What's that in your mouth?

7. January 2010 William Davis (17)



Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.

De Novo Lipo-what?

5. January 2010 William Davis (16)
Humans have limited capacity to store carbohydrates. Beyond the glucose and glycogen in our blood and tissues, we have relatively little carbohydrate to draw from in time of energy need. That's why long-distance runners and triathletes have to carry sugar sources to keep blood sugar from plummeting.

Fat, of course, is different. We have virtually unlimited capacity to store energy as fat.

Because we have limited carbohydrate storage capacity, what can the body do with the excessive quantities of carbohydrates that Americans ingest? What becomes of a bagel for breakfast, wheat crackers for snacks, a whole wheat sandwich for lunch, pretzels, and whole wheat pasta that many people eat every day, not to mention the chips, soft drinks, and juices?

Excess carbohydrates are diverted to an interesting metabolic pathway called de novo lipogenesis (DNL). This refers to the liver's ability to make triglycerides from excessive carbohydrates in the diet. Triglycerides are packaged for release into the blood as VLDL. VLDL, in turn, interacts with other lipoproteins, creating small LDL particles, reduced HDL and smaller, less protective HDL. High VLDL will be measured on a standard cholesterol panel as higher triglycerides.

A University of California (Berkeley, San Francisco) group has done much of the work describing DNL.

A diet weighed towards carbohydrates, especially if 50% or greater calories are carbohydrate, is sufficient to provoke plenty of DNL, even in slender people. DNL is a big part of the reason why low-fat (and, thereby, high-carbohydrate) diets result in higher triglycerides. DNL really gets turned on many-fold if the carbohydrates are "simple," rather than "complex."

Overweight people, however, can demonstrate five-fold greater DNL even with lesser quantities of carbohydrate intake (e.g., 40% fat, 46% carbohydrate, 14% protein):





From Schwarz et al 2003. Mean (± SEM) fractional de novo lipogenesis in lean normoinsulinemic (NI), obese NI, and obese hyperinsulinemic (HI) subjects after 5 d of consuming a high-fat, low-carbohydrate diet and in different lean NI and obese HI subjects after 5 d of consuming a low-fat, high-carbohydrate diet. Values with different superscript letters are significantly different.


Excessive carbohydrates, a la standard low-fat diets, are good for nobody. The concept of de novo lipogenesis fills in a theoretical hole that now explains why people who eat carbohydrates have higher triglycerides, VLDL, and, eventually, insulin resistance and diabetes.

Gretchen's postprandial diet experiment II

3. January 2010 William Davis (37)
I previously posted Gretchen's postprandial diet experiment, in which she consumed a low-fat diet for a day, followed by a low-carbohydrate diet for a day. Grethen monitored blood glucose and triglycerides with fingerstick checks. (Blood glucose can be checked on any widely available glucose monitor; triglycerides can be monitored with the Cardiochek device.)

Let's now discuss what happened.

On the low-carb, high-fat day, there was an initial surge in triglycerides to 250 mg/dl late morning, followed by a secondary peak several hours following dinner. Because fat is mostly triglycerides, Gretchen's high-fat (sausage, bacon, butter, whole-fat yogurt) breakfast provided a large quantity of triglycerides that needed to be absorbed. This generally occurs over approximately 6 hours, varying depending on body weight, how accustomed you are to fat, activity level during the day, the kind of fat in the meal. The high content of saturated fat in Gretchen's high-fat breakfast likely caused the somewhat slower drop in triglycerides over approximately 7 1/2 hours.

As Gretchen herself had noted, triglycerides the following day were lower, a typical low-carb response. Blood sugar throughout showed only minor variation, with only small postprandial increases.

Thus, Gretchen experienced what we'd expect with a low-carb, high-fat diet: an initial high surge in triglycerides, followed by a decline in fasting levels, while blood sugar shows a normal contour.







Now, the more confusing low-fat experience:



Blood glucose makes a striking peak at 200 mg/dl after the low-fat breakfast of pasta and rice, in contrast to the low-carb breakfast. Triglycerides behaved very differently from the low-carb experiment: While there was no initial postprandial surge, there was a late surge developing 6-24 hours later. The late surge continued into the next day, with fasting levels the following morning (210 mg/dl) exceeding the starting triglyceride level (60 mg/dl).

