Unforgiving small LDL particles

21. October 2011 William Davis (39)
Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.
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Comments (39) -

  • ChrisB

    10/21/2011 3:45:39 PM |

    Great Article.  As I'm sure you know by now, I've been kind of a lipidpanelaholic since having a MI 2 yrs ago.  The hardest information to find is that of how long it takes for lipids to respond to diet changes and how sensitive they can be to even the smallest amount of carbs.

  • Howard

    10/21/2011 4:44:48 PM |

    Are you sure that sort of response is not due to gluten/gliadin/lectin/transfat? Four crackers doesn't sound to me like much of a carb load, but for a gluten-sensitive person like me, that could set off some inflammation.

  • Marc

    10/21/2011 7:08:35 PM |

    Dr. Davis,
    How does alcohol fit in to the above "equation"? Specifically wine.

    Marc

  • Sam Sinderson

    10/22/2011 12:12:39 AM |

    I have been on a wheat-free and carb restricted diet for about 7 weeks, and being concerned that I might be Apo E4, and therefor need to also limit saturate fat as you explained in an earlier blog, I asked my doctor to order a small LDL test.  No independent lab here that I consulted knew what that was, nor obviously did my doctor, since he just ordered "small LDL".  The local hospital lab finally found the following, which is what I will have blood drawn for tomorrow:
    Lipoprotein Fractionation Panel 1, Ion Mobility
    Which includes:
    Choesterol; HDL Cholesterol; Triglicerides; :Lipoprotein (a); Lipoprotein Fractionation Panel 2, Ion Mobility (LDL, Total; LDL, Medium and Small; LDL, VerySmall; HDL, Large; LDL Peak Diameter, LDL Phenotype)

    I hope that this is what I need.  Probably it is overkill, but in this case apparently my Medicare Advantage plan will cover it since it has been more than 3 months, since I had a simple panel done.

    Is there a simpler test for small LDL?  By the way the CPT codes are 80061, 83695, 83704

  • Fat Guy Weight Loss

    10/22/2011 4:41:38 AM |

    Sounds like cheat days may not be that good of an idea...

  • Dr. William Davis

    10/22/2011 12:39:39 PM |

    Yes, it does cast cheat days in a new light!

  • Dr. William Davis

    10/22/2011 12:45:11 PM |

    That's it, Sam.

    It shouldn't be that hard. The information is actually fairly straightforward and provides crucial information.

  • Dr. William Davis

    10/22/2011 12:51:45 PM |

    Hi, Marc--

    Alcohol does indeed slow or stop weight loss, especially if more than a serving or two are consumed. So it pays to minimize during a weight loss effort.

  • Dr. William Davis

    10/22/2011 12:56:34 PM |

    Probably not, Howard, since those components have not been associated with triggering of small LDL. The trans fat component can indeed trigger small LDL, but it seems to occur even with foods minus trans fats.

    However, I am impressed that gluten/gliadin/lectin rolled off your tongue!

  • STG

    10/22/2011 1:36:14 PM |

    The problem is carb creep. I experienced this a few months ago when I received the results of my HbA1c test. I was still in the prediabetic range and it was higher than the HbA1c test I had a few years earlier. I didn't get it? I thought I was consuming less carbs then I was. When I actually looked at my diet there were carbs creeping in: dark chocolate and small "safe starches" (e.g, potatoes, yams). Another factor that may have impacted my blood sugar was the stress of travel/visiting family during that three month time period. My understanding is that elevated cortisol levels can raise blood sugar. In any case, my recent HbA1c is in normal range. I think this is because I eliminated even small amounts of dark chocolate and "safe starches" (see Jimmy Moore's comments about safe starches).

  • jethro

    10/22/2011 2:01:01 PM |

    How low should we go in carbohydrates to avoid increasing small LDL?

  • Davide

    10/22/2011 3:01:26 PM |

    I'm not sure that wheat has this acute effect on everybody. In fact, I know it doesn't happen with me. I keep a close eye on my lipids and my small LDL particles remain "relatively" low despite the fact that I consume wheat/sugar products. Then again,  my blood sugar does not significantly rise after carbohydrates, so maybe that's why. If I eat a massive plate of pasta, a glass of fruit juice, and dessert, my blood sugar may (keyword, "may") rise to 120, if that, but then it goes down to about 80 about 45 minutes after the meal. No joke. In other words, I'm thinking this effect may have to do with the degree of people's volatility to rising blood sugars. Just a guess.

