Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)
Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

10. December 2009 William Davis (32)
Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

4. December 2009 William Davis (0)
Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil


Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

1. December 2009 William Davis (31)
Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)
The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

28. November 2009 William Davis (13)
According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

27. November 2009 William Davis (11)
Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.
I Wish I Had Lipoprotein(a)!

I Wish I Had Lipoprotein(a)!

8. August 2012 William Davis (33)
Why would I say such a thing? Well, a number of reasons. People with lipoprotein(a), or Lp(a), are, with only occasional exceptions:

--Very intelligent. I know many people with this genetic pattern with IQs of 130, 140, even 160+.
--Good at math--This is true more for the male expression of the pattern, only occasionally female. It means that men with Lp(a) gravitate towards careers in math, accounting, financial analysis, physics, and engineering.
--Athletic--Many are marathon runners, triathletes, long-distance bicyclists, and other endurance athletes. I tell my patients that, if they want to meet other people with Lp(a), go to a triathlon.
--Poor at hydrating. People with Lp(a) have a defective thirst mechanism and often go for many hours without drinking water. This is why many Lp(a) people experience the pain of kidney stones: Prolonged and repeated dehydration causes crystals to form in the kidneys, leading to stone formation over time.
--Tolerant to dehydration--Related to the previous item, people with Lp(a) can go for extended periods without even thinking about water.
--Tolerant to periods of food deprivation or starvation--More so than other people, those with Lp(a) are uncommonly tolerant to days without food, as would occur in a wild setting.


In short, people with Lp(a) are intelligent, athletic, with many other favorable characteristics that provide a survival advantage . . . in a primitive world.

So when did Lp(a) become a problem? When an individual with Lp(a) is exposed to carbohydrates, especially those from grains. When an evolutionarily-advantaged Lp(a) individual is exposed to carbohydrates, more than other people they develop:

--Excess quantities of small LDL particles--Recall that Lp(a) is a two-part molecule. One part: an apo(a) made by the liver. 2nd part: an LDL particle. When the LDL particle within the Lp(a) molecule is small, its overall behavior is worse or more atherogenic (plaque-causing).
--Hyperglycemia/hyperinsulinemia--which then leads to diabetes. Unlike non-Lp(a) people, these phenomena can develop with far less visceral fat. A Lp(a) male, for instance, standing 5 ft 10 inches tall and weighing 150 pounds, can have as much insulin resistance/hyperglycemia as a non-Lp(a) male of similar height weighing 50+ pounds more.

Key to gaining control over Lp(a) is strict carbohydrate limitation. Another way to look at this is to say that Lp(a) people do best with unlimited fat and protein intake.
Tags :

Comments (33) -

  • Bill Davis

    8/8/2012 1:17:58 PM |

    I have Lp(a) and am working on reducing it.
    Have been off wheat for several years now and on a low-carb diet. Hope I find that diet as well as fish oil, thyroid treatment, niacin and DHEA will bring it down.
    Thanks for making me feel special with this article! I have cross posted it. Scan coming up next month to give me a look at how I'm doing.
    The other Bill Davis

  • Joe

    8/8/2012 5:05:52 PM |

    I know this is probably a stupid question: but who doesn't have Lp(a)? My last VAP said that I have a Lp(a) of 7.0 and that <10.0 is preferred. Do some people actually have zero Lp(a)?

    Thanks!

  • randallbb

    8/9/2012 3:01:37 PM |

    I too am high Lp(a) and fit largely the profile Dr. Davis has outlined.  Am working on the Lp(a) with all guns blazing!  My new TYP lifestyle along with high amounts of fish oil and Niacin have brought it down markedly in just six months (from 61mg to 46mg on the NMR profile).  Am eating lots of cheese, nuts, etc, so am glad to hear that fats are a good thing!  Dr. Davis' post here reminds me to keep limited my carb intake!

  • Holly

    8/9/2012 10:44:08 PM |

    Any ideas why these traits would correlate with Lp(a)?

  • aerobic1

    8/11/2012 2:28:01 PM |

    Joe:

    Yes, some people do have "zero" Lp(a).  It is partly determined by your genetics which you have no control over.  But, as Dr. Davis suggests you gain gain control over your Lp(a) with dietary interventions such as elimination of wheat and other refined carbs, along with taking a few targeted supplements.  His interventions do not involve pharmaceutical drugs as there are no drugs that effectively treat Lp(a).

    Three years ago my first VAP test revealed a Lp(a) level of 22.  Three years of following Dr. Davi's advice my level is now 3.  For more information go to http://www.trackyourplaque.com/default.aspx.