The one potentially confusing aspect of all this is Gretchen's late rise in triglycerides on the low-fat diet. This phenomenon is due to something called de novo lipogenesis, or the liver's conversion of carbohydrates to triglycerides that occurs when an excessive carbohydrate load comes through diet. Because the human body cannot store anything beyond a minor quantity of carbohydrates (as glucose and glycogen), carbohydrates are converted to fats.

Another factor causing the late triglyceride increase is insulin resistance, given the high blood sugar response. When insulin resistance is present, the activity of the enzyme, lipoprotein lipase, is reduced. Less lipoprotein lipase activity allows slower VLDL degradation, allowing VLDL (and thereby triglycerides contained in VLDL) to "stack up" in the blood. Thus, the higher triglycerides late after eating and into the next morning.

One issue to be aware of: Acute responses can differ from chronic responses. In other words, had Gretchen had the luxury (and time and money) to conduct the experiment over, say, 4 weeks, rather than a single day, there would be somewhat different responses. The best data on this come from Dr. Jeff Volek of the University of Connecticut, in which 4 weeks of low-carbohydrate eating modify fasting and postprandial responses over time.

Several conclusions can be made from Gretchen's experience:

1) Low-carb, high-fat acutely generates extravagant postprandial triglyceride responses.
2) Low-fat causes a late triglyceride surge and higher fasting triglycerides.
3) Low-fat leads to high blood sugars and, by implication, diabetes.


Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease. Which is worse? I believe that low-fat is more destructive, since it leads over time to both high triglycerides and diabetes, while low-carb/high-fat only leads to postprandial triglyceride surges, at least acutely.

How to best balance the responses to reduce risk for heart disease? That's a discussion for future.


Again, my thanks to Gretchen and the substantial amount of effort that went into generating these numbers. More of Gretchens' own writing can be found on her blogs:
http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

A wheat-free 2010

2. January 2010 William Davis (22)
A Heart Scan Blog reader sent this fascinating description of his wheat-free adventure.

Whenever I discuss this notion of going wheat-free and the incredible health effects that develop, I invariably receive comments or emails saying something like "I eat wheat and feel fine. That can't be true." The problem is that not everybody needs to go wheat-free. 20-30% of people can include wheat in their diet and suffer little more than weight gain, some not at all.

But stories like Michael's (below) are commonplace in my experience. I've had many patients who, at first, refused to believe that wheat exposure might be the underlying cause for health struggles. But they finally give it a try and find that rashes, arthritis, acid reflux, irritable bowel symptoms, mood swings, anger, etc. are miraculously improved or gone.

Anyway, hear what Michael has to tell us:


Dr. Davis,

I want to thank you. I was browsing the web a while back and happened to stumble upon your blog post about wheat belly. The first thing that caught my attention was that I thought you had somehow gotten a photograph of me. The young man you posted an image of looked exactly like me. So I read what you had to say. After reading, I thought "Four weeks isn’t so bad. I think I can handle this."

It has now been nine weeks and all I can say is that I am completely amazed. Let me say first that twice in the past twenty years I have been tested for allergies. The first time I was tested I showed a slight reaction to Timothy Grass, but not enough to cause me any problems. The second testing I did not show a reaction to anything. So, I have always assumed that my chronic sinus problem were due to sensitivities to environmental pollutions. Now I am not so sure. I would like to list for you everything that has happened to me since I eliminated wheat from my diet.

