Optimal medical therapy

I was re-reading some of the details behind the recently announced COURAGE Trial comparing angioplasty/stent in 1100 people compared to "optimal" medical therapy in another 1100. You'll recall that no difference was found.

In particular, over approximately 5 years, 20% of participants in each group died, experienced heart attacks, or strokes. Of those treated with "timal" medical therapy, 32% ended up getting a procedure like stents or bypass anyway due to deteriorating symptoms.

What is "optimal" medical therapy? I bring this up again because the study investigators in COURAGE, as well as in similar trials, say this with a straight face. Optimal medical therapy means aspirin and/or Plavix (the anti-platelet, aspirin-like blood thinner); "aggressive" statin drug therapy to reduce LDL cholesterol to 60-85 mg/dl; and "anti-ischemic" therapy (that reduces angina and the phenomena of poor coronary blood flow) using nitroglycerin preparations, beta blockers, and other drugs.

I do give credit to the investigators for having the courage to perform this trial in a world hell bent on doing procedures and still reporting the neutral outcome. But the notion of "optimal" medical therapy begs for comment.

Indeed, this is regarded as optimal by most practitioners. Some would even argue excessive, based on the low LDL target achieved. Would you be satisfied with a 20% likelihood of heart attack, stroke, or death or 5 years, a 1 in 5 roll of the dice? I would not. Recall that we aim for near-total elimination of risk.

What could have been further "optimized"? Plenty. For instance:

--What is the real LDL, not the fabricated, calculated LDL? The two can be commonly 100 mg/dl different.

--How about raising HDL to 60 mgd/?

--What about reducing the proportion of small LDL particles? After all, small LDL is the number one cause of heart disease in the U.S., not high LDL.

--What is Lp(a)? If you treat LDL with a statin drug, Lp(a) is unaffected and continues to trigger huge plaque growth. You will fail if this is not identified and corrected.

--What is vitamin D3? One of the most powerful facilitators of plaque reversal I know of.

--What are triglycerides? Triglycerides create hidden particles in the blood like intermediate-density lipoprotein, potent triggers for coronary plaque growth. Speaking of intermediate-density lipoprotein, that's another very important pattern to identify, the after-eating persistence of dietary fats.

--Why aren't they taking fish oil? With a 28% reduction in heart attack and 45% reduction in sudden death from heart attack, this alone would have halved the number of "events" in the "optimal" medical treatment group.

Of course, there's more. But the idea that aspirin, statins, and anti-ischemic therapy is somehow optimal is silly and sad at the same time. But that's the bias. The COURAGE Trial does represent a step forward, a step away from the "stent everyone and everything" mentality that motivates my colleagues, aided and abetted by their co-conspirators, the hospitals. But you and I know better. "Optimal" medical therapy, in truth, can mean a far better approach that can dramatically reduce, perhaps eliminate, risks for events like heart attack. The conventional "optimal" medical therapy will suffice only if you're content with a 20% likelihood of heart attack, death or stroke, or a 32% likelihood of an urgent procedure in your future.

Niacin, postprandial patterns

For a detailed report on the very important postprandial (after eating) patterns that contribute hugely to heart disease risk, read my recent article in Life Extension Magazine, available (no cost) at:

Uncovering a Hidden Source of Cardiovascular Disease Risk
at http://www.lef.org/magazine/mag2007/mar2007_report_heart_01.htm


For a report on using niacin to reduce risk of heart disease, see another report in the same issue of Life Extension:

Ask the Doctor: Using Niacin to Improve Cardiovascular Health
at
http://www.lef.org/magazine/mag2007/mar2007_atd_01.htm.

Also, keep your eyes open for a lengthy report focused exclusively on the Track Your Plaque program in an upcoming issue of Life Extension. I'll provide links in this Blog when it comes out.

What's better than fish oil?

One of the recent questions on our Track Your Plaque Forum related to what to do about a triglyceride level of 101 mg/dl while on fish oil.

Recall that, contary to conventional thinking like that articulated in the ATP-III cholesterol treatment guidelines, we aim to reduce triglycerides to 60 mg/dl or less. This is important to suppress the formation of abnormal triglyceride-containing lipoprotein particles, especially small LDL, reduced HDL, lack of healthy large HDL, VLDL. ATP-III advises a level of 150 mg/dl or less. Unfortunately, triglyceride levels this high guarantee appearance of all these undesirable particles and an increasing heart scan score.

What's better than 4000 mg of fish oil for its 1200 mg of EPA and DHA (omega-3 fatty acids)? More fish oil. In other words, the 4000 mg fish oil providing 1200 mg EPA + DHA is our minimum. A simple increase to 6000 mg to provide 1800 mg EPA + DHA is usually all that is necessary to reduce triglycerides and put a halt to the cascade of abnormal lipoprotein particles that trigger plaque growth. Occasionally, a somewhat higher dose may be required. Doses are best divided into two, with meals (e.g., three capsules twice a day).

