Eat triglycerides

8. June 2011 William Davis (31)
Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.

 

 

 

 

 

 

 
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Comments (31) -

  • Kurt

    6/8/2011 2:51:47 AM |

    There must be genetic variations, though, as my triglycerides have measured between 78 and 90 on every test since 1993. For the past two years, I've been eating a 20% fat diet (with about 50% carbs), and on my latest VAP test, my triglycerides were 78. The diet, by the way, lowered my LDL 30%.

  • Ian Goldsmid

    6/8/2011 2:55:47 AM |

    Dr. Davis

    Could you please clarify:

    If I have one slice of gluten free mixed grain /seed toast - and very liberally heap Organic Coconut Oil & Almond Butter on it - am I still going to get the exaggerated carbohydrate to triglyceride conversion effect from the toast?

    Thanks, IJG

  • Gene K

    6/8/2011 3:28:45 AM |

    Dr Davis,

    How much TG-rich foods is it safe for APOE 4 people to consume? Will this amount depend on their fasting TG? Will it be per meal or a day's total?

    Thank you.

  • Markus Damian

    6/8/2011 7:16:16 AM |

    I think this article is excatly on target- I ate a low-fat, high-carb vegetarian diet for years, and at one point my measured triglyceride levels were > 300. After I started omitting most refined carbs from my diet (and upping my fat/protein intake correspondingly), my last reading has been 88. So, for me at least, dietary intake of triglycerides is not substantially related to blood levels.

  • Markus D

    6/8/2011 7:32:02 AM |

    ... having said that, there is something which I don't quite understand. Given that virtually the entire human population is on a high-carb feast, it must be that some of us react differently to high-carb diet than others, otherwise everyone would have elevated triglyc levels, right? My mother, who is certainly genetically quite close to me, eats a high-carb, low-fat diet, and her triglyceride levels are normal ...  Many thanks, M.

  • Might-o'chondri-AL

    6/9/2011 12:18:07 AM |

    EPA (eicosa-pentaenoic fatty acid)  an omega-3  poly-unsaturated fatty acid reduces the amount of glucose that is made into tri-glycerides ("trigs") , thus decreasing de-novo lipo-genesis put out by the liver.  When I added daily concentrated fish oil  with 1,500 mg EPA & 750 mg DHA to my moderate carb diet my NMR  tested measurement of trigs went from 90 mg/dL down to 42 mg trigs/dL (tests  were 4 months apart).  

    EPA also increases the amount of insulin related glucose transporters inside skeletal muscle cells, which allays insulin resistance;  it (EPA) induces the skeletal muscles to "burn" more glucose for ATP energy  in oxidative phosphorylation , which decreases irritating lactate output that contributes to body "aches".  Insulin in circulation can then also work as a co-fact0r with EPA,  together they go on to increase functional  leptin  levels  (leptin = anti-appetite);  thus  we get less impulse to "graze"   between meals on  carbs that make  trigs.

  • carb sane

    6/9/2011 11:57:11 AM |

    Actually, it has been established that DNL is NOT a major source of fatty acids in VLDL.

    http://carbsanity.blogspot.com/2011/05/where-do-triglycerides-come-from-part-i.html

  • majkinetor

    6/9/2011 1:49:40 PM |

    Actually, its around 20%

    http://ajpendo.physiology.org/content/286/4/E577.full

  • majkinetor

    6/9/2011 1:49:59 PM |

    Nice. I didn't know that. Thats pretty big amount of EPA/DHA, it is therapeutic amount often used for COX-2 inhibition.

    Can you tell more about the dosage ? Did you try smaller dose ? Is it fish oil or fish capsule or simply fish ? What are you thoughts about potential problems with PUFA and oxidation in regard to fish oil ?

  • carb sane

    6/9/2011 5:05:24 PM |

    Firstly, that's not about VLDL.  Secondly, that means around 80% comes from dietary fat.    Did you read my link?