1. I have lost a total of 12 pounds in the last 9 weeks.
2. I have lost 1 ¼ inches of belly fat
3. I have lost a tremendous amount of fat from my neck.
4. My entire life I have had problems with oily hair. I could wash my hair and three hours later I looked as if I hadn’t washed in a week. Now my hair stays clean and soft for two to three days without shampoo.
5. My hair was always flat and stringy. Now it has lots of body.
6. I used to have thick layers of dry skin on my scalp. It would come loose in chunks as large as a fingernail. That dry scalp is gone.
7. I used to have dry flaky skin that seemed to secrete oil. That no longer happens. My skin is now soft and smooth.
8. I have lived with bad acne for at least 35 years. Now it is hard to find a pimple on my body.
9. I have always had to fight dehydration. That is no longer a problem.
10. I used to drink two large cups of coffee every morning just to be able to function. I now have enough energy that I have eliminated caffeine from my diet.
11. I sleep more soundly than ever before and my dreams are clear and vivid.
12. My thought processes are more active and clear than they have ever been.
13. My chronic sinus issue is now a thing of the past.
14. I used to have problems with getting the “shakes” if I had gone more than a couple of hours without eating. It was as if I was suffering from low blood sugar. I would even be afraid that I would pass out. Now all I feel is hunger. I can go all day without eating and never feel in danger of losing consciousness.


Today is Thursday. This past Monday my wife and I were eating out and I ordered a burger without a bun. What I didn’t realize was that the burger would arrive covered in onion rings. I knocked the mountain of onion rings onto the plate but there were still a couple that were embedded in the cheese. I decided, what the hell, a couple of onion rings shouldn’t make that much of a difference. I will not make that mistake again anytime soon. Within 30 minutes I felt like there was a steel spike going through my left eye socket. I don’t remember ever being in that much pain. My sinuses were exploding. This morning, as I write this, I still feel the vestiges of that pain. Just enough that I know it is there. But after two and a half days, I am at least able to function again.

I owe you a debt of gratitude. You may have just saved my life. In the very least you have given me the means to improve my life in ways that I never thought possible.

Thank you so much,
Michael B.


Now, if wheat exposure can do that in Michael, what damage can it do in other people?

Personally, I previously experienced many of the same symptoms that Michael suffered, all gone with wheat elimination.

My advice: If you have any inkling that you might have a wheat sensitivity, make a New Year's resolution to stay wheat-free for 4 weeks and see whether you can feel any difference. Not everybody will, but many will be telling us about the dramatic health turnarounds they experienced.

Lipoprotein lipase and you

30. December 2009 William Davis (0)
Lipoprotein lipase can make the difference between having heart disease and not having it. Having sky-high triglycerides or normal triglycerides. It can mean dinner hanging around for over 12 hours in the bloodstream, rather than the usual 4-6 hours.

If you take niacin, you must exercise

30. December 2009 William Davis (23)
We use a lot of niacin in the Track Your Plaque program.

Niacin:

--Increases HDL and shifts HDL towards the large, protective fraction

--Reduces small LDL--In fact, niacin is the best treatment we have to reduce small LDL after wheat elimination and carbohydrate reduction.

--Reduces fasting and postprandial (after-eating) triglycerides

--Reduces heart attack risk by 20-28%--even as a sole agent.


But . . . niacin also triggers higher blood sugar because it partially blocks the effects of insulin (insulin "resistance").

While the net effect of niacin remains positive, the provocation of insulin resistance is not such a good thing. Can it be minimized or eliminated?

Yes, through exercise. Here's one interesting observation in obese (BMI 34.0), sedentary men given placebo, exercise, niacin (1500 mg Niaspan, once per day), or niacin + exercise:





From Plaisance et al 2008.

Blood was drawn following a high-fat meal challenge. (Yes, a high-fat challenge, not a carbohydrate challenge. In this study, there were only 17 grams carbohydrates in the test meal, but 100 grams fat. More on this in future.) Exercise consisted of walking for 50 minutes at a moderate pace one hour prior to the meal challenge.

You can see from the graph that exercise partially corrected the increased insulin level provoked by niacin.

Judging from this and other studies, exercise can help minimize the insulin-blocking effects of niacin. It doesn't take much, just moderate exercise for at least 30 minutes.

Adequate sleep can also help, since sleep deprivation is a potent trigger for insulin resistance, only worsened in the presence of niacin. Vitamin D supplementation to achieve desirable blood levels (which I define as 60-70 ng/ml) is also an effective means to minimize this effect.

To track small LDL, track blood sugar

24. December 2009 William Davis (28)
Here's a trick I learned after years of fussing over people's small LDL.

To gain better control over small LDL, follow blood sugars (blood glucose).