Another important issue: An over-reliance on wheat products can also increase triglycerides. This includes any flour product like breads (regardless of whether it's white, whole wheat, or whole grain--they all raise triglycerides), pretzels, bagels, breakfast cereals, and pasta. A dramatic reduction in wheat-containing products will reduce triglycerides substantially, help you reduce your abdominal fat, reduce blood pressure, raise HDL and reduce small LDL, clear your mind, provide more energy, avoid afternoon "fogginess" . . . Huge benefits.

Valve disease and vitamin D

There are two common forms of heart valve disease: aortic valve stenosis (stiffness) and insufficiency (leakiness), and mitral anular calcification.

Both valve issues are regarded as evidence of senescence, or aging--the older you are, the more likely you will have one or both. Both conditions involve progressive calcium deposition and, to some degree, cholesterol deposition. They might be regarded as phenomena of "wear and tear" just like hip arthritis.

There are no known therapies to stall or stop the development of mitral anular calcification. However, several attempts have been made over the years to identify treatments that can slow or stop the progression of aortic valve disease, which is becoming increasingly common and is addressed by surgical valve replacement when severe. The most recent trials have examined whether high-dose Lipitor (80 mg) has any effect (it did not) and high dose Crestor (40 mg), which slowed but did not stop the deterioration of stiff valves.

It's been my suspicion that vitamins D and K2 may play a crucial factor in valve health. After all, vitamin D is the master controller of calcium deposition. Preliminary data also suggest that people who are intentionally made vitamin K deficient with the drug, Coumadin, develop twice the calcium deposition on aortic valves that non-Coumadin takers develop.

I saw a patient Friday, Marianne. In addition to a moderate heart scan score of 379 at age 71, Marianne had a leaky (insufficient) aortic valve. By an echocardiogram 18 months ago, the valve was moderately leaky. I put Marianne on vitamin D, 4000 units, to raise her blood level to 50 ng/ml.

Last week, I asked Marianne to have another echocardiogram. This time, no leakiness whatsoever--none. I have never seen this happen before. Although Marianne is only one example and we don't want to extrapolate too far from the experience of one person, it's hard not to attribute this phenomenal response to vitamin D supplementation.

I wonder what would have happened if we had added vitamin K2, as well?

Anyway, just another potential wonderful effect of vitamin D restoration.

Homocysteine and coronary plaque

If you’ve watched the news over the past year, you know that doubt has been cast over the idea that reducing homocysteine blood levels with high doses of B vitamins (B6, B12, and folic acid, or B9) results in reduced risk for heart attack.

Is the homocysteine concept dead? Shall we empty our bottles of costly B vitamins into the trash and move on?

I don’t think so. As detailed in one of our Track Your Plaque Special Reports from a few months ago, I think the homocysteine issue still deserves lots of respect and further investigation. After all, hundreds of clinical studies have connected higher homocysteine levels with greater risk for heart disease, stroke, and aneurysm. Numerous studies, for example, have repeatedly and consistently demonstrated a tripling of heart attack risk when homocysteine levels exceed 14 ?mol/l. Can we dismiss this association because several more recent studies—NORVIT, HOPE, and VISP—suggested that, when starting homocysteine levels are 12.5, that B vitamin supplementation does not reduce heart attack risk?

I think there’s lots more to know about the homocysteine connection. That said, I have never seen a patient who I thought had heart disease strictly because homocysteine was increased.

I believe that we can at least use homocysteine as an index of lifestyle: the higher the homocysteine, the poorer the diet, or the less effective the absorption of B vitamins (especially vitamins B12 and folic acid). Homocysteine levels of <9 micromol/l suggest both adequate intake and absorption of these B vitamins.

If homocysteine is tightly connected with risk for heart disease, yet supplementation of B vitamins fails to reduce risk, might there be another means of connection? Or, could both homocysteine and heart disease be connected in some way that has nothing to do with B vitamins?

Don’t close the book on homocysteine. Just because conventional experience fails to draw connection does not necessarily mean that none exists. If it’s any consolation, taking B vitamins has been correlated with better memory, concentration, and other health benefits, even if no reduction in heart disease develops.

Big heart scan scores drop

High heart scan scores of, say, greater than 1000 are more difficult to reduce than lower scores.

I learned this lesson early in the experience of trying to drop scores. In the first few years of trying to drop scores, I saw relatively modest scores of 20, 50, or 100 drop readily, even when the usual targets were not fully achieved, and even before the incorporation of some of the more exciting recent additions to the Track Your Plaque program, like vitamin D.