    Fyi, I'm the apo E/4 person who's LDL amount/particle number (226, 2,000) is extremely sensitive to saturated fats and thus I'm always lost in the conundrum of balancing fats with carbs. Difficult!

  • Teresa

    10/22/2011 3:05:34 PM |

    I know that if weight loss is involved, it can take a few months after weight stabilizes for lipids to normalize.  If minimal or no weight loss is involved, how long does it take?

  • Fat Guy Weight Loss

    10/22/2011 5:31:19 PM |

    With the example about 4 crackers would be as low as 10g carbs.  Curious of the overall effects of say 10g carbs of sweet potatoes....

  • Dr. William Davis

    10/23/2011 11:49:09 PM |

    Then it depends on which parameter you are talking about, Teresa.

    Small LDL requires just days to respond, while triglycerides require weeks to months, while HDL requires months to years.

  • Dr. William Davis

    10/23/2011 11:51:13 PM |

    Hi, Davide--

    No doubt: Individual tolerances to various foods, including carbohydrates, can differ. And the apo E4 person has a tougher time of it.

  • Dr. William Davis

    10/23/2011 11:53:40 PM |

    Unfortunately, Jethro, there's no quick and easy way to decide this, since individual sensitivity varies.

    Although imperfect, you can use HbA1c, an index of glucose and not of small LDL, to gauge whether you've been triggering higher blood sugars that often parallel the triggering of small LDL particles. You could, of course, obtain lipoprotein testing 48 hours after ingesting a known amount of carbohydrates, e.g., 20 grams, but that is logistically difficult.

    That all said, most people can get away with 15 grams carbohydrates per meal, while some can't tolerate more than 10, yet others do fine with 30+ grams.

  • Dr. William Davis

    10/23/2011 11:54:15 PM |

    Excellent point, STG! And I like the "carb creep"!

  • Barbara

    10/24/2011 12:14:06 AM |

    Did you see this, Dr. Davis?

    http://medicalxpress.com/news/2011-10-common-link-autism-diabetes.html

  • Teresa

    10/24/2011 1:14:14 AM |

    And it takes years to unlearn all the inaccurate stuff learned in school, and to find and learn the good stuff that is out there.  Thanks.

  • Stephanie

    10/24/2011 2:27:52 PM |

    How does one check to see if they are apo E4?

  • ChrisB

    10/25/2011 1:19:25 PM |

    How does it affect lipid results?

  • steve

    10/25/2011 10:52:06 PM |

    Dr Davis:  What is the small LDL profile for native populations that consume tons of of carbs and no signs of heart disease; also, the Japanese consume lots of carbs- easily 3 cups of rice per day which is about 120 carbs from rice alone.  Low level of CAD; what are their levels of small LDL.  I know for myself ApoE 3/3 that carbs do affect the small LDL level i have and in any event in the absence of a statin i produce tons of LDL particles large or small depending upon carb levels.  I believe genetics plays a large role.
    Thanks

  • Dr. William Davis

    10/26/2011 3:19:22 AM |

    No doubt, Steve.

    However, I'm unaware of lipoprotein assessment done to answer these questions. That would be interesting, however.

  • Dr. William Davis

    10/26/2011 3:21:50 AM |

    Yes, agreed, Teresa: New lessons to learn every day in this Information Age!

  • Dr. William Davis

    10/26/2011 3:23:44 AM |

    Thanks, Barbara. No, I hadn't seen this. But I'm not the least bit surprised!

    I find it wonderfully satisfying that the puzzle pieces are falling in place, just like that 1000-piece jigsaw puzzle we struggled to put together, with the last few pieces fit just perfectly!

  • Dee

    10/28/2011 1:57:49 PM |

    Dr. Davis,
    Have you heard or read about Lumbrokinase helping to lower small "a" particles?
    Just wondering.
    Dee

  • Tim

    10/28/2011 7:14:08 PM |

    Dr. Davis,

    There seems to be a lot of mention of the E4 ApoE genotype.  What about those of us that are E2/E4?  Any different instructions for us?