  • Joe

    8/11/2012 4:59:41 PM |

    Thanks for the feedback!
    On the other hand, aren't you on the way to having no Lp(a)?  From 22 to 3?
    I'm still not sure why having "high" Lp(a) is a good thing. I'm still confused. Frown

  • jpatti

    8/11/2012 9:08:51 PM |

    We're also good-looking.  And very sexy.  And surprisingly modest!  ;)

    So why the heck would the thirst thing be going on?  I don't get it.  

    I have this issue; I have to carry drinks all the time or I completely forget about drinking.  I never go anywhere without carrying drinks cause I don't remember until I've got a killer headache.  I've got a giant mug of coffee and a liter of ice water flavored with lime shrub sitting next to me right now.  

    It's not that I'm not thirsty, if you ask me, I become aware of thirst.  It's just that "thirsty" is not something I am aware of at all.  I don't notice it unless I ASK myself if I'm thirsty.  

    I'm also ridiculously picky, I can have a drink sitting next to me, but if the ice has melted, I don't "want" it no matter how thirsty I am.  

    I don't understand why I'm like this.

  • aerobic1

    8/12/2012 2:48:06 AM |

    Joe:  
    There is nothing good whatsoever about having any measurable level of Lp(a).  Zero Lp(a) level should be your goal.  The personality characteristics Dr. Davis pointed out are just some typical observations of Lp(a)er's but do not assume the higher your Lp(a) is that the more intelligent, better at math or athletics, etc. you will become.  Lp(a) offers no advantage in that regard.

    There is plenty of good reading and advice from Dr. Davis on this subject on this blog on what Lp(a) is and how to self-manage it.  http://blog.trackyourplaque.com/category/lipoproteina.  Most all doctors are not well informed on this subject and therefore do not know how to treat it.

  • aerobic1

    8/12/2012 4:52:33 AM |

    jpatti:

    The sensation of thirst is governed by the Hypothalamus and Limbic System of the brain.  I do not have an understanding of why people with Lp(a) demonstrate this unusual thirst pattern that Dr. Davis has observed in people with Lp(a).  Here is a good explanation of how the typical thirst mechanism works.  http://www.enotes.com/thirst-reference/thirst.  

    Perhaps the normal brain hormone driven thirst mechanism in people with Lp(a) "malfunctions" and may not be producing enough arginine vasopressin to enhance thirst.  The relationship of renin, angiotensin II, and aldosterone also control water retension and thirst and may play a role too.

  • Joe

    8/12/2012 6:36:30 PM |

    Aerobic:
    Thanks again. I followed that link and it reiterated Dr. Davis' protocol, of: " i.e., wheat elimination followed by elimination of cornstarch, oats, and sugars; high-dose fish oil (total daily EPA + DHA of 6000 mg/day); vitamin D supplementation sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml; iodine supplementation; and thyroid normalization which, in Ted’s case, required supplementation with the T3 thyroid hormone, liothyronine, at a small dose. "

    And I follow that protocol pretty closely (I don't take quite that much fish-oil).  My thyroid is fine. I have Pattern "A" LDL. Vitamin D of 90ng/ml. My TC is "high" but I have great trig and HDL numbers and ratios. My Lp(a) again is 7, which is well under the "reference range" of  <10 (according to VAP). But I'm unable to find anything anywhere that explains why having a zero Lp(a) is best, or what the mechanism is that makes it best. I'll keep looking around. Thanks for the help!

  • Joanna

    8/13/2012 8:16:28 PM |

    So we requested our doctor order an Lp(a) test along with several other blood tests that were being done - and later find out that our insurance company (Humana) will not cover the cost of the test, they gave some reason like it wasn't scientifically proven to be useful!!!  It's $65 so not sure if it would be worth fighting them on this one since they have been pretty good about covering most things.

  • Mark

    8/14/2012 2:59:56 AM |

    Hi Dr. Davis,
    I’m 47 yrs old. I’ve had migraines since I was a teen and I developed Athsma this past January (hate it). During the process of discovery the drs found I have a 50% blockage in one of the 5, non critical, arteries running along the back of my heart. Scared me, to say the least. I’ve always eaten quite healthfully (for what I knew), am thin @ 6′ 1″/155lbs (was 175lbs in Jan.). Had:
    Total Cholesterol of 200
    LDL of 146
    HDL of 50

    Drs wanted me to do Lipitor. Researched and said, “No, thanks.” Started exercising 5-6 days/wk (lifting + walk/run), taking red yeast rice, fish oils, fish, no meat, no dairy, no eggs, lots of veggies/fruit, etc., but still eat beans, oats (every AM), occasional wraps. After 6 wks my blood work (VAP) was as follows:
    LDL=86
    HDL=43
    VLDL=17
    TOT. CHOL=146
    Trigycerides=66
    Non-HDL (LDL+VLDL)=103.

    Seemed GREAT to me! The dr wasn’t impressed. Said my ‘particle size’ was small: LDL1(a)=8.1, LDL2(a)=0, LDL3(b)=39.5, LDL4(b)=24.9. Density Pattern=B.