But big scores of 1000, 2000, or 3000 are a tougher nut to crack. In the first few years, what I usually saw was a slowing , or "deceleration," of growth from the expected rate of annual score increase of 30% that would continue for a year or two, followed by zero change. In the first year of effort, for example, a score increase of 18% was common. 10% was common in year two, then finally zero change in year three. Somehow, the more plaque you begin with, the more "momentum" in growth is present and the longer it takes to stop it. Kind of like stopping a compact car versus stopping a freight train.

But more recently, I'm seeing faster drops. Today, Charlie came to the office to discuss his second heart scan. 18 months earlier, Charlie's first scan showed a score of 3,112, high by anybody's standard.

His repeat score: 3,048. While the drop is relatively small on a percentage basis and may even fall within the expected rate of error for heart scans (which tends to be <2% at this high a score), I told Charlie that it still represented a huge success. Not only did he not increase his score by the expected 30% per year, he also brought a charging locomotive to a rapid stop.

Next year, Charlie is targeting a big drop. Given the tools he now has available, I'm optimistic that he will succeed.

Watch for the Track Your Plaque May, 2007 Newsletter in which we will detail Charlie's story further.

Does the American Heart Association diet reduce heart disease?

If you have a heart attack and land in the hospital where, invariably, you will have a heart procedure. Or, if you get a stent or coronary bypass operation, sometime before your discharge from the hospital, a well-meaning hospital staff dietitian will provide instruction in the American Heart Association (AHA) diet.

Does this diet reduce the risk of heart disease?

The answer depends on where you start. If you begin with a conventional American diet that is enormously influenced by convenience, food manufacturers like Nabisco, General Mills, Quaker Oats, ADM, and Cargill, or food distributors like McDonald’s, Pizza Hut, and Taco Bell, then the American Heart Association diet is indeed an improvement. But just a small one. If LDL cholesterol is the yardstick, the average reduction in LDL is between 10 and 15 mg/dl. This is the same amount of change you’d experience by adding 1 tablespoon of oat bran to your diet. Hardly worth boasting about. HDL, triglycerides, blood glucose, and body weight do not change.

The diet could be substantially better. After all, it’s become common knowledge that other diets, such as the so-called Mediterranean diet, the South Beach Diet, and similar broad projects result in far greater changes than the AHA diet dispensed by your hospital and cardiologist. These diets more effectively reduce LDL, raise HDL, reduce triglycerides, reduce C-reactive protein, reduce blood pressure. Diets like South Beach also yield substantial weight loss and reversal of diabetic tendencies, with the magnitude of benefit dependent on the amount of weight lost.

Why this stubborn adherence to the outdated concepts articulated in the AHA diet? Cardiologists would argue that insufficient data has been generated to permit widespread application of these diets. They also differ on whether they really work. Of course, the majority remain ignorant and dismiss them as fad diets.

A little digging into the financial disclosures of the AHA suggests another, more malignant influence: who is paying the bills? Until recently, drug manufacturers were major contributors to the AHA. However, more recently AHA administrators have become sensitive to the public perception that they might be nothing more than a voice box for the drug industry. They have since limited contributions from the drug companies to 8% of annual charitable revenues.

The drug manufacturers have been replaced by the food industry. In addition to food manufacturers that make the cereals on your grocery shelf, it includes the multi-national conglomerates that produce unimaginable revenues and carry enormous political clout, like ADM and Cargill. Ever wonder how it is that Honey Nut Cheerios received a “Heart Healthy” endorsement from the AHA?

The AHA diet does not provide the answers we’re looking for, not even close. It is a perversion from an organization that has its strings pulled by industry. The answers to health will not come from the AHA, AMA, the American College of Cardiology, the American Hospital Association, and it won’t come from your doctor. It won’t come from a titillating report on the evening news or Good Morning America. It will come from collective and expanding wisdom placed directly into the hands of the public. It will be untainted by the temptation of drug industry dollars. It will not be dirtied by million dollar contributions, or the multi-million dollar behind-closed-doors lobbying of the food manufacturers. It will come from the truth relayed to the healthcare-consuming public. I hope you recognize it when you see it.

If you want a healthy diet for your heart, throw away the pamphlets from the AHA unless you are partial to bread, breakfast cereals, corn, and the supporters of their misguided nutritional advice.

Vitamin K2 and coronary plaque

The vitamin K2 story, though still preliminary, is becoming increasingly interesting from the perspective of CT heart score reduction.

The origin of this concept came from some unexpected observations. One, the observation that osteoporosis (lack of bone calcium that leads to fractures) arises from deficiency of vitamin K2. Two, deficiency of K2 leads to unrestrained calcium deposition in animal models, leading to heart attack in just weeks.