  • Might-0'chondri-AL

    6/9/2011 6:15:27 PM |

    Hi majkinetor,
    I only went from no fish oil supplementation as an experiment to taking 1 tsp of Natural Factor's "pharmaceutical grade"  (  concentrated Canadian product's total fish oil=4,400 mg.  with 2,630 Omega 3 fatty acids of which 1,500 = EPA & 750 = DHA)  taken, as free  poured liquid along with morning food and evening food in 1/2 tsp measuring spoon slurps. Intake  of liquid oil was at the same time ate carbs , and carb intake was similar for when had 1st measured trigs when wasn't supplementing with fish oil  .  

    I personally don't think PUFA oxidation is an issue in diets that have lots of substrate for gut bacteria to make short chain 4 carbon fatty acid butyrate. It (butyrate) up-regulates many distinct  GST (glutathione S-transferase) genes;  these go on to tackle multiple lipid peroxidation by-products  (ex:  activity neutralizes 4-hydroxy- nonenal &  trans-alk-enals/dienals ),  while  micro-somal GST promotes the glutathione conjugation to electro-philes  which then can act to decrease lipid hydro-peroxide activity.

  • majkinetor

    6/10/2011 7:25:50 AM |

    Ah, sorry, I missread your post.

  • majkinetor

    6/10/2011 7:30:08 AM |

    Secondly, that means around 80% comes from dietary fat
    Not at all.
    80% from dietary fat AND cho.

  • Jimmy

    6/10/2011 11:11:24 AM |

    Might: Do you live in Canada?
    Jim

  • Helen

    6/10/2011 11:25:24 AM |

    M-Al,

    I used to take fish oil, but now that I'm measuring my glucose daily, I find that even a small dose immediately raises my fasting glucose 10-15mg, and somewhat worsens my post-prandial readings.  My own observation is in keeping a study that showed that prediabetic women's glucose control was worsened by a fish oil supplement.  (I don't have the link handy.)  Can you explain?

    I have the same troubles with modest supplements of vitamin C and niacin, though I'm sure for different reasons.  I find it interesting, and I don't mean that in any coded way, that two of Dr. Davis' recommended supplements  (fish oil and niacin) impair glucose control in me and in some studies.  I am wondering if this might explain in part his advice to shun carbs.  In the context of those supplements, carbs are not well tolerated.

  • Dr. William Davis

    6/10/2011 12:12:00 PM |

    Several commenters make the point that there is genetic variation in susceptibility to triglyceride intake and carbohydrate intake.

    Absolutely. Two people on the same diet can have wildly different results. Part of this is attributable to apo E genotype, apo C genotype, lipoprotein lipase and hepatic lipase genotypes, among others. Body weight and previous eating habits will also enter the equation. However, in most people increased triglyceride intake does not result in substantial increase in serum triglycerides.

  • Might-o'chondri-AL

    6/10/2011 9:59:19 PM |

    Hi Helen,
    I've heard some respond as you mention;  I wonder if they were all overweight during the data collection period, as pre-diabetic could imply.  In your circumstances (ie: blood glucose goes up with supplements)  it would be instructive to know if  you've a tendency for excess weight.

    My own niacin use went from none to 3x per day of 500 mg.  niacin taken with meals;   my own 2011 NMR lipid tests done 4 months apart were as follows.  Without any niacin fasting NMR cholesterol test results:  LDL = 139,  HDL=45,  total number of LDL particles  = 1,676,  with the number of small LDL particles  = 1,021 nmol/dL .  As for NMR cholesterol test with 1,500 mg daily total  niacin :  LDL = 100, HDL = 64,  total number of LDL particles = 976 , with the number of small LDL particles = nmol/dL.

    The nice plunge in small LDL doesn't seem to be due to a massive restriction of carbs;  in fact,  both my  HbA1c  and fasting serum glucose test result ciphers  went up slightly after I had  instituted niacin &  EPA/DHA fish oil  (started both at same time).   Incidentally,  I've never had  weight gain problems  and unintentionally lost 10 pounds I didn't intend to  since started taking the fish oil;  losing so much small LDL was more than thought possible and maybe wasn't 100% due to the niacin  (also daily  added  6,000 IU vitamin D3 from none, taken as 2,000 IU  with each meal).