    I’ve continued but don’t know how to elevate my HDL and reduce the particle size/change the pattern to the more favorable ‘A’. Getting down about this. Working hard but, seems like I can’t find answers that work, anywhere! What might you would work in my situation? Also, Is niacin ANDRed Yeast Rice a bad idea?
    I’ll hang up and listen. Thank you,
    Mark

  • Will

    8/14/2012 3:03:09 PM |

    Dr. Davis,

    Do you have any comments or response to the study released yesterday at the University of Western Ontario, comparing the risk of regular consumption of egg yolks to smoking on the increase of arterial plaque?

  • JoAnne

    8/15/2012 1:08:25 AM |

    Dr Davis, I recently had had a NMR LipoProfile done, but I don’t understand the numbers. I think it’s saying my LDL particle size is pattern A (good), but the total LDL-P number of 1985 nmoI/L is bad. And the HDL at 79 mg is good, but the TC at 307 is bad…. I’m so confused. Can you please summarize? I’ve been looking at the TYP website and I’m ready to join.

    LDL-P    1985 nmoI/L  (LDL Particle number)

    LDL-C    212 mg/dL  (calculated)
    HDL-C  79 mg/dL
    Triglycerides  82 mg/dL
    Total Cholesterol  307 mg/dL

    LDL & HDL Particles
    HDL-P   40.8 μmoI/L  (total)
    Small LDL-P  106 nmoI/L
    LDL size  22.1 nm

    Lipoprotein markers assoc with insulin resistance & diabetes risk
    Large VLDL-P  0.7 nmoI/L
    Small LDL-P    106 nmoI/L
    Large HDL-P  15.8 μmoI/L
    VLDL size    32.9 nm
    LDL size    22.1 nm
    HDL size    9.9 nm

    Insulin resistance score  0-100
    LP-IR score    5

  • kimsuoil

    8/15/2012 2:15:14 AM |

    Dr. Davis, I have Lp(a) and all of the traits above. Don't really know my IQ, but I am a Petroleum Geologist, been a runner for over 32 years,  can go many hours without water (ran a marathon in 3 hrs and 3 minutes when I was 24 in New Orleans and only had a small cup of water at the halfway point).  I have no problem eliminating foods and have high willpower to food.

    Before joining your Track Your Plaque program 3 years ago, I was on the "low fat"  high carb Am. Heart Assoc. recommended diet for many years.  At 48 I discovered that I had massive heart disease and received 6 stents.
    I now have to limit my carbs to very low to keep my small LDL particles somewhat low.

    Good news is now at 53 years old my carotids are getting better flow since on the TYP diet when I got my last carotid echo.

  • Gene K

    8/15/2012 5:59:29 PM |

    @Joanna
    We have coverage thru Blue Cross Blue Shield, and they require extensive review of why I would need an NMR or an Lp(a) test, after which they will decide whether to cover or not. I decided it was too much of a pain, so I order these tests thru privatemdlabs, and use their receipt to get reimbursed from my flexible spending account. If you have an FSA, you could do that, too.

  • Joanna

    8/15/2012 8:18:23 PM |

    Nope, no FSA account so that's not an option and they already have extensive records of why it would be warranted (if they even looked at medical expenses for the past year it would be obvious!)  Thanks for the tip though.

  • Dr. Davis

    8/17/2012 2:36:21 AM |

    Hey, Kim!

    Yes, we have to reverse this incredibly stupid tidal wave of low-fat that is enormously destructive.

    The proof is in the (carotid) pudding!

  • Dr. Davis

    8/17/2012 2:40:41 AM |

    There are a number of possibilities to explain this pattern, JoAnne.

    Among them:

    --Hypothyroidism
    --Apo E4 genetic type
    --Other genetic patterns

    Unfortunately, this is a pattern that may be difficult to correct with diet. You might also consider an HDL Labs sterol absorption panel to decide what role diet plays.

  • Dr. Davis

    8/17/2012 2:43:50 AM |

    This is a pattern that is highly responsive to diet, such as the diet used in the Track Your Plaque program, the diet discussed in these pages, and the diet I articulate in my book, Wheat Belly.

    By the way, you are currently on a diet that makes this pattern worse. Your diet of avoiding meats and eggs with lots of fruits causes the small LDL pattern and heart disease. And it sounds like you have an intellectually challenged doctor who wants to prescribe drugs but doesn't understand that your diet is contributing or outright causing your pattern.

  • Dr. Davis

    8/17/2012 2:45:54 AM |

    Nobody does.

    It is likely that the gene for the apo(a) protein of Lp(a) is somehow linked to a gene for thirst triggering and nothing more.

    More of a curiosity than anything else.

