Self-empowerment is coming!

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


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

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


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

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

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.

Large new clinical study launched to study. . .niacin


Oxford University has issued a press release announcing plans for a new clinical trial to raise HDL cholesterol and reduce heart attack risk. 20,000 participants will be enrolled in this substantial effort. The agent? Niacin.

How is that new? Well, this time niacin comes with a new spin.

Dr. Jane Armitage, formerly with the Heart Protection Study that showed that simvastatin (Zocor) reduced heart attack risk regardless of starting LDL, is lead investigator. She hopes to prove that niacin raises HDL cholesterol and thereby reduces heart attack risk. But, this time, niacin will be combined with an inhibitor of prostaglandins that blocks the notorious "flushing" effect of niacin.

The majority of Track Your Plaque participants hoping to control or reverse coronary plaque take niacin. Recall that niacin (vitamin B3)is an extremely effect agent that raises HDL, dramatically reduces small LDL, shifts HDL particles into the effective large fraction, reduces triglycerides and triglyceride-containing particles like IDL and VLDL. Several studies have shown that niacin dramatically reduces heart attack. The HATS Study showed that niacin combined with Zocor yielded an 85-90% reduction in heart attack risk and achieved regression of coronary plaque in many participants.

In our experience, approximately 1 in 20 people will really struggle using niacin. Flushes for these occasional people will be difficult or even intolerable. Should Dr. Armitage's study demonstrate that this new combination agent does provide advantages in minimizing the hot flush effect, that will be a boon for the occasional Track Your Plaque participant who finds conventional niacin intolerable.

But you already have access to niacin, an agent with an impressive track record even without this new study. And you have a reasonably effective prostaglandin inhibitor, as well: aspirin. Good old aspirin is very useful, particularly in the first few months of your niacin initiation to blunt the flush.

Although this study is likely to further popularize niacin and allow its broader use, it's also a method for the drug companies to profit from an agent they know works but is cheap and available.

You don't have to wait. You already have niacin and aspirin available to you.

The dark side of CT heart scans

"I just got a heart scan!" declared Eric to his doctor. He handed the report to him.

"Oh my. Your score is 154." The doctor paused, then looked at Eric with a serious look on his face. "If we're going to understand whether or not you're in danger, you'll need a heart catheterization."


I've seen this happen countless times. How can I say this diplomatically? THIS IS WRONG!! In my view, it's absolutely criminal for this to happen. Physician ignorance, profiteering, whatever--it is wrong.

There's very few reasons why someone who has no symptoms should go directly to the cath lab for a procedure. (A rare exception might be an exceptional quantity of plaque in the left mainstem artery, e.g., >100. This is highly unusual.)

Even a nuclear stress test (e.g., thallium) at this level of scoring is only 10-15% likely to be abnormal. That means 85-90% likelihood of being normal. There's rare reasons to perform a heart catheterization in a person with no symptoms and an entirely normal stress test. The vast majority of people like Eric do not need a heart catheterization to discern risk.

If Eric's doctor had been up-to-date on the published literature on the prognostic value of heart scans, he could have advised Eric what the risks were--without a catheterization. Many doctors simply don't want to be bothered. Or, they opt for the more profitable method--a hospital procedure.

Always discuss your heart scan with your doctor--but be armed with information in case your doctor is uninformed or unscrupulous. Unfortunately, that's not uncommon. The Track Your Plaque program is your advocate, a source for unbiased information.

The dirty little secret about aneurysms

Jake had an abdominal aneurysm identified--by accident.

While getting a CT scan of his abdomen for unexplained abdominal pain, a 4.4 cm aneurysm was discovered. Jake's abdominal pain eventually passed without explanation, but he was left with this aneurysm.

Jake's primary care doctor referred him to a surgeon. "It's too small to require surgery right now. Wait a few years and it'll probably get bigger. When it gets to around 5.5 cm, that'll be the time to operate. Let's schedule an abdominal ultrasound or CT scan every 6 months."