    So,  before you decide that niacin & EPA/DHA supplements driving up your post-prandial glucose is positively detrimental it might be good to have your own baseline data (ie:  NMR for cholesterol & HbA1c for accretion of  blood sugar) .  If you are in the USA you can get a valid blood draw order in ANY state at all and the emailed results by using  cheapest online arrangement from summitcountymedicalsociety.prepaidlab.com ;  their doctor orders the blood test for you and,  of course, I have no financial interest in this .

  • Might-o'chondri-AL

    6/10/2011 10:04:42 PM |

    edit,
    see 2nd paragraph's last sentence to Helen above, missing number in last set of data is for number of small LDL nmol/dL and should be 96 (ninety-six) ... in other words  that data shows that with niacin the  small LDL  "plunged" to 96 from being 1,021 nmol/dL without niacin supplementation.

  • Helen

    6/11/2011 5:27:07 AM |

    Hi M-Al,

    I'm different from a lot of visitors to this blog in that I have never had cholesterol problems.  I don't remember my exact numbers but my HDL and LDL split has been deemed "ideal," and my triglycerides range from 44-48, with total cholesterol being about 157.  

    My current BMI is 20 or less (haven't checked the charts lately) and my highest ever was 25, about a year ago.  Generally, I've been in the 23 range.  So, no, I don't have a propensity to weight gain.  On the other hand, I'm borderline diabetic.  Last year, at my highest BMI, my A1C was 6.4.  On low-carb, it slowly got down to 6.0, and my last test, on low-fat, was also 6.0, although according to my meter readings, taken at least three times a day, it should be 5.3.  I'm definitely right on the border with the diabetes, though have pushed it back some over the past year.  My blood sugar *sometimes* shoots to 200 or over within the first hour of eating (a "diabetic" number, though my endocrinologist says it has to be 200 at two hours to be considered clinical diabetes), but it quickly goes down again.  My liver seems to pump out a lot of glucose.  I tend to have a fasting glucose between 109 and 125.  Sometimes it gets as low as 99.  On low-carb, it ranged from 125 to 145, and was 160 a few times.  

    Needless to say, my biggest concern is my glucose level.  Metformin didn't help, low-carb didn't help much (and definitely made my tolerance for any amount of carbs next to zero - I once went to 198 on a carrot and half an orange, but I don't anymore.  It also gave me heart palpitations, worsened my insomnia, and greatly impaired my exercise tolerance), and I wonder if I'm just stuck with what I've got at this point.  Not that I'm throwing in the towel.  Fortunately, my cholesterol profile has  been ideal, my resting heart rate and blood pressure are low-normal, and my weight is okay without a struggle.  But I'm getting aches and pains in my joints and think the fish oil could help there.

  • Peter

    6/11/2011 1:32:44 PM |

    Dr. Davis, at one point you were concerned that you were eating too many nuts
    because your ratio of omega 3 and 6 was off.  What is your current thinking about the trade-offs?

  • Might-o'chondri-AL

    6/11/2011 10:02:26 PM |

    Hi Helen,
    lost 2 replies, says server error ... sorry

  • Might-o'chondri-AL

    6/11/2011 10:14:46 PM |

    Hmm Helen,
    Sounds like epigenetic or good old genetic polymorphism ... appears that Hexokinase II (HK II) is NOT staying inside skeletal muscle mitochondria and glucose-6-phosphate (G-6-P) is working to keep HK II in cell cytosol in a loop,  whereby HK II engenders glycogen output and instigates lots of G-6-P ... that cell has own glucose from glycogen so GLUT 4 (glucose transporters) move too far away to pick up blood glucose  ... liver glycogen  for it's part involves HK IV (glucokinase) and G-6-P too, but may not be root of  your syndrome ... too slow a rate of G-6-P degradation and /or too many carbon or nitrogen terminals on HK II would allow G-6-P to yank HK II  into metabolism cranking out glycogen ...  hey - twice wrote this already.

  • Might-o'chondri-AL

    6/12/2011 12:49:42 AM |

    Helen, Hi-
    Metaformin probably did not work for you because it functions to increase glucose uptake by provoking anaerobic glycolysis to create additional glucose demand;   you may already be doing plenty  of anaerobic glycolysis  as a consequence of your extra ordinary local glycogen synthesis.  The carbon from glucose with anaerobic glycolysis engenders a lot of lactate being produced; your aching joints and body pain syndrome fit the profile of excessive lactate in circulation.