Vitamin K2 has been largely ignored for years, since the more widely understood K1 is rarely deficient. K1 deficiency can occur from prolonged antibiotic use, or from severe malnutrition. But deficiency in otherwise well people is very uncommon. Vitamin K2, however, may be a different story. Deficiency may be common.

The Rotterdam Heart Study of cheese-eating Dutch showed that greater K2 intakes resulted in a halving of heart attacks. Cheese (traditional varieties, not Velveeta or other make-believe cheese products) is a modest source of K2, as is the Japanese native food, natto. (If you've ever seen natto, I dare you to eat it. I have a pretty strong stomach and curiousity for food, but natto is the one thing I could not eat--it is truly horrible.)

The weight of evidence suggests that vitamin K2 supplementation may prove to be a useful addition to your coronary plaque control program. Clearly, more data are needed, particulary therapeutic obserations, i.e., observing people who take dose X of a K2 prepartion and tracking some feedback measure, e.g., bone density, CT heart scan score, "events" like heart attack, etc.

Nonetheless, the K2 story is clearly worth reading about, perhaps even considering supplementation. Please watch for the Special Report on the www.cureality.com website in the coming days.

Exercise and blood pressure

The media has gotten a hold of a case report from the University of Maryland describing a 51-year old physician who, despite being a long distance runner, had a high heart scan score.

An example of the report can be found at

Heart Disease In A Marathon Runner: Is Too Much Exercise A Bad Thing?

http://www.sciencedaily.com/releases/2007/03/070315091100.htm in Science Daily.



"The mystery was all the more intriguing because his resting blood pressure and fasting cholesterol levels, the usual measures of cardiovascular health, were in the normal range."


When this man was put on a treadmill for a stress test, his blood pressure skyrocketed from a normal 118/78 to 230/78--extremely high, even for exercise. The physicians reporting the case raised the question of whether long-distance running represents a risk for heart disease and if the high blood pressure with exercise is a contributor or cause of the high heart scan score.

These are phenomena we are very familiar with. We have stressed the importance of exercise blood pressure as a trigger for coronary plaque for years. While 230/78 is clearly too high, we find that any blood pressure over 170/80 with exercise adds to the fire and can trigger plaque growth.

However, I think it is absurd to suggest that marathon running itself is a trigger of coronary plaque. I think it is far more likely that the person described in the report had lipoprotein(a), a potent trigger for both exercise-induced hypertension and high CT heart scan scores in seemingly well people. He likely also suffered from a deficiency of vitamin D deficiency, another contributor. There's no need to indict exercise.

If you are in the Track Your Plaque program, you know that stress tests are of questionable helpfulness for the detection of hidden heart disease. But they are useful for assessment of blood pressure responses during exercise. If BP exceeds 170/80 at 10 mets (a measure of exercise effort achieved by walking 3.4 mph at a 14% grade for 3 minutes), then blood pressure may be a contributor to your heart scan score.

"Fish oil is stupid"

"Fish oil is a waste of time and money. It's stupid. Just stop it."

So a patient of mine was advised by another physician when he complained that he occasionally experienced a fishy aftertaste.

This attitude perplexes me. After all the confirmatory data that support the enormous health benefits of omega-3 fatty acid supplementation, including the 11,000 participant GISSI-Prevenzione Trial, you'd think this attitude would be history. What's a little fish aftertaste when heart attack risk is slashed 28%?

Perhaps the tendency to pooh-pooh fish oil is because it's available as a nutritional supplement. This shouldn't make fish oil appear inconsequential. Far from it.

If you witness the extraordinary power for fish oil to reduce triglycerides, you will be immediately convinced of its effectiveness. The ability of omega-3 fatty acids from fish to eliminate intermediate-density lipoprotein (IDL), the persistent abnormal lipoprotein which signals an inability to clear dietary fats from the blood, can also convince you. More than 90% of people with excessive IDL have it completely eliminated by 4000-6000 mg of fish oil (providing 1200-1800 mg EPA + DHA) per day.

The fact that fish oil is available as a prescription "medication," as well as an over-the-counter supplement, causes some physicians to dismiss the power of the supplemental form. This is nonsense. The over-the-counter form is every bit as effective as the prescription form.

The makers of prescription Omacor also make the claim that their preparation is safer and purer. That may be true, but I'd like to see independent verification from the FDA, USDA, or an unbiased organization like Consumer Reports before I accept their marketing as fact--particularly at $120 to $240 per month! If Omacor proves to contain substantially less mercury and pesticide residues, then that will need to be factored in. (Please note that both Consumer Reports and Consumer Labs measured no substantial mercury or pesticide residues in their analyses of 16 and 41 brands, respectively.)