  • steve

    8/19/2012 1:36:11 AM |

    Hi Dr. Davis:
    Can LDL-P level ever be to low? I have heard lower is better, but when you get below 500, most of that can be small LDL-P.
    Thanks

  • Dr. Davis

    8/23/2012 2:00:59 PM |

    Yes, it can.

    But it should be mostly, if not all, large particles if you are following the diet advised here.

  • steve

    8/26/2012 8:39:17 PM |

    i do follow the diet, but unfortunately generate much in the way of small LDL-P
    I eat no wheat, small amounts of rice and potatoes, no other grains or sugars.  TRGS  were 26 which i thought  is an indication of carb intake.  Am guessing it is just genetics.
    How low is low for LDL-P and do you have any studies you can point that indite small particles?  All research I have seen indite LDL-P and say size does not matter.  Would be interested in seeing studies that show otherwise
    Thanks

  • jpatti

    8/28/2012 7:46:26 PM |

    Yes, I knew the hypothalamus was involved with thirst and the adrenals involved with electrolyte balance.

    Except... just last week, I had a board-certified endocrinologist tell me that ONLY the heart, liver and kidneys are involved in fluid/electrolyte balance:  
    http://gapsfort2.blogspot.com/2012/08/i-am-just-so-freaking-angry.html

  • Susan

    10/4/2012 9:59:33 PM |

    My pattern is very similar and I have had the sterol absorption panel, though I don't know what it means. Campesterol is optimal at 2.22, Campesterol ratio is Hypo at 63, Sitosterol is Hyper at 3.23, Sitosterol ratio is optimal at 88, Cholestanol is Hyper at 5.89 and Cholestanol ratio is Optimal at 172. What does this tell us?

  • Kindred

    10/31/2012 4:53:42 PM |

    My LP(a) was 167.  I got it down, in three months, to 22 using the strict vegan, Forks Over Knives approach coupled with 1500 mg of niacin before going to bed.  My math skills are deplorable as I have severe discalculia (the math version of dyslexia which I also have.)  I'm not competitive at all so, although very coordinated and active, I'm not athletic.  I drink lemon water or dandelion/chicory coffee frequently and frequently get up in the middle of the night for a glass of lemon water. I'm not diabetic and am tested for this annually.   I graze between  meals on celery sticks.   Also, I'm 1/8 Native American Indian. We are suppose to have low levels of LP(a.)

    I lightened up on the vegan diet using olive oil for cooking and my LP(a) rose in 3 months to 67 so it's back to Forks Over Knives again.

  • darin

    12/29/2012 5:47:33 PM |

    Confused, would this be the same thing as Lp(a) mass (mg/dl) i had on a recent Health diagnostics test?
    Mine is showing 44 and its supposed to be less than 30.

    There was also a Lp (a) cholesterol (mg/dl) and mine was 8- supposed to be <3

    Thanks

  • Fred Rutherford

    6/17/2013 5:00:36 AM |

    I have a lipid disorder. My doctor checks lpa once a month. Says thou I have minimal body fat I have to take cholesterol meds. Because my lpa is 14 times higher than what is considered high risk. This putting me at risk of blood clots. I under go quarterly ulta sounds of vascular system as well as annual Hart caths. A high price for being smarter than the average bear. Don't ya think?

  • Dr. Davis

    6/18/2013 1:29:29 AM |

    No, you have been misled.

    What you need are new doctors, plain and simple.

  • Mathieu Gagné

    6/18/2013 5:17:58 PM |

    That is very interesting! I never heard of this before, but it seems to fit to me pretty well. I have high IQ, I'm a physicist, don't drink enough water and would be fairly athletic if it wasn't for my crohn disease. The impact of giving up grains was huge on my health! A quick search and I've found this link between high Lipoprotein(a) and crohn disease:
    http://www.ncbi.nlm.nih.gov/pubmed/11742189

    It would be interesting to ask my doctor about it!

  • Mary Ann Joyce

    2/15/2014 8:07:55 PM |

    I've the Berkley tests three or four times, and my Lp(a) was 217 in 2007; the latest test shows 80Lp(a).
    I have been on Crestor for a very long time, and now realize it does noting to lower the Lp(a).  On the latest test, my small particle was 21.2 and the large was 11.4.  What does this mean?
    I want to get off the Crestor and onto the niacin, etc., including pomegranate juice which, I understand, has properties that will lower the Lp(a).  I am aiming to cut carbohydrates out completely as well as reduce sugar to near zero.  Do any of you have suggestions for me?  Even though I am 70 years old, I am not ready for a stroke nor MI.  Thanks!

  • Sandra Tremulis- Founder Lipoprotein(a) Foundation

    5/7/2014 6:12:44 PM |

    For those of you interested there is now a foundation for high Lipoprotein(a)  www.lipoproteinafoundation.org

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