    There is no easy way to determine what phase of the G-6-P dynamic with Hexokinase forms is not working normally, if even involved.  When we wean to real food our skeletal muscles start to run glucose metabolism with HK II and GLUT 4,  rather than the HK I and GLUT 1  we started with;  this change over occurs when we  starts to relatively "burn" both carbs and fats  and skeletal muscles develop  their insulin sensitivity.

    I am not  a clinician, and you have your personal physician to guide you; if I had a distorted  HK II  and G-6-P pattern ( that was unresponsive to low carbs)  I would try to end run it,  and not have skeletal muscle cells utilizing glucose to stop ratcheting up G-6-P and short out the negative feedback loop . I'd  significantly increase my consumption of  dietary fat in the explicit form of unheated virgin coconut oil  and fatty fish (for the EPA/DHA);  if taking EPA causes  blood sugar to rise it is probably because the EPA is driving skeletal muscles to "burn" fat , and thus skeletal muscles are using less of the HK II glycogen  which itself then used even less blood glucose as substrate  (ie: EPA  reduces blood glucose commonly used so glucose level in blood measures higher if cell metabolism aberrant  in the manner like I surmise).

  • Might-o'chondri-AL

    6/12/2011 4:28:39 AM |

    Hi Jim,
    Am not  residing in Canada.

  • majkinetor

    6/12/2011 7:04:12 AM |

    Vitamin C can give falsely higher values when measuring bunch of markers, most notably glucose. Its because it is so similar with glucose (very similar net formula, the same transporters in the body - GLUT, its made from glucose in animals etc...)

    About oil, it can only slow down carb absorption and let the body tolerate better. Did you experiment with other fish oil manufacturers ? Perhaps something in the product apart from fish oil makes you feel that way. For instance, ascorbyl palmitate is typical antioxidant used (along with Vitamin E) so this can be responsible for false higher reading.

  • majkinetor

    6/12/2011 7:22:27 AM |

    Helen, did you try megadosing with Vitamin C (~10g per day as frequent as you can). Vitamin C influences beta cells in the pancreas and deficiency is common in diabetes. Scorbutic guinea pigs show defects in insulin metabolism in vitro. Higher glucose levels compete with C for transporter. Add chromium if you didn't. Daily exercise will surely help. Since low carb made your glucose problem worst (most probable is higher hepatic insulin resistance that is consequence of low carb diet) you might try to return some safe starches back (for instance potato or rice) and keep CHO between 50 and 75 g per day.  Ashes and pains in the joint might be consequence of your too low carb diet since carbs are used for joint functions. Carbs are also used for intestinal mucus which so on very low carb you might have some micronutrient deficiencies.

  • Dee

    6/13/2011 7:47:05 PM |

    Have you tried adding D-ribose to your mix of supplements?  It has helped with my muscle aches from exercise.

  • Kris - Health Blog

    6/14/2011 7:52:50 AM |

    It seems that a lot of doctors would do well by going back a few years in time and re-reading Biochem 101.

  • Jim Anderson

    6/14/2011 7:05:22 PM |

    My wife and I have both been following a low-carb eating plan.  For me, that has meant increased fat consumption from the start.  I have felt full and satisfied after meals, and can go longer without feeling hungry.  I have also lost weight steadily.  My wife, however, has had a harder time of it.   She claims that is because women just have a harder time losing weight than men do.  That's true, I guess, in general, but I have also noticed that she seems to be avoiding fat a lot more than I do.  (Well, I don't avoid it at all!)  So she gets hungrier more often.  It is very difficult to overcome years and years of anti-dietary fat propaganda!