    Thanks.

  • Dr. William Davis

    10/29/2011 10:48:39 PM |

    With this very tough pattern, you are best following lipoproteins and glucose measures like HbA1c to gauge response to various dietary manipulations. The basic diet approach, however, is largely the same; it just may require some adjustments, e.g., fat intake.

  • Dr. William Davis

    10/29/2011 10:49:12 PM |

    Sorry, Dee, no info.

    Where did you hear this?

  • Dee

    10/30/2011 5:20:26 PM |

    Here is the quote.  Appently it just helps lower the LP[a]  and does not have any terrrble side effects.  I may try it, nothing else is working.  My little a is 43 and rising in spite of all I do.

    "The one nutraceutical that has shown promising clinical results in actually lowering Lp(a) is a lumbrokinase product made by Canada RNA Biochemical called Boluoke. Like its chemical cousin nattokinase, lumbrokinase is an enzyme that helps break up fibrin—a fibrous protein that helps form blood clots—to avoid too much clotting and keep blood flowing optimally."

    :

    Dee

  • Sam Sinderson

    10/31/2011 7:32:29 PM |

    I have my results.  My PCP reported these to me "for my records" with no further comment.  Maybe he can't interpret them?
    Total Cholesterol: 231 (My PCP surely would think this is high.)
    I find it strange that they did not report LDL direct, though perhaps it is not done because of the breakdown below.  
    Calculated LDL: 133 H MG/DL
    HDL: 85 Mg/dl  This is higher than I have ever had measured.
    Triglycerides: 64 Mg/Dl  Even Simvastatin only got it down to 84.  I conclude that I am not Apo E4.
    The range after \ below  is the range they cite, I presume, as normal.
    Lipoprotein Innocent: <10  NMOL/L \ <75  I presume this is a good result.
    LDL, Total: 2268 H NMOL/L  \ 440-1600
    LDL, medium and small: 651 NMOL/L \ 144-787
    LDL, Very Small: 277 NMOL/L \ 75-419
    HDL large: 9315 H NMOL/L  \ 469-5258
    LDL Peak Diameter: 227.5 Angstrom  \216.-234.3
    LDL Phenotype A  Pattern A     I believe this to be the preferred pattern, low small LD and Triglycerides.  Ref: Obesity (2009) 17 9, 1768–1775. doi:10.1038/oby.2009.146--Reversal of Small, Dense LDL Subclass Phenotype by Normalization of Adiposity
    Patty W. Siri-Tarino1, Paul T. Williams2, Harriet S. Fernstrom1, Robin S. Rawlings1 and Ronald M. Krauss1

    Does this calculate to large LDL = 2268-651 =1617 (Not including medium)?
    When should I do this test again?
    Comment?

  • Dr. William Davis

    11/1/2011 2:03:32 AM |

    Hi, Sam--

    The "pattern A" comment is misleading. About 40% of your LDL particles are small, too much.

    It means going back to the strategies to reduce small LDL, such as wheat elimination and limiting carbohydrate exposure. It is worth repeating about 2 months after weight has stabilized following a diet change.

  • Sam Sinderson

    11/1/2011 12:49:43 PM |

    I have been on a no-wheat, limited, very-low carb, diet now for 6 to 7 weeks already.  I cringe to think of what the numbers may have been before.  I initially lost about 12 pounds in less than 2 weeks to get to 148, I am 72-in tall, and have stabalized there by eating more high-fat non-carb stuff.  You say 40% small.  You must be using the medium and small (640) over total (2268) to get 40%.  Apparently medium and small includes the very small, which must be a fraction of small?  How long should it take for the very small to approach zero?  Isn't that the more important number?  I will be out of the country for 2 weeks.

    Thanks

  • Dr. William Davis

    11/2/2011 1:43:14 AM |

    Yes, exactly, Sam: Combine medium and small.

    Dietary and weight changes usually exert effects on small LDL within a few weeks, much faster than most other parameters.