I try to persuade my colleagues that the idea of taking supplements is a wonderful trend that allows people to express ownership of their own health. What people need is guidance, not salesmanship for a more expensive version, nor dismissal of nutritional preparations that actually possess considerable benefits.
Heart Scan Blog readers take impressive doses of omega-3s

Heart Scan Blog readers take impressive doses of omega-3s

Here are the results from the latest Heart Scan Blog poll:

What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)

The 479 respondents answered:

Less than 1000 mg per day
65 (13%)

1000-1999 mg per day
145 (30%)

2000-2999 mg per day
98 (20%)

3000-3999 mg per day
79 (16%)

4000-4999 mg per day
33 (6%)

5000-5999 mg per day
14 (2%)

6000 mg per day or more
45 (9%)


The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.

We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It's clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.

Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no "right" or "wrong" dose of omega-3 fatty acids.

However, there are several factors that enter into knowing your ideal omega-3 intake:

--Higher triglycerides require higher doses
--Lipoprotein(a) can respond to higher doses
--Having coronary or carotid plaque means you desire a "therapeutic" dose of omega-3s, not just a "preventive" dose

Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.

But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL.

Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.

Comments (28) -

  • Mike

    10/24/2009 3:52:01 PM |

    "But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL."

    So what?

    Wolf, Sears, and Poliquin recommend a high fish oil dose of 0.5g-1.9g EPA/DHA per 10lbs BW; this generally equates to 9-10g range.  All three have had amazing success with sedentary, chronically ill individuals and elite level athletes.

    I believe you yourself have stated in the past that fish oil causes a shift from VLDL and IDL to large particle LDL---a benign, if not beneficial action.

    So is the raising of LDL in high dose fish oil even a concern?  Some clarification on this would be appreciated.

  • Dr. B G

    10/24/2009 4:44:35 PM |

    Gosh... what an ODD response to fish oil! *wink* Do you actually believe it?  The reports would be contrary to the literature.  At least fish oil would have a strong role in stabilizing plaque and prevents soft ruptures in growing plaque (just like the Tokelau and Masai, high carb H-G societies)!

    Nowhere in the literature that I can find reports omega-3 increases dense LDL. Perhaps there is a TYP program-omega3 interaction? Or perhaps this only occurs in those who take high-dose statins and fail to convert to Pattern A (due to the overstatination phenomenon, as reported by researchers where TG <  150)) and complain annually about their EBCT plaque progression 10-25%??  I have tried to admonish the statin overuse but apparently that doen't go over well with this individuals as you are aware. Oh well.

    I have noticed that in the summers people's HDLs drift down.  Have you Dr. Davis in your practice?  I suspect a strong fruit-effect on splaying out dense LDL. Thoughts?

    IMHO many on the TYP members consume WAY way way too much grains, orange juice, oat bran, oatmeal, FRUITY SHAKES (e.g. JJ) and consume several servings of fruit all day (e.g Jeg). Do you think this may play any part of complaints related to higher dense LDL?  My first thoughts are ALWAYS... diet.  

    Your observastions are always UNIQUE!!  Thank you putting the highlights on the omega-3 index and the role of n-6 to n-3 on inflammation, the root cause of CAD!  You are certainly the biggest quantum EVOLVER.

    http://drbganimalpharm.blogspot.com/search/label/Evolver

  • Dr. B G

    10/24/2009 4:44:35 PM |

    Gosh... what an ODD response to fish oil! *wink* Do you actually believe it?  The reports would be contrary to the literature.  At least fish oil would have a strong role in stabilizing plaque and prevents soft ruptures in growing plaque (just like the Tokelau and Masai, high carb H-G societies)!

    Nowhere in the literature that I can find reports omega-3 increases dense LDL. Perhaps there is a TYP program-omega3 interaction? Or perhaps this only occurs in those who take high-dose statins and fail to convert to Pattern A (due to the overstatination phenomenon, as reported by researchers where TG <  150)) and complain annually about their EBCT plaque progression 10-25%??  I have tried to admonish the statin overuse but apparently that doen't go over well with this individuals as you are aware. Oh well.

    I have noticed that in the summers people's HDLs drift down.  Have you Dr. Davis in your practice?  I suspect a strong fruit-effect on splaying out dense LDL. Thoughts?

    IMHO many on the TYP members consume WAY way way too much grains, orange juice, oat bran, oatmeal, FRUITY SHAKES (e.g. JJ) and consume several servings of fruit all day (e.g Jeg). Do you think this may play any part of complaints related to higher dense LDL?  My first thoughts are ALWAYS... diet.  