When you think about it, all the foods that trigger increases in blood sugar also trigger small LDL. Carbohydrates, in general, are the most potent triggers of small LDL. The most offensive among the carbohydrates: foods made with wheat. After wheat, there's foods made with cornstarch, sucrose (table sugar), and the broad categories of "other" carbohydrates, such as oats, barley, quinoa, sorghum, bulghur, etc.

Assessing small LDL requires a full lipoprotein assessment in which small LDL particles are measured (NMR, VAP, GGE). Not the easiest thing to do in the comfort of your kitchen.

However, you can easily and now cheaply check your blood sugar. Because blood sugar parallels small LDL, checking blood sugar can provide insight into how you respond to various foods and know whether glucose/small LDL have been triggered.

Here's how I suggest patients to do it:

1) Purchase an inexpensive blood glucose monitor at a discounter like Walmart or Walgreen's. You can buy them now for about $10. They're even sometimes free with promotional offers. You will also need to purchase lancets and test strips.

2) With a meal in question, check a blood sugar just prior to the meal, then again 60 minutes after finishing the meal. Say, for example, your pre-meal blood sugar is 102 mg/dl. You eat your meal, check it 60 minutes after finishing. Ideally, the postprandial (after-meal) blood sugar is no more than 102 mg/dl, i.e., no higher than pre-meal.

Perhaps you're skeptical that oatmeal in skim milk with walnuts and raisins will do any damage. So you perform this routine with your breakfast. Blood sugar beforehand: 100 mg/dl. Blood sugar 1 hour post: 163 mg/dl--Uh oh, not good for you. And small LDL will be triggered.

This approach is not perfect. It will not, for example, identify "stealth" triggers of blood sugar and small LDL like pasta, for the same reasons that pasta has a misleadingly low glycemic index: sugars are released slowly and not fully evident with the one-hour blood sugar.

Nonetheless, for most foods and meals, tracking your one-hour postprandial blood sugar can provide important insight into your individual susceptibility to sugar and small LDL-triggering effects.

C-reactive protein: Fiction from the drug industry?

21. December 2009 William Davis (0)
C-reactive protein (CRP) is the liver product of inflammatory responses anywhere in the body. If there's an inflamed left knee, CRP will be increased. If viral bronchitis is making you cough, then CRP will be increased.

The argument put forward by the drug industry is that, because CRP indicates underlying inflammation, very low-grade levels that can be measured in the absence of overt inflammation like the sore knee or bronchitis is associated with increased risk for cardiovascular events. There are now many studies that conclusively demonstrate that, the higher the CRP, the greater the cardiovascular risk.

Naturally, any marker of risk is followed by the inevitable study: Do statin drugs reduce the excess cardiovascular risk of excessive CRP?

And, yes, indeed they do. My statin-crazed colleagues rave about the so-called "pleiotropic," or non-lipid, effects of statins. CRP reduction and the reduction of risk associated with CRP result with statin treatment.

But is life really statin vs. placebo, as most statin trials are constructed? Are there strategies that can outdo statins like Crestor for reduction of CRP?

Watch your fish oil labels

17. December 2009 William Davis (36)
A quick quiz:

How much omega-3 fatty acids, EPA + DHA, are in each capsule of fish oil with the composition shown on the label below:





If you said 1340 mg (894 mg + 446 mg), sorry, but you're wrong. There are 670 mg EPA + DHA per capsule.

Did you notice that the composition, or "Supplement Facts," lists the contents of two capsules? Rather than the usual one capsule contents, this product label lists two capsules.

I don't know why some manufacturers or distributors do this. However, I have seen many people tripped up by this kind of labeling, taking half the omega-3 fatty acids they thought they were taking. This can be important when you are trying to obtain a specific dose of EPA + DHA to reduce triglycerides, reduce Lp(a), control abnormal heart rhythms, reduce bipolar mood swings, or other important effects.

I liken this to pulling up to a gas station where the sign says gasoline for $1.25. Wow! Can't beat that! You then find out that it's really $1.25 for a half-gallon, or $2.50 a gallon.

In truth, the labeling is accurate; it's just very easy to not notice the two capsule composition.