Jake then got himself a heart scan. His high score of 879 then led him to my office. Lipoprotein testing, a stress test, correction of his lipoprotein patterns, changes in lifestyle followed. One year later, Jake's heart scan score was unchanged.

How about his abdominal aneurysm? 4.2 cm--a modest quantity of regression. When Jake's surgeon learned of the change, he just shrugged. "Okay, we'll just watch it from here."

Shockingly, the conversation surrounding aneurysms is just like the one Jake received: Let's just watch it grow until you need surgery.

If you've every seen anyone have abdominal aneurysm surgery, you know it is an awful, painful, barbaric process with high risk for major complications like kidney failure and loss of the legs. Waiting for an aneurysm to grow is a lousy solution. Surgeons point out that, although surgery is imperfect, it's better than the alternative: rupture, which is catastrophic with a 50% chance of dying.

But what about stopping the growth of the aneurysm? Or even reversing, or shrinking, it?

Surgeons say it can't be done. Yet we've done it--many times. And it's not that difficult.

The steps to take are very similar to that in the Track Your Plaque program for coronary plaque regression, with a few different strategies. Suppression of inflammation, for instance, plays a more important role and blood pressure must be abolutely normal, even during exercise.

More to come on this important topic in the future, including an upcoming Special Report on the www.cureality.com membership website.

Heart scan scores dropping like stones!!

I saw two instances of dramatic coronary plaque regression today.

John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume!

Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction.

Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events".

Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.
Gretchen's postprandial diet experiment II

Gretchen's postprandial diet experiment II

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

Comments (37) -

  • Pythonic Avocado

    1/3/2010 3:53:05 PM |

    Why do you say the low-carb response  is leading to increased risk for heart disease?

  • Stan (Heretic)

    1/3/2010 5:34:56 PM |

    Re: Both the low-carb and the low-fat responses are undesirable, both leading to increased risk for heart disease.

    With due respect, I would disagree that BOTH are undesirable, but I agree that the one caused by the low fat high carb diet (only) is indeed dangerous!  

    It was never proven that high triglycerides alone cause heart disease.  The available trials such as Framingham (1)  may have shown some correlation with the total cholesterol but correlation is not causuation, especially that the statistics do not distinguish between various diets. Furthermore, Framingham's correlation is restricted to men only (not women) and only for the age group 30-55.  For older men and for women of all ages the correlation becomes insignificant or reversed.

    Given the above data, I think the most plausible interpretation leads me to a conclusion that the most likely direct cause of atherosclerotic cardiovascular disease is excessive blood glucose with hyperinsulinemia  (see the following papers, and Stout's papers(2) ).

    Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease.  That I believe has nothing to do with dietary fat.

    Regards,
    Stan (Heretic)

    -----------
    Refs:

    1) JAMA. 2004 May 12;291(18):2243-52. Drug treatment of hyperlipidemia in women. Walsh JM, Pignone M.

    2) INSULIN-STIMULATED LIPOGENESIS  IN ARTERIAL  TISSUE  IN RELATION  TO DIABETES AND ATHEROMA,
    R.W. STOUT, Lancet Sept 28, 1968, p702.

    and

    INSULIN STIMULATION OF CHOLESTEROL
    SYNTHESIS  BY ARTERIAL TISSUE,
    R.W. STOUT, Lancet Aug 30, 1969, p467.

  • Nigel Kinbrum BSc(Hons)Eng

    1/3/2010 5:41:31 PM |

    As serum TG's with the HF meal are lower at the end of the day than at the beginning, does this suggest that successive days of HF meals produce progressively lower & lower TG's?

  • Anonymous

    1/3/2010 6:02:56 PM |

    I would love to hear about how to balance the risk between these extremes!  Wow, nice post.

  • Dr. William Davis

    1/3/2010 10:11:35 PM |

    Pythonic and Stan--

    It's not that triglycerides per se are atherogenic, but the POSTPRANDIAL PARTICLES that triglycerides represent are atherogenic.

    In other words, high triglycerides signals extravagant chylomicron remnants and VLDL, both of which are atherogenic.