  • pb

    2/6/2012 3:47:25 PM |

    Get a VAP test....this measures your small particle/large particle LDL.
    labcorp code 804500

  • pb

    2/6/2012 3:51:39 PM |

    I am going to try to get a VAP test.  No doctors know of it....only folks on the web.  Why?  It seems like a very important test to measure your LDL properly.  Can someone elaborate on this further?

  • Dr. William Davis

    2/7/2012 3:18:11 AM |

    Easy, Pb: There are no drugs--read: "no financial incentive"--to treat the abnormalities generally uncovered by lipoprotein testing like VAP. Thus, no push to get it tested.

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Homocysteine and coronary plaque

8. April 2007 William Davis (4)
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

6. April 2007 William Davis (0)
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?

5. April 2007 William Davis (0)
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

4. April 2007 William Davis (1)
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

4. April 2007 William Davis (5)
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"

3. April 2007 William Davis (13)
"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.

More Vitamin D and HDL

2. April 2007 William Davis (8)
I’m seeing more and more of it and I am convinced that there is a relationship: significant boosts in HDL cholesterol from vitamin D supplementation.

To my knowledge this remains an undescribed and uncharacterized phenomenon. There have been several observers over the last two decades who have noticed that total cholesterol shows a seasonal fluctuation: cholesterol goes up in fall and winter, down in spring and summer; year in, year out. This phenomenon was unexplained but makes perfect sense if you factor in vitamin D fluctuations from sun exposure.

I have come across no other substantiating evidence about fluctuations of HDL. But I am convinced that I am seeing it. Replace vitamin D to a blood level of 50 ng/ml, and HDL goes up if it is low to begin with. If HDL is high to begin with, say, 63 mg/dl, it doesn’t seem to change.

But, say, starting HDL is 36 mg/dl. You take niacin, 1000 mg; reduce high-glycemic index foods like breakfast cereals, breads, cookies, bagels, and other processed carbohydrate foods; exercise four days a week; add a glass of red wine a day; even add 2 oz of dark chocolate. You shed 15 lbs towards your ideal weight. After 6 months, HDL: 46 mg/dl. Better but hardly great.

Add vitamin D at a dose of, say, 4000-6000 units per day (oil-based gelcap, of course!), and re-check HDL two or three months later: 65 mg/dl.

I’ve seen it happen over and over. It doens't occur in everybody but occurs with such frequency that it’s hard to ignore or attribute to something else. What I’m not clear about is whether this effect only occurs in the presence of the other strategies we use to raise HDL, a “facilitating” effect, or whether this is an independent benefit of HDL that would occur regardless of whatever else you do. Time will help clarify.

We are tracking our experience to see if it holds up, how, and to what degree on a more formal basis. Until then, a rising HDL is yet another reason—-among many!-—to be absolutely certain your 25-OH-vitamin D3 level is at 50 ng/ml or greater.

How high is an ideal vitamin D blood level? If 50 ng is good, is 60 or 70 ng even better? Probably not, but there are no data. We have to wait and see. Unlike a drug that enjoys plentiful “dose-response” data, there are no such observations for vitamin D into this higher, though still “physiologic,” range.

Thin ice

2. April 2007 William Davis (0)
How long can an industry built on ignorance and deception continue its practices in the new Information Age?

I don’t think it can for long. I talk to hospital administrators who believe that their source of competition is the hospital across town, battling for the same patients. I speak to my colleagues, the cardiologists, who believe that the current model is sustainable—take every willing body to the catheterization laboratory or operating room for heart procedures, the revenue-generating engine of income and expanding heart programs.

I speak to primary care physicians, who are dumbfounded and perplexed and have no idea which way things are going. They are trapped in a peculiar position: most have signed contracts and are employees of the hospital. They are legally bound to support the cardiologists who take anybody possible to the catheterization laboratory or direct patients to other profit-making procedures.

Much of this system depends on the willingness of the participant, meaning you and the health care seeking public. What happens when the truth comes out and disseminates widely through the thinking populace? What happens to hospitals and physicians and the vast structures they’ve built when the bottom drops out for 50% of their “market?

The proverbial cow manure will hit the fan. Upheavals in the medical industry will rival the changes that the automobile or telephone brought early in the last century. Cardiologists, immense hospital heart programs, and the vast economic infrastructure they spawned will go the way of stage coach manufacturers and the telegraph.