Why do I need a prescription for Olava?

16. December 2009 William Davis (0)
Imagine this:





What is OLAVA?

Olava is prescription olive oil. It is the purest, highest concentration of olive oil available.




Why Do I Need a Prescription for OLAVA?

Studies show that olive oil contains essential fatty acids, "good" fats that:



--Contain natural compounds your body needs for good health but can't produce on its own.

--Has antioxidants that may provide protection from heart disease.



So, it is common for people to ask why they need a prescription for OLAVA if it is made from a natural ingredient--olive oil. It's time to get the facts about OLAVA. Learn why OLAVA is different from olive oil you can buy at a store.



OLAVA Is an FDA-Approved Medication

OLAVA is the only FDA-approved medicine made from olive oil that's proven, along with diet, to reduce risk for heart disease


The FDA enforces standards to make sure that prescription medications like OLAVA are safe, effective, and quality controlled.


The way OLAVA is manufactured is reviewed and approved by the FDA.


OLAVA uses a 10-step purification process that helps remove lead and other environmental toxins that can be present in olive oil.


Each 1-gram capsule of OLAVA contains 1000 mg of pure olive oil.


The FDA-approved dose of OLAVA is 4 capsules per day. It could take up to 2 tablespoons per day of regular olive oil to provide the same amount of active ingredients proven to lower heart disease risk.




What Else You Should Know About Olive Oil

Regular olive oil has not been approved by the FDA to treat any specific disease like heart disease.



Olive oil doesn't have specific dosing information; it has a food label.



Olive oil does not go through an FDA-approved manufacturing process.





Talk to Your Doctor About OLAVA

If you have very heart disease, you may need a prescription medicine, along with diet, to treat your condition. Talk to your doctor about OLAVA. Print a trial offer to use on your first prescription of OLAVA.

Prototypical Lipoprotein(a)

Prototypical Lipoprotein(a)

25. February 2010 William Davis (23)
Here's the prototypical male with lipoprotein(a):



Several features stand out in the majority of men with lipoprotein(a), Lp(a):

Slender--Sometimes absurdly so: BMIs of 21-23 are not uncommon. These are the people who claim they can't gain weight.

Intelligent--Above average to way above average intelligence is the rule.

Gravitate to technical work--Plenty of engineers, scientists, accountants, and other people who work with numbers and/or technical details are more likely to have Lp(a).

Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Are rabid fans of Star Trek.


Okay, I made the last one up. But the rest are uncannilly true, shared by the majority (though not all) men with Lp(a).

Why? I can only speculate that the gene(s) for Lp(a) are closely linked to gene(s) for intelligence of a quantitative kind and some factor that enhances aerobic performance or yields a desirable emotional state with exercise.

Oddly, the same patterns tend not to occur in women in Lp(a). I have yet to discern a personality or body configuration phenotype among the ladies.
Tags :

Comments (23) -

  • Anonymous

    2/24/2010 8:24:18 PM |

    arthur ashe and steve larsen (the cyclist who recently died at age 39) seem to fit the profile...

  • Jolly

    2/24/2010 8:57:16 PM |

    Great, I fit most of this risk profile.  (BMI is 17), although I prefer rock climbing to aerobic work.  

    Maybe I should get my Lp(a) levels tested.

  • Bob

    2/24/2010 9:41:58 PM |

    Dr. Davis,

    Thanks for sharing this, very interesting. Are these your personal observations or do you know of any studies indicating any of the above?

  • Anonymous

    2/24/2010 11:44:25 PM |

    Doctor Davis,

    While many people are sensitive to profiling, I think you are on to something and it should be investigated. The rate of how a person ages definitely seems to be indicative of how healthy their heart. I look at pictures of John Ritter in his younger years and compare them to just before he died. Yikes, he looks like a mess! How our chins droop and stomachs grow shows something. Being pruney is one thing. Looking old is another.

    -- Boris

  • Onschedule

    2/24/2010 11:56:56 PM |

    The profile you outline for your typical lp(a) patient describes me perfectly. I'll even admit to liking Star Trek...

    My lp(a) = 88 mg/dl (prior to treatment). I've lowered it significantly, in part, by following the advice on your blog.