  • Joe Lindley

    6/30/2011 2:04:03 PM |

    Yes!  Thanks for the complete explanation of the fats vs. carbs impact.  I'm successfully on a low carb diet now after quitting Atkins years ago because my wife was worried I'd keep over from a heart attack.  With the right information out there now that dietary fat won't hurt you, people can stick to a low carb diet and get enough satiety (food satisfaction) with fats in the diet to stay on a diet.  It's truly been a disaster that the nutrition authorities shooed us away from dietary fats starting in the 1970s.  It's taken decades to get the word out that dietary fats are OK.  I published a nostalgic post on this about how Barney Fife got it right back in 1963:  http://bit.ly/m5eAhE

  • James Roberts

    7/30/2011 12:59:43 AM |

    Great post, great site.  I made my way to focusing on triglycerides by starting with Lipitor.  I had some bad though serious side effects (mostly insomnia),  so I dropped it and worked really hard on reducing fat intake.  That pretty much worked, but surprise (to me)... triglycerides went way up.  Now that I've also worked on cutting empty calories my levels are down to borderline.  Once you make it to a genuinely healthy diet everything seems to work out Wink
    cheers,
    James

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What if your lipoproteins are perfect?

16. June 2006 William Davis (0)


Sandy is a 56-year old woman--fit, slender, physically active, with no bad habits. A retired teacher, she has time to devote to her health. She bikes several days per week, mountain bikes, walks, and takes fitness classes. In short, she's the picture of perfect health.

Her heart scan score was not terribly impressive: 41. However, at her age, this modest score placed her in the 77th percentile. This suggested a heart attack risk of around 2-3% per year.

So we measured Sandy's lipoproteins. They were shockingly normal. In fact, Sandy is among the very rare person with absolutely no small LDL particles. All other patterns were just as favorable, including an HDL in the 80s.

This may seem like good news, but I find it disturbing. People are often initially upset by seeing multiple abnormal lipoprotein patterns. But lipoprotein abnormalities are the tools that we use to gain control over coronary plaque.

So what do we do when there are no abnormalities?

There are several issues to consider:

1) Your heart scan score reflects the sum total of your life up until that point. What if you were 20 lbs heavier 10 years earlier and your lipoproteins were abnormal during that period? Or you smoked until age 45 and quit? As helpful as they are, lipoproteins and related patterns are only a snapshot in time, unlike the heart scan score.

2) You have a vitamin D deficiency. This is unusual as a sole cause of coronary plaque. Much more commonly, it is a co-conspirator.

3) The heart scan is wrong--highly unlikely. Heart scans are actually quite easy, straightforward tests. (The only time this tends to happen is when scoring that appears in the circumflex coronary artery is actually in the nearby mitral valve. This really occurs only when there's very minimal calcium in the valve.)

4) There's a yet unidentified source of risk. Probably very rare but conceivable. For instance, there's an emerging sense that phopholipid patterns may prove to be coronary risks. One clinically available measure that we've not found very useful is phospholipase A2, known by the proprietary name "PLAC" test. (See http://www.plactest.com for more information from the manufacturer/distributor of the test.) But there's probably lots of others that may prove useful in future.

How often does it happen that someone fails to show any identifiable source for their coronary plaque? I can count the number of instances on two fingers--very unusual. (Thank goodness!)

Sandy's case is therefore quite unique. How should we approach her coronary plaque? In this unusual circumstance, lacking a cause, we tend to introduce therapies that may regress plaque independent of any measurable lipoprotein parameters. But that's a whole new conversation.

Fly to India for a bypass operation?

16. June 2006 William Davis (1)

In the June 19, 2006 issue of People Magazine, there's an article called "The Doctor is in . . .INDIA". The report talks about how, with health care costs in the U.S. spiralling out of control, more and more Americans are leaving the country to have their procedure performed.

They tell the story of Mr. Carlo Gislimberti of New Mexico and cite these numbers:

Heart Surgery
Cost in U.S.: $200,000

Cost in India: $10,000

Mr. Gislimberti opted to have his coronary bypass operation in India for cost reasons.

But the People magazine report left out one other option: The Track Your Plaque program: $39.00

Do your part to save ballooning health care costs: Engage in a truly powerful program of heart disease prevention like the Track Your Plaque program. The cost difference is laughably huge. And you won't require a 12-inch chest incision.

Follow conventional guidelines and guess what? You're going to have a heart attack. Follow the American Heart Association diet and you'll have heart disease.

Cut to the chase. The only program that is able to detect, track, and control coronary plaque better than any other process I know of is this program.

