting it back to the liver for disposal. There are also particles designated Apo A-II and Apo A-IV that are also associated with HDL, but their function is not well understood. All the HDL-associated apo A particles are described with the upper case "A".

    Finally, there is the LDL pattern A, which indicates that the LDL particles are mostly large, whereas LDL pattern B indicates that LDL particles are mostly small. These are usually designated with an upper case "A" and "B", and the A pattern is thought to be less atherogenic than the B pattern.

    It is easy to confuse these "A" types, especially Apo A and Apo a, which are two very different particles, the large A apo is good and the small a apo is bad.

  • Kent

    7/2/2010 3:21:25 PM |

    My LP(a) started a year and a half ago at 198 nmol/L, it is now down to 35 nmol/L. Thanks to Dr, Davis's advice that I followed in the Track Your Plaque book, including 4800mg combined EPA, DHA fish oil and 2000mg Niaspan, etc.

    I also want ot mention though that I have been following the Linus Pauling protocol as well, which I believe has a synergistic effect with the other principles applied.

    An interesting thing happened that is worth mentioning, my LP(a) had been gradually dropping over that period of a year and a half from 198 to 45 nmol/L, then I switched to immediate release niacin and my LP(a) jumped back up to 150 nmol/L. That was the only change I made, so I switched back to Niaspan and that is when it went back down to 35 nmol/L.

    Kent

  • Alfredo E.

    7/2/2010 3:35:40 PM |

    Hi All.The following paragraphs were taken from http://www.drlam.com/opinion/Lp(a).asp

    Lipoprotein A, commonly called Lp(a), is a major independent risk factor for cardiovascular disease. The optimum laboratory level should be under 20 mg/dl and preferably under 14 mg/dl.

    Currently, there is no medicine or drugs that to effectively lower your Lp(a). A high Lp(a) is genetically linked. Fortunately, Mother Nature has provided us a much better non-toxic alternative. It consists of large doses of vitamin C, L-lysine, and L-proline.

    Many conventionally trained physician uses niacin to reduce Lp(a). This does work to a limited extend. Niacin reduces the production of lipoprotein A in the liver, and helps to bring down the lipoprotein A in the blood. This is what most conventional doctors use. However, this approach has its limitations because until the endothelial wall is optimized and cleared, the lipoprotein A level will not be able to reduce significantly. The effects of niacin usually hit a plateau after 6-9 months of therapy. If you are on niacin, make sure the liver enzyme levels are taken periodically to make sure the liver is able to handle the high dose of the niacin.

    This last flower:
    Replacing carbohydrates with proteins ignores the fact that protein, once in the intestinal tract, converts to amino acid. Amino acids increase insulin secretion. It is unclear, however, whether proteins are as potent as carbohydrates in stimulating insulin secretion.

    My comment: Is it possible that protein can produce high insulin secretion? So, what is left for simple humans? No carbs, no protein?

  • Anonymous

    7/2/2010 3:52:13 PM |

    Is the LDL carried in the blood by a protein or has it already been oxidized. I'm trying to understand what form chlorestral is in the blood.

  • David

    7/2/2010 6:17:02 PM |

    Alfredo,

    It's true that protein stimulates insulin, but the key is that it doesn't only stimulate insulin. Glucagon, insulin's counter-regulatory hormone, is also stimulated. Insulin secretion  is undesirable in the context of low glucagon (which is what we have with high carbohydrate intake), but it's not such a big deal when the ratio of the two are more balanced (which is what we have with low-carb protein intake).

    David

  • Jack C

    7/3/2010 12:03:08 AM |

    The VAP cholesterol profile, which gives the distribution of LDL and HDL particle sizes a other information, shows an upper limit of 10 mg/dl for Lp(a)cholesterol.

    In recent tests, my wife had an Lp(a) of 6 while mine was 8. Through no fault of our own I might ad.

  • Dr. William Davis

    7/3/2010 12:13:49 AM |

    HI, Kent--

    Great results!

    You are living proof that Lp(a) can indeed be tamed. It sometimes requires some unusual strategies, but huge reductions are possible . . . and Lipitor is not part of the equation.

    Long-term commitment to the effort is the key.