    Your observastions are always UNIQUE!!  Thank you putting the highlights on the omega-3 index and the role of n-6 to n-3 on inflammation, the root cause of CAD!  You are certainly the biggest quantum EVOLVER.

    http://drbganimalpharm.blogspot.com/search/label/Evolver

  • TrueDharma

    10/24/2009 5:50:45 PM |

    My EFA results showed an Omega3 index of 11.7% and a Omega 6:3 ratio of 2.3/1. I supplement with 1600mg EPA and 800mg DHA daily. I follow a low carb (high fat) I can't afford to eat "grass fed", but I do avoid processed foods whenever possible and my dietary fats are from coconut oil, lard, beef tallow, butter, olive oil and small amounts sesame oil. The Omega 3 Index test was a bit pricey, but...it did give me some comfort that I am on the right track.

  • Jae

    10/24/2009 5:53:26 PM |

    For those who witnessed an increase in LDL, what was the profile of small, dense VLDL vs large, fluffy VLDL reflected in the increase?

    Also, first-time commenter. Thank you for a great, informative blog.

  • Adam Wilk

    10/24/2009 8:59:52 PM |

    "But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL."

    I'm hoping (and wondering if...) that while those diligent enough to take that high a dose of omega-3's may have higher measured LDL levels, they indeed have much larger, fluffier particles now than when they began the megadosing.  That would be something marvelous to hear.
    Good stuff here, as usual!
    -Adam

  • Steven Horvitz, D.O.

    10/24/2009 9:35:20 PM |

    If one's LDL's raise dramatically on omega-3's, without the corresponding increase in hdl, or decrease in trigs, is it better to lower the omega 3's?

    Ex:

    pre-omega
    tc 240
    hdl 45
    ldl 165
    tg 70

    during 2000mg omega-3's
    tc 320
    hdl 58
    ldl 240
    tg 90

    Also, the pattern size of the ldl's are type a with a low carb, no grain diet.

  • homertobias

    10/24/2009 11:29:56 PM |

    I'd very much like to know what subfraction of LDL was elevated in the TYP followers on 9,000 plus omega 3's a day.  My experience is that large fluffy LDL increases but not small dense.

  • Kevin

    10/25/2009 8:36:26 AM |

    What about lipid peroxidation on high dose of fish oil?

  • Dr. William Davis

    10/25/2009 2:52:27 PM |

    The form of LDL that increases depends.

    It seems to depend on the genetic basis for small LDL. In other words, if the triggers of small LDL have been removed along with other efforts aimed at reducing small LDL like niacin, and there is no genetic basis for small LDL, then large LDL increases.

    If small LDL is genetically programmed (a lot more common than many think), then small LDL can increase explosively.  

    Having performed many thousands of lipoprotein panels, the latter situation in which small LDL increases is worrisome.

    I am unsure of the implications of the first situation. Sure, we can extrapolate and speculate that it might not be related to increased risk. But I am not willing to gamble someone's health and life on pure speculation with no human data.

  • homertobias

    10/25/2009 5:07:57 PM |

    The only references to an increase in LDLC with fish oil supplementation is from WS Harris who authors 95% of the omega 3 index studies including a 2008 review which concludes that the omega 3 index is superior to omega 3/omega 6 ratio.  When 95% of literature comes from one man who promotes a pricey lab test I can't help but wonder if he gets part of the profits. I have no data to say he does though.

    He has two 1997 publications,one showing that Omnacor given at 4 g epa/dha a day raised ldlc by 10%. 1997 was the predawn era of advanced lipids.  In his second publication individuals with severe hypertriglyceridemia (baseline fasting levels on statins of 500 to 2000) did have a 32% rise in LDLC.  
    Harris has ties to Big Pharma (the maker of Lovasa/Omnacor) and to Monsanto.
    Data that I can easily access ascide from Harris shows effecacy of fish oil supplementation up to 4 grams of epa/dha a day.  5 grams a day for plaque stabilization/ antiinflammatory effect.  9 or 10 grams a day only in obese heart failure patients.  
    My bottom line:  if your baseline tg's are 500-2000, watch out for your ldlp on high dose fish oil.  If you are an obese heart failure patient, lose weight.

  • William Trumbower

    10/25/2009 5:31:50 PM |

    I believe that when people use theraputic levels of fish oil (more than 3gm EPA=DHA)  they should follow their omega profile and lipoprotein analysis closely.  It is possible to push the eicosanoid synthesis pathways toward the arachadonic acid side depending on your diet.   Once you know your optimal dose, then you can adjust it up in certain circumstances.  I attended a football tailgate and found some of the mixed nuts were cooked in soy oil, so I took an extra dose of fishoil when I got home to compensate.