    Many thanks for all of the time you spend sharing your wisdom and experience with the world!

  • Dr. William Davis

    2/25/2010 12:16:44 AM |

    Hi, Bob--

    Pure, unadulterated anecdote. No data whatsoever.

    Nonetheless, I marvel at how often it holds true. I see several people a week who fit the description.

  • ramon25

    2/25/2010 1:03:09 AM |

    Hello doctor, I know this is a little off topic and for that I apologize. I ask because I am a little desperate for an answer. I hope it would not be an inconvenience to answer. I take a vitamin k supplement from the LEF brand, this one-http://www.lef.org/Vitamins-Supplements/Item01224/Super-K-with-Advanced-K2-Complex.html
    It has a lot of K. I wanted to know If that high amount of k would require me to take HIGHER levels of vitamin D? Or would the regular 6000- 8000 iu would suffice, I ask that knowing that Vitamin D status is an individual thing ( I am an avid reader of your blog) But as a general rule for how they interact, I cant find any info on this. Thank you very much for your time, and keep up the good work!

  • Stan (Heretic)

    2/25/2010 3:00:32 AM |

    Dr. Davis,

    Thank you for very thought-provoking posts, but I have to say I have a slightly different slant on this:  the type of people you show have so little body fat that our (yes, I am one too) metabolism runs exclusively on what we put on our plate rather than using our body fat (intermittently) for ketogenic cycling in between meals. We lack ketone bodies.

       If we consume a high carbohydrate diet then our body has to use glucose for energy 100% of the time.   Our abnormal (on high carb) lipid profile may be (probably) a consequence of that rather than of some genetical differences.  This is the simplest explanation and may be sufficient to explain the entire plethora of observations.

    That is why I used to have hypoglycemia (and beginning of angina) at the age of 42 on a  low fat vegetarian diet, 11 years ago.  That's probably why you were developing diabetes on Ornish diet.  That's why many if not most low fat vegetarians are not doing particularly well especially after a couple of years once they loose their body fat.

    Regards,
    Stan (Heretic)

    Refs:

    Carbohydrates and Diabetes

    Snacking and glucose/ketogenic cycling

    Very-Low-Fat Diets: What Are the Benefits?

    Diabetes, liver, fructose and omega-3

    It's the glucose, stupid!

    Food Choices and Coronary Heart Disease

  • Dr. William Davis

    2/25/2010 3:13:28 AM |

    Hi, Ramon--

    To my knowledge, there is no interaction. Many of my patients are on the combination and I've not noticed any shift in dose requirements. I DO believe, however, that there is an important synergy between the two in both prevention/reversal of coronary disease and bone health.

  • Dr. William Davis

    2/25/2010 3:15:52 AM |

    Hi, Stan--

    Not so fast.

    Recall that Lp(a) is "activated" by the presence of small LDL. Small LDL particles are spectacularly created by  . . . carbohydrates!

    So I wouldn't be so eager to live on carbohydrates if you are a super skinny Lp(a) person.

    With small LDL and Lp(a), the basic theme is fat, fat, and more fat.

  • ramon25

    2/25/2010 4:12:36 AM |

    Dr. Davis, thank you so much for your response! But even with such a high level of K? the dosage I am taking is over 2500% of the DV. Do you think that amount has health benefits?
    thanks Dr. Davis I really appreciate you help.

  • Anonymous

    2/25/2010 4:29:36 AM |

    Dr. Davis,

    What of someone who initially fit the profile but then managed to add a fair amount of muscle tissue through hard training and enough calories and nutrients? Does this change anything?

    I'm not advocating going hog wild, but do you feel that a formerly golden fit for this profile who now has more muscle mass and is quite active has a bit more of a buffer zone in terms of carbohydrate consumption?

    I ask because in my work in gyms, I have known many men who would initially be carbon copies of the profile you proposed, but after 6 months to 2 years or somewhere in that range, people who just met them would never guess they had fit the profile at some point in the past.

    -Steve Janzek

  • Mat

    2/25/2010 5:25:03 AM |

    I am not sure of HeartHawk's BMI but he sure looks like has this problem.  From his blog:

    "I have high Lp(a) with an otherwise world-class lipid panel."