  • Anonymous

    7/3/2010 1:29:29 AM |

    what kind of doctor shoudl i see to get the right tests done.  I know I have high Lipo(a) from a previous test at Mayo.  They recommended that I take drugs and I declined.  Now I'm realizing I don't have the complete story.  I need to know more than just my lipo(a) is high.

    thanks!
    Linda

  • Anonymous

    7/3/2010 6:04:15 AM |

    Hi
    Are there stats on people with lp(a) that don't develop any plaque?
    Also does the same happen with lp(a) as with ldl? that is that is better to have a higher mg/dl with big paricles than a lower mg/dl with small particles?
    Santiago

  • Hans Keer

    7/3/2010 7:28:36 AM |

    I would say apoprotein(a) is normal phenomenon. What is not normal is the abundance of small dense LDL which apoprotein(a) binds to. So the best way to avoid LP(a), is to avoid the abundance of sugars and starch in the diet. All the other (still costing) treatments for Lp(a) won't be necessary then.

  • jd

    7/3/2010 5:39:38 PM |

    Hi,   I recently had a VAP test done via LEF -- I seem to have some very good numbers and some bad LDL ones.  Any comments would be appreciated.

    all values in mg/dl
    LDL 105
    HDL 71
    VLDL 14
    Total Cholesterol 190
    Triglycerides 51
    LP(a) 4.0
    IDL 3
    HDL2 18
    HDL3  53
    VLDL3 8
    LDL1 PatternA 5.4
    LDL2 PatterA 7.5
    LDL3 PatternB 61.6
    LDL4 PatternB 22.4


    LDL Density pattern = B, flagged abnormal

    Vit D  65.4 ng/ml
    Homocysteine 6.2
    C-Reactive Protein 0.2

    I am 55 yr of age, 6'0", 165 lbs, exercise regularly.

    Heart disease in family, mother's father died of heart attack at 66, other 3 grandparents lived into 90s.  father died leukemia cancer 53, mother living at 80 in good health.  Thanks,   Jim

  • Anonymous

    7/7/2010 4:40:46 PM |

    I use Lugols solution 2% and I have absolutely no idea what dosage I should be using.  I have been using one drop about twice a week, but I would like to have a better idea of proper dosage.  Can you help?

  • James L.

    7/13/2010 9:52:15 PM |

    My cardiologist is treating my high Lp(a) with Niaspan, but even with high doses, it has not had much effect. What do you mean by items 3 and 4 on DHEA and T3? Please be more specific. Thanks.

  • Anonymous

    7/29/2010 9:06:55 PM |

    Could you give some dose for T3 and DHEA that you are recommending?

    Thanks!

  • Anonymous

    8/10/2010 8:38:43 AM |

    "If your Mom gave the gene to you, you will have the same type of apoprotein(a) as she did. "

    Does that mean that high levels of Lp(a) is not inherited from the father?

    Thanks

  • LisaMichelle

    8/24/2011 11:46:03 PM |

    Dear Dr. Davis,

    I'm a 44 yr old female.   I recently had a consultation w/ a cardiologist here in Canada.   I was sent for the consultation because of some strange left jaw and low chest tightness I'd experienced at work the week prior (had been seen then in the ER, normal ECG x 2, normal CXR, normal bloodwork).  Prior to the appt I was told I needed to have fasting bloodwork (so that results were available for the cardiologist to review at my appt).  

    HDL good, LDL good (though at the higher end of the normal range).  Lipoprotein A was 0.55 g/L (which i guess works out to 55 mg/dl which is what the usual unit of measurement is for this one in the U.S.).  The cardiologist told me that all of my bloodwork was normal and that I was very low risk for a heart attack but I requested a copy of my results just to have on file.   I am surprised she didn't mention the elevated Lipoprotein A (normal range for this lab is: 0.00 to 0.33 g/L).   So that got my on my search for info on what exactly Lipoprotein A is, and what it indicates.

    My question is:   I was only told to fast for 12 hours prior to my bloodwork, nothing was said about ensuring I didn't smoke.   Well I did smoke over the 12 hours up until the blood was drawn (even about 30 minutes prior to).   Now I'm reading online that one should not smoke prior to blood being drawn for Lipoprotein A, HDL and LDL, etc.    So could my smoking right up to the time bloodwork done have negatively impacted the results?   Could smoking have made my LDL and Lipoprotein A higher?    Should I have these redone but ensure I don't smoke for 12 hrs prior to blood draw?  (I have a 'quit date' set for next Saturday, so don't worry, I will be quitting).

    Thanks so much,
    Lisa

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