What form will the broad exposure of detailed information in health take? I’m not sure, but it will certainly come. The collaborative efforts that created the Linux operating system and have challenged the monopoly of Microsoft Windows, or the emergence of the extraordinary Wikipedia as a repository of human knowledge that dwarfs the venerated Encylopedia Brittanica, will eventually overtake the American medical system, the heart disease industry in particular.

If you base your future on the welfare of your local hospital or the manufacturers of stents, operating room equipment for heart bypass, or similar industries, watch out. The ice is thin. And as the spring warms the air around you, it gets thinner.

The Track Your Plaque program is our first step in broadcasting the message of self-empowerment in heart health care and an attempt to wrestle control away from the profit-seeking forces that dominate. As we grow, we not only hope to broadcast the message more widely, but expand the message to other areas of health. I predict that the collaborative, let’s-all-pitch-in-and-help spirit of the Information Age, “version 2.0,” will spark the change.

Vitamin D and cancer

30. March 2007 William Davis (0)
Although this is a Blog about heart scans and heart disease, I came across a helpful video from Dr. Joseph Mercola about vitamin D and cancer that's worth viewing. Though I do not agree with many of Dr. Mercola's on-the-edge views, he does come up with some good thoughts and, in this instance, a useful educational tool about vitamin D.

You can view his video (which he claims crashed his server, due to the excessive demand for downloads) by cutting and pasting the address into your URL bar (above):

http://v.mercola.com/blogs/public_blog/How-to-Reduce-Your-Risk-of-Cancer-By-50--8790.aspx

Also, for my many patients who I've directed to look in my Blog for Dr. Reinhold Vieth's webcast presentation on vitamin D, here's the address:

http://tinyurl.com/f93vl

Perhaps I carry on too much about vitamin D. But I've come to respect this "nutrient" as among the most powerful strategies I've seen for dramatically improving control over coronary plaque growth as well as other aspects of health, as Drs. Mercola and Vieth eloquently detail.

Lipoprotein(a), menopause, and andropause

30. March 2007 William Davis (0)
Lipoprotein(a) is a curious lipoprotein. Not only is it a genetic pattern with numerous variations, it is also one that shows a predictable age-dependent rise.

Women in particular are prone to this effect, men to a lesser degree. As we age, many hormones recede, particularly growth hormone, testosterone, the estrogens (estradiol, estriol, estrone), progesterone, and DHEA, among others. This is not a disease but the process of senescence, or aging.

When we're young, estrogens, testosterone, and DHEA all exert suppressive effects to keep lipoprotein(a), Lp(a), at bay. But as a woman proceeds through her pre-menopausal and menopausal years, and as a male passes through his fourth decade, there is an accelerated decline of these hormones. As a result, Lp(a) crawls out of its cave and starts to sniff around.

Typically, a woman might have a Lp(a) of 75 nmol/l (approximately 30 mg/dl) at age 38. Ten years later, at age 48, her Lp(a) might be 125 nmol/l (app. 50 mg/dl), all due to the decline of estrogens and DHEA. A parallel situation develops in males due to the drop in testosterone. For this reason, it may be necessary to re-check Lp(a) once after the fourth decade of life if you've had a level checked in your younger years.

This opens up some interesting therapeutic possibilities. If receding hormones are responsible for unleashing Lp(a), hormones can be replenished to reduce it. In males, this is relatively straightforward: supplement human testosterone and Lp(a) drops about 25%.

In women, however, it's a bit murkier, thanks to the negative experince reported using horse estrogens (AKA Premarin) in the HERS Trial and Women's Health Initiative. You'll recall that women who take horse estrogens and progestins (synthetic progesterone) do not experience less heart attack and develop a slightly increased risk of endometrial and breast cancer. There was, however, a poorly-publicized sub-study that showed that women with Lp(a) experience up to 50% fewer heart attacks on the horse/synthetic combination.

Wouldn't it be nice to have a large trial examining the safety/advisability of human estrogens and progesterone? To my knowledge, no such confident study in a significant number of women exists, since there's so little money to be made with human hormonal preparations.