  • Mike

    10/25/2009 5:40:54 PM |

    Thanks for your thoughts on this.  Regarding LDL particle size, how dependable would TG/HDL ratio be?  Sears indicates a ratio less than 2 indicates large benign LDL.  In my own experience over the past few years, as I've increased my fish oil intake (along with a Paleo diet) my HDL has gone up, my LDL has gone up, and my TGs have decreased.

  • Boris

    10/26/2009 1:30:58 AM |

    I have increased my intake of omega-3 since I answered the poll. My problem was that I couldn't take it all at once. Too much fish oil gave me a super upset stomach. Granted, it was the impure Nature Made brand sold at Walmart (34% pure). Now that I am using Omapure, I take one capsule with every meal and then one before bed time. It 6x more expensive than the Nature Made junk but I'm not getting sick from it.

    Does it matter that I break up my intake over the course of the day rather than swallow four capsules all at once?

  • Anonymous

    10/26/2009 1:49:07 AM |

    great information here, thanks all.

    To follow on Dr.BG's note on statin overuse :  there is an interesting presentation of baylor college's lipidsonline.org with discussion of guidelines for statin dosage.  The presenter notes how very little value is obtained from subsequent doubling of a statin dose and the risks for side effects.

    http://www.lipidsonline.org/slides/slide01.cfm?tk=82

    Dr. D.  Thank you for the caution on fish oil. I take 1650mgs EPA/DHA twice per day.  Might be a good idea to cut out a dose if I eat salmon or other oily fish.

    Would love to see more info on MK4/Mk7 K2 and MCFAs like coconut oil.

  • Dr. William Davis

    10/26/2009 1:58:12 AM |

    Hi, Mike--

    While the Triglyceride/HDL ratio can serve as a useful measure of small LDL in a population, it performs poorly when applied to specific individuals. This is because small LDl, while influenced by the situation creating low HDL and high triglycerides, can also behave independently.

    Small LDL is, in my view, best measured specifically.

  • Ross

    10/26/2009 5:52:24 AM |

    It's pretty straightforward to end up in the middle of the pack on that poll.  But don't take gels or you'll be there all day.  One tablespoon of Carlson's Finest has 4800mg O-3's with 2400mg EPA and 1500mg DHA.  One swallow just as I'm sitting down to breakfast makes for a great start to every day.

  • Anonymous

    10/26/2009 1:54:50 PM |

    I was told than an ApoE 4 Patient should not be on therapeutic doses of fish oil (for reasons which you have stated- raising LDL).

  • homertobias

    10/26/2009 2:46:23 PM |

    Dr Davis:

    I would like to know which WS Harris 2008 you referenced and the reference for the females in the Harvard School of Public Health please.
    I also would like to know if there was a correlation between baseline tg levels and those who experienced a more marked elevation of sd LDL on fish oil.

  • homertobias

    10/26/2009 4:14:20 PM |

    I guess that this is my day to ask you questions.
    When you read a MDCT, do you also measure pericardial fat?
    What do you think of Dr. Ding's new MESA findings re pericardial fat.  Thanks in advance.

  • Alan S David

    10/26/2009 6:16:55 PM |

    I take 6000 units daily or more, but I also consume a few tablespoons of ground flax seed daily as well.
    AND still eat fish a few times a week, especially oil rich sardines.

  • jegesq

    10/26/2009 9:28:03 PM |

    Homertobias:

    Lots of interesting work being done on pericardial adipose tissue (PAT) and using CT imaging done in conjunction with CAC scoring to more precisely determine the relationship between PAT and the development of CAD and calcified plaques, i.e., in order to more precisely "score" the level of PAT and to determine association and/or causality with calcific lesions.

    Dr. Lerber at University Hospital in Munich, Germany has observed that PAT accumulation precedes the development of calcified plaques, that increased volume of PAT are associated with reduced levels of  adiponectin and higher CRP.   So the idea is that with more precise measurements and concomittant imaging of both PAT and CAC, we might be able to better detect the presence of disease in an earlier stage.   There is also some push among those doing such research to link PAT thickness assessment with administering routine echo stress testing but this hasn't gained much traction yet other than in a small circle of folks.   The hope though is that PAT can also be used as another surrogate marker for diagnosing preclinical atherosclerosis.

    But as of now, I don't think anyone who does a routine CAC scan, whether with MDCT or EBT is doing any form of assessment of PAT, at least not until there is more data on the reliability of using this as a clinical marker of disease.

    Personally, I think there's a lot of interesting info that can come from this, and the idea of deposition of fat into muscle tissue and necrosis of that tissue, inflammation and the relation to levels of saturated fats consumed from dietary sources is an area that is just begging to be better researched.