Note: I am not proposing that a heart disease prevention program like Track Your Plaque can replace a procedure like coronary bypass when a dangerous situation has developed. The Track Your Plaque program is designed to be implemented in the years before heart surgery is required. That's when you have the greatest control over your fate.

Surprise: Heart scan score reversal

14. June 2006 William Davis (0)
Gene is a jovial, fun-loving railroad worker who didn't take anything too seriously--including his heart scan score of 767.

This score placed Gene solidly in the 99th percentile (in the worst 1%). It came as no surprise to Gene. After all, his father died at age 36 of a heart attack and Gene's brother died at 60 of a heart attack. So Gene took life as it came and long ago decided not to fret about his fate.

But Gene's wife prodded him and prodded him to get the heart scan. That's when I met him.

Of course, Gene had been prescribed Lipitor by his doctor for a somewhat high LDL cholesterol. Our assessment uncovered several additional patterns including lipoprotein (a), small LDL, a pre-diabetic tendency, and a severe deficiency of vitamin D.

At 224 lb and 5 ft 6 inches in height, I felt that Gene was at least 40 lbs overweight.

One year later and with reasonable correction of all his patterns except weight loss and Gene's heart scan score was 590--a reduction of 23%!

Gene was thrilled, as was I. But, frankly, I was also surprised. Dramatic regression of coronary plaque tends to not occur so readily as long as pre-diabetic patterns persist and weight is not controlled.

The lesson: Often the only way to tell if you've achieved control or regression of coronary plaque is to have another heart scan. The tremendous variation in human responses never ceases to amaze me.

Call me when you're having chest pain

13. June 2006 William Davis (0)

I met a patient, Anna, yesterday. She was quite frustrated and frightened.

At age 50, Anna suffered a heart attack and received a stent to her left anterior descending coronary artery. What she found upsetting is that, because several members of her family had suffered heart attacks in their 40s (Dad--heart attack at age 45, paternal uncle--heart attack age 40, and even another uncle with heart attack in his late 20s), she had repeatedly asked her doctor whether she was okay.

She received the usual array of false assurances: "You're feeling fine, right? Then don't worry about it." "Look. Your cholesterol is in the normal range. Even your cholesterol/HDL ratio is fine." "Women don't get heart disease until later in life."

All proved absolutely false. As we talked, Anna exclaimed, "I think what I've been told all along is that we'll take you seriously when you finally have a heart attack!"

She's exactly right. The vast majority of times, heart disease is discovered by accident, usually because of an "event" like heart attack. This is like changing the oil in your car when it finally breaks down--it's too late.

CT heart scan, followed by lipoprotein testing and associated values, then correction of your specific causes. It's that simple.

Self-empowerment is coming!

11. June 2006 William Davis (0)
I've discussed this before: The coming wave of self-empowerment in health. Health that is driven by you, not a hospital, not a doctor, not by procedures, but by information and access to tools that are powerful and effective.

The seeds are being planted right now and won't take full root for many years or decades. But it's going to happen.

I previously cited several broad trends that are examples of this emerging wave:

--The nutritional supplement movement. Contrary to the media's ill-informed bashing, nutritional supplements are getting better: improved quality, better substantiation of when/how to use them, new agents that appear rapidly, since introduction is not slowed by the molasses of the FDA.

--Medications moving to over-the-counter status. Health insurers are driving this one. OTC means not paid for by insurance. That also means access to you.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The mind-boggling rapidity and depth of information available on the Internet today is fueling the self-empowerment movement by providing sophisticated information to health care consumers. Information here is uneven at present. But, as consumer sophistication increases and the system of checks and balances evolves, internet-driven information will be often superior to what you get from a doctor or other health professional.

--High-deductible health insurance plans. If health care consumers bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention and minimize long-term costs.

This trend does not mean treating your own infection, taking out your own gall bladder, repairing your own broken leg. It means that conventional routes of health delivery will recede into providing only catastrophic care.

It means that you and your family will take a larger role in learning how to eat and exercise properly, use foods to maintain and promote health (the "designer food" and "nutraceutical" movement), take supplements that have real benefits, use medications for treatment of many everyday ailments.