For these reasons, we use lots of DHEA, generally at doses of 25 to 50 mg per day. It makes most people feel good, boosts energy modestly, increases muscle, and reduces Lp(a) up to 18% in women, a lesser quantity in men.
High LDL cholesterol--only

High LDL cholesterol--only

11. May 2007 William Davis (3)
As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cause of coronary plaque and a heart scan score?

In other words, how often does someone prove to have only LDL cholesterol as the cause of a heart scan score . . . and nothing else? No low HDL, small LDL, lipoprotein(a), a post-prandial (after-eating) intermediate-density lipoprotein, inflammatory responses, phospholipase A2, high triglycerides, vitamin D deficiency, etc.

Rarely. In fact, I can truly count the number of people who have only LDL cholesterol as their sole cause of coronary atherosclerotic plaque on one hand. It is really an infrequent situation.

Far more commonly, people have 5, 6, 7 or more reasons for coronary plaque.

Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits.

In my view, an effort to identify all the causes is relatively easy, makes far better sense, and provides you much greater assurance that you will succeed in conquering heart disease and removing its evil influence from your life.
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Comments (3) -

  • Anonymous

    5/11/2007 7:21:00 PM |

    Dr. Davis, two things check out this web site http://www.traceminerals.com/research/synx.html it appears to have some good data on Metabolic Syndrome-X:
    I would like to share some good data that I have had by following the TYP program, I was diagnosed with type 2 diabetes Feb. 15 and after that I got my second heart scan, over 600 (my age 57) a 43% increase in 18 Mo. Not good needless to say, than I found TYP in march of this year I started slowly following and implementing a TYP plan,
    Background
    In February I did not feel well and I went to the doctor(2/15) I had lost 12 lbs my % body fat was going up  the muscles in my stomach were sore at times I was so thirsty I could not stand it and my eye site was changing. Needless to say I was diagnosed as a type II diabetic   glucose 344 A1C 11.2, was prescribed new medications for both the diabetic condition( Januvia 100mg 1X per day actoPlus Met 2X per day 15mg 850mg) along with cholesterol ( Advicor 20/1000 ). I started a life style changing program.
    Life style changes
    Modified eating program- went to a low GI high Vegetable protein including soy no or almost no Fats, eat as much as I want .(needless to say I have changed this plan)
    Quit smoking
    Increased exercise- walking on treadmill 7%grade 3.75mph from 30 min. to 30 min twice a day
    My Medications were changed Advicor 20/1000; Lisinopril-hydrochlorothiazide tablets 10-12.5 mg and a 325mg aspirin
    April started on the TYP plan, my Glucose average was way up, my total cholesterol number was 100 but my LDL-P was 1015 and my small LDL-P was 913 along with a HDL-C of 30  went on the TYP program
    Had my Vitamin D checked -it was low , had my DHEA checked it was low, had my Magnesium checked it was low, after my discussion with you came off Lisinopril , ( we are seeing were this settles out to pick the right med's) stopped talking all diabetic med's added two other supplements R-ALA , PGX Fiber Blend (instead of oatmeal too many carbs) along with Vit D, Magnesium, DHEA , 15 grams of soy protein Fish oil, healthy Fats, no wheat products, Dark chocolates L-Arginine.   I have had a additional blood test for these items (Vit D magnesium, DHEA) adjusted supplements body fat down to less than 14% WHAT A DIFFERENCE, in the last 11 days  my fasting glucose numbers are between 84 and 103 that’s normal, before they were above 125 solidly Diabetic (since Feb even with diabetic medications) my doctor has never seen this much improvement without medication, on someone that had a 12 week ave of over 340.I do not know who is more anxious to see my next lipid profile me or my doctor  . I'am scheduled in three weeks.
    Needless to say i also beleive that very few people can just take one pill and be cured. I hope i'am alive when they do find the magic cure (and i think they will) but right now the TYP plan is the best game in town. Eugene

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    11/3/2010 3:12:33 PM |

    Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits.

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    4/19/2011 8:16:49 PM |

    I knoe a lot about the Cholesterol!
    LDL particles vary in size and density, and studies have shown that a pattern that has more small dense LDL particles, called Pattern B, equates to a higher risk factor for coronary heart disease!!My grandpa died for this reason, I think that it was terrible!!

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