    Oh, and by the way, don't believe everything you read here from BG about what foods I consume, how much statin I take, or much else when it comes to me.  In fact, I'd prefer that she simply not make references to me in her writings wherever they appear.  This will obviate the need for me to continue to correct her misstatements about me, my lipids, and drug and supplement usage, as well as the fact that she continues to misrepresent that I have not achieved plaque stability and/or demonstrated regression through serial MDCT CAC scoring over a period of three years despite very low dose use of rosuvastatin.

  • jegesq

    10/27/2009 12:16:24 AM |

    A correction....  My serial scan scores show that I have achieved stability and optimally regression of coronary calcium.   My point is that Dr. BG continues to claim that those taking rosuvastatin at doses of ~10mg daily cannot possibly achieve regression on EBT/MCDT scanning, and that just isn't so.

    I happen to be one of those whom I believe Dr. Davis was referring to with "too much of a good thing" with reference to EPA/DHA dosing.  My dose was upped from ~1-2 grams per day (of EPA/DHA) to ~10 grams based on recommendations from Dr. BG.  This occurred in or around December 2008 and continued until very recently. Based on five consecutive, quarterly NMR's and VAP's, my sdLDL-P remained at >85% of LDL-P, and my trigs went from ~40 to ~75, and, more significantly, my overall LDL-P rose from ~1000 to ~1300.   No other significant impacts were noted, other than CRP dropping to 0.7, which I attribute not to the n-3's, but instead to continued use of rosuvastatin together with combined high dosing of both boswellia and 5-Loxin and large doses of aspirin (taken specifically as an anti-inflammatory due to nerve and muscle pain from a herniated cervical disc in the month immediately prior to the last VAP testing).

    The point though is that in some, excess fish oil can convert to higher trigs and higher LDL, and will not improve the concentration or ratios of sdLDL-P/LDL-P.

    Yes, n=1, but I'm the n, so that's really most important to me, not what Wolf, Sears or anyone else has to say about this.  After all, what we're after is personalized medicine, not epidemiological observations that may be valid in large population studies but which may have no relevance to a particular individual.

  • homertobias

    10/27/2009 4:05:13 PM |

    Hi JEG,
    Thanks for the references.  I am truly upset that you andBG seem to be having a cybertiff.  She has a big heart, alot of enthusiasm, alot of intelligence and makes me laugh. You are a sincere intellectual, very bright, searching for truth in medicine and are doing a good job of it.  I can learn from both of you and want to continue to do so.
    As to omega 3 and dosage.  I can't seem to find any solid benefit to doses over 4g to maybe 5g per day. This seems to max out tg lowering, ldl improvement in particle size, minimal increase in hdl, bp lowering, improvement in tnf alpha, interleukin 6.  Reports on irs effect on HSCRP are conflicting.  One interesting report, Thies F, in Lancet 2003 took 188 patients scheduled for carotid endarterectomy and treated them with either DHA/EPA, sunflower oil, or placebo for an average duration of 42 days prior to surgery.  There was a significant difference in thickness of the fibrous cap over the plaque,the degree of monocyte  infiltration of the fibrous cap, percent DHA etc.  This directly addresses plaque stability.  I love it.

  • Dr. B G

    10/30/2009 5:06:04 AM |

    Homertobias,

    That is a great plaque stablization article -- will have to ck out!



    Jeq,

    I must be correct again as indicated by the length and duration of the post!

    Let me get this straight -- the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results....  

    Gosh... I wonder if the high dose fish oil had anything to do with it?

    EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins.  I think you have seen some them, personally IMHO.

    -G

  • Dr. B G

    10/30/2009 5:06:04 AM |

    Homertobias,

    That is a great plaque stablization article -- will have to ck out!



    Jeq,

    I must be correct again as indicated by the length and duration of the post!

    Let me get this straight -- the lipoproteins were less than desirable for both you and JJ/Jim for the past 2008 to 2009 (you reported increased sdLDL?), yet both of you posted regression recently on BOTH of your EBCT/MDCT results....  

    Gosh... I wonder if the high dose fish oil had anything to do with it?

    EPA DHA get infiltrated directly locally into calcified plaque and has immense immeasurable benefits for regression BEYOND lipoproteins.  I think you have seen some them, personally IMHO.

    -G

  • Dr. B G

    10/30/2009 5:14:21 AM |

    By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find...

    Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?

    I wonder what the omega-6:3 ratio is now off the fish oil?

  • Dr. B G

    10/30/2009 5:14:21 AM |

    By the way, congratulations to you two gentleman, JJ and Jeg, for achieving regression with Pattern B! I have looked for regression in Pattern B forum posters, but turned up none. You two are the FIRST at TYP that I can find...

    Do you think omega-3 had any role in your success since that appears to be the common link as well as major supplement change you guys identified?

    I wonder what the omega-6:3 ratio is now off the fish oil?

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