It also means seizing control of diseases that previously were only treated in hospitals, like coronary heart disease. This, of course, is where our program, Track Your Plaque, is an example of how you can have a powerful and effective role in your heart health. Track Your Plaque goes so far beyond the "eat low-fat, exercise, and know your numbers" media mantra that it's like comparing a brand-new Mercedes to a rusted, run-down '87 Ford Escort. There truly is no comparison. (Sorry if you're an Escort driver!) But you get the idea.

Another option for lipoprotein testing

9. June 2006 William Davis (0)

For those of you who have been frustrated in trying to get your lipoprotein analysis performed, here's another option.

The Life Extension Foundation at www.lef.org provides access to the VAP test, or Vertical Auto Profiler. This is the lipoprotein test run by the Atherotech company in Birmingham, Alabama. The name refers to the method used, a form of centrifugation, or high-speed spinning of your blood (plasma) to separate the various components by density.

This is a fine technique that works well. Though our preferred method is NMR (www.Lipoprofile.com, Liposcience Inc.), the Atherotech VAP is a reasonable alternative.

If you go through the Life Extension process, they will direct you to blood draw sites in your area. They charge $185 for Life Extension members, $247 for non-members. (Membership in Life Extension costs $75.) Drawback: No billing for health insurance reimbursement.

A full description of the significance of lipoproteins can also be found in my article posted on-line at the www.lef.org website at http://www.lef.org/magazine/mag2006/may2006_report_heart_01.htm

Weight and lipoproteins

8. June 2006 William Davis (0)
Tom, an accountant, came into the office eager to know what his 2nd heart scan score showed.

A year ago, Tom's view of himself as a healthy, middle-aged man was shattered when he found out his heart scan score: 1236. Tom had severe coronary plaque with a heart attack risk of 25% per year (without intensive preventive action).

In the way of lipoprotein abnormalities, he had several: low HDL, deficient large HDL, small LDL, high triglycerides, IDL (the after-eating inability to clear dietary fats), and a high blood sugar in the pre-diabetic range. In addition, Tom was hypertensive, with blood pressure so high it even landed him in the emergency room last winter.

In addition to our approach to correct all these patterns, Tom was urged to lose a significant quantity of weight. Starting at 225 lb., at 5 ft 7 inches, Tom was clearly at least 40 lbs over his ideal weight.

I stressed to Tom that the entire spectrum of causes of coronary plaque were weight-related. I likened his patterns to throwing gasoline on a fire: As weight increased, his lipoprotein and other abnormalties flared dramatically.

But each time Tom came back to the office over the ensuing year, he'd gained another 3 to 6 lbs. And each time he had an explanation. "My daughter just got married. I couldn't turn down wedding cake, now could I?" Or, I just survived another tax season. I was working day and night--no time for exercise!" "It's getting too hot to walk anymore."

Well, despite multiple treatments, Tom's repeat heart scan showed a score of 1677, a 35% increase. That's a dangerous rate of growth that virtually guarantees that plaque is building up momentum to "rupture", which results in heart attack.

I therefore stressed to Tom that weight loss was crucial. Control of coronary plaque was simply not going to occur without weight loss to our target. Alternatively, we could add several new prescription medicines and hope that they could achieve the same effect, though at a price (side-effects, expense).

I tell Tom's story to highlight again just how important weight loss can be for a number of lipoprotein abnormalities.

What measures specifically are sensitive to weight? They are:

--HDL cholesterol
--Triglycerides
--Small LDL
--VLDL
--Blood pressure
--Blood sugar and insulin
--C-reactive protein
--LDL

Weight exerts profound influence on these patterns. In Tom and people like him, weight can be a "make it or break it" issue.

If you, like Tom, have any of the above patterns, consider weight loss as a potent tool you can use to gain control of coronary plaque.

Variation in vitamin D requirements

7. June 2006 William Davis (0)

For Track Your Plaque followers, you know we are very concerned about vitamin D blood levels. My prediction is that, in 10 years, vitamin D will be regarded as an important item on the list of coronary artery disease risk factors.

In our experience of trying to stop or reverse heart scan scores, restoration of vitamin D to a blood level of 50 ng/ml appears to have increased our success rate dramatically.