    "I am proactively fighting my extraordinarily high Lp(a)"

  • Dr. William Davis

    2/25/2010 3:46:54 PM |

    Hi, Mat--

    Yes, indeed. Our beloved Track Your Plaque Heart Hawk does indeed have Lp(a). He also fits the physical/mental pattern, including the Star Trek part.

    Anonymous--

    Lp(a) is genetically-determined. Muscle mass has no effect, unfortunately.

  • Kent

    2/25/2010 4:26:16 PM |

    Dr Davis,

    I've received mixed messages concerning LP(a) and LDL. Many have said that lowering one's LDL will not lower LP(a), yet I'm a little curious as to what happened with my LP(a).

    LP(a) started at 198 nmol/l, with LDL at 105 or so. I started 2000mg Niaspan, 4800mg fish oil, Pauling therapy, no wheat and a few other things you reccomended in your book for LP(a). In 3 months LP(a) was down to 109 nmol/l. In 9 months my LP(a) was down to 45 nmol/l! But my LDL was down to 26! My liver enzymes had gone from 20 to 60, my Testosterone had dropped sigmicantly and my energy was zapped.  

    Therefore, I went from 2000mg Niaspan to 2000mg Niacin IR because I was told it was easier on the liver and wouldn't shoot the LDL so low while keeping HDL high. Well next test LDL was back up to 89, and felt better, but LP(a) had jumped back up to 150 nmol/l. That would lead me to believe it is tied to LDL. Would you agree?

    Thanks,
    Kent

  • StephenB

    2/25/2010 7:01:44 PM |

    It's quite funny how well I fit the criteria: 46, electrical engineer, BMI of 22, and a marathon runner. I have eliminated wheat, have 62 mg/dl 25-H levels, and enjoy extra saturated fat with my saturated fat. I may have to spring for LpInnocent testing next time around.

  • jd

    2/25/2010 7:49:54 PM |

    I am getting mine tested shortly, once LEF puts their blood tests on sale.   I fit that profile very closely although I can gain weight if I pig out over a period of days.  I do stay away from all empty carbs but do get carbs from fruit and veggies like butternut squash & sweet potatoes.  I always eat my carbs with a protein and/or fat source to slow the assimilation into the bloodstream.

  • Drs. Cynthia and David

    2/25/2010 9:25:18 PM |

    Very interesting observations!  It might explain why some healthy-looking people have heart attacks anyway.  I am curious whether the observation will hold up as you gather more info, and what other insights it might bring.

    @ramon25, take a look at Chris Masterjohn's post about D, A, K1 and K2. Apparently D increases the use of and need for K, but is somewhat modulated by A. It's really interesting stuff. http://blog.cholesterol-and-health.com/2009/04/tufts-university-confirms-that-vitamin.html

    Cynthia

  • zach

    2/26/2010 3:34:21 PM |

    Wow. I just realized that all of myteachers of higher math and physics were all really, really skinny guys. You're right!

    @Stan

    That makes a lot of sense.

  • shelley

    5/21/2010 8:04:17 PM |

    Interesting stuff.  I am a 46 year old woman, runner, fit, low weight/body fat, good cholesterol levels, but have Lp(a) levels of 62mg/dl.  Huge family history of early death from sudden cardiac arrest.  I'd say add women to the profile. Smile

  • Viagra Online

    8/23/2010 10:41:10 PM |

    I had a friend like this men he was so intelligent but when we were talking about something he said that he always was right and everybody was wrong it was a really bad problem I wouldn't like to be intelligent if I were like him.

  • papermoz

    9/20/2010 12:24:38 PM |

    Thanks for this great post it was very informative and helped me with my own project I am attempting to complete.
    Dissertation | Thesis | book report

  • buy jeans

    11/2/2010 7:35:48 PM |

    Enjoy high levels of aerobic performance--I tell my Lp(a) patients that, if they want to see a bunch of other people with Lp(a), go to a marathon or triathlon. They'll see plenty of people with the pattern among the aerobically-elite.

Add comment

Loading