As we've talked about before, on the bell curve of vitamin D dosing in a northern climate, the majority of women require 2000 units per day, men require 3000 units per day to achieve a level of 50 ng. However, there are "outliers" on this bell curve, i.e., people who require much more or much less.

This week, I saw two people who were very instructive cases of extreme requirements on the high end of vitamin D dosing. Both started with unmeasurable blood levels, i.e., essentially zero ng/ml. On 5000 units of vitamin D per day, both raised their blood levels to around 17-18 ng/ml--in the range of severe deficiency (defined as <20 ng/ml). I advised both to increase their oral dose of vitamin D to 8000 units per day.

Notably, both people avoided sunlight and lived in Wisconsin, a terribly sun-deprived locale 10 months a year. Both were also substantially overweight (around 300 lbs each).

The vitamin D issue continues to be endlessly fascinating in all its nuances and twists.

Heart attacks in your own backyard

7. June 2006 William Davis (0)
Two men from my community just died of heart attacks. Both were in their 40s.

What bothers me most about these all too frequent stories is that it is so preventable. You can bet that both had little or no symptoms prior to their deaths. You can also bet that they've had cholesterol panels taken by their doctors.

Followers of the Track Your Plaque program know that these are sure-fire paths to failure. The absence of heart disease symptoms should provide no reassurance whatsoever. High cholesterol, in-between cholesterol, low cholesterol--none are confident indicators in a specific individual.

Stress test? How about the patient I saw today who, until I met him, had been undergoing stress test after stress test, every year--all while the quantity of coronary plaque tripled. False reassurances provided by his cardiologist led him to believe that all was well--while this stack of oily rags was just waiting for the spark to ignite.

Too little time, too much money, too far away--there's a hundred excuses for not getting a heart scan. Or, you've had a heart scan and no one can tell you what to do about it. If you're reading this, however, you've found the most intensive source of information available on how your heart scan can serve as the start of a program of heart attack prevention for a life free of dangers.

It's not that tough. But it won't just go away on its own. I just have to look around me in my own community, watch the local news, talk to friends, and I'll heart about all the people just in my neighborhood who should be learning these lessons. I rant and rave about this but some people need to hear it from a friend, colleague, neighbor, rather than some crazy doctor bucking the standard line.

You, too, should be telling anyone who will listen about how heart disease can be identified and controlled.

Pilot lands safely after heart attack, then dies

6. June 2006 William Davis (1)
That was the disturbing headline on a report from MSNBC, also reported nationally on all the major news networks.

The story goes on:

"A pilot suffering a heart attack made an emergency landing on a highway, saving his three passengers shortly before he died...He landed the single-engine Cessna 185 on Utah 30 near Park Valley and was taken to Bear River Hospital in Tremonton, where he died."

We track these sorts of stories and it's frightening just how common they are. A school bus driver recently had a heart attack while driving 30 children; the bus crashed but no one was hurt. A 52-year old commercial bus driver suffered a heart attack while transporting 49 conference attendees; the bus plunged 400 feet down a ravine. Remarkably, 17 passengers suffered only minor injuries and there were no deaths.

There have even been incidents where the pilot of a jet liner suffered a heart attack in-flight. In 2000, the 53-year old pilot of a Northwest Airlines DC-10 died while in-flight from a heart attack while landing in Minneapolis. The 290 passengers were landed safely by co-pilot.

Most incidents where the driver or pilot has been incapacitated or died resulted in the deaths of only a handful of people. No major catastrophe has yet occured. But--mark my words--it will. These incidents just happen too frequently.

Virtually all of these and similar incidents could have been prevented. If the FAA, for instance, would insist that all pilots have a simple CT heart scan, it would become immediately obvious which pilots should be grounded and who should fly. Similar requirements could easily be applied to persons in charge of the welfare of many people, most notably school bus drivers.

It's not that tough! The FAA currently requires stress testing and cholesterol testing. Well, guess what? Followers of the Track Your Plaque program know that these tests do not effectively identify the person at risk for heart attack in the majority of individuals. Just ask former President Bill Clinton how helpful his stress tests (five in a row!) were. Or how valuable his cholesterol monitoring was--all prior to his emergency bypass surgery.