    In the ongoing debate over what constitutes a healthy or unhealthy diet, the entire issue of postprandial patterns has been ignored. Yet much of heart disease develops IN THE POSTPRANDIAL PERIOD.

  • shel

    1/3/2010 10:55:38 PM |

    i eat copious amounts of fat with positive effects. i'm a layman, but "postprandial" or not, i'm having a hard time accepting this, as the evidence i've read seems to contradict what you're saying regarding overall benefits.

    why did no one pick up on the "postprandial particle" issue until now?

    will this be a new controversy sweeping through the paleo/low carb blogging community now? ;)

  • Dr. William Davis

    1/4/2010 2:15:45 AM |

    Anyone desiring a full accounting of the hundreds of studies documenting this effect will need to refer to the Track Your Plaque Special Report, Postprandial Lipoproteins: The Storm After the Quiet.

    This literature is, unfortunately, relatively difficult to understand. But just because nobody else has incorporated these findings into diet advice doesn't mean it isn't important.

    Keep in mind that most dietary advice is NOT based on observation of postprandial phenomena.

  • Eric

    1/4/2010 5:53:50 AM |

    I had a stroke last month. (Very minor, I went immediately back to work.)  As a 35 year old non-smoker/non-drinker who generally ate low carb and avoided sweets before the stroke (and had been exercising regularly for 6 weeks), I'm baffled as to why my triglycerides are between 600 and 900.  I'm now on Lovaza.  Against my doctor's advice, I decide to do a paleo type diet.  We'll see how the lipid panel does at the end of this month, but so far avoiding wheat and grains has generally made me feel better.  I've lost some weight as a bonus.

    The doctor is blaming my triglycerides for the stroke, and just calling it hereditary.  It'd be nice to know just what gene I have that causes strokes!  No blood clotting disorders, no diabetes, no pancreaitis, and no hole in my heart either.

  • Alen Kcatic

    1/4/2010 10:58:09 AM |

    First let's take a brief overall look at heart disease because you need to combine two other major lifestyle habits with diet to truly make a difference in reversing or preventing heart disease.


    But here's the good news. You can prevent or reverse heart disease by following care

    Avoid tobacco
    Be more active and walk 30 minutes
    Choose healthier food, including more fiber, less saturated fat, and less salt.

  • Peter

    1/4/2010 12:38:21 PM |

    If it were as simple as low fat leads to diabetes, the Japanese who ate the traditional low fat high rice diet would have had extremely high levels of diabetes, but they hardly had any. I would be more inclined to wonder if our diabetes epidemic is due specifically to flour and sugar rather than low fat in general.

  • shel

    1/4/2010 4:27:36 PM |

    ~Dr Davis, i wonder if this finding is going to point toward advocation of "grazing", rather than two or three meals per day (in a low carb context).

  • kris

    1/4/2010 6:04:12 PM |

    Dr. Davis,
    Happy new year.
    here is the link to videos about FDA and drug giants. An eye opener. just in case you have not looked at it. total of 8 videos.
    http://www.veoh.com/search/videos/q/generation+rx#watch%3Dv18919526gZ4fkAAk

  • StephenB

    1/4/2010 7:16:32 PM |

    Dr. Davis, the abstract of the study you linked read: "Ten men consumed a low-carbohydrate diet rich in monounsaturated fat (MUFA) and supplemented with n-3 fatty acids for eight weeks."

    As you know, there are multiple low carbohydrate diets. This particular study did not examine a high saturated fat diet. I would love to see the result of chronic dieting featuring quality saturated fats like tallow, lard, butter, and coconut milk and avoiding hydrolyzed fats.

  • mark

    1/4/2010 7:19:28 PM |

    Dr. Davis wrote:
    "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."

    We don't see triglycerides being converted to glucose. It's a one way street.

    Would having increased carbohydrayte storage space in the body be preferable to storing triglyceride? We have an example of that in hyperglycemia. That's storage in the bloodstream. But the body works quickly to CORRECT that.

    So it's not that the body lacks glucose storage and triglyceride is the bad alternative. Not that at all. The body works hard to push glucose out of blood storage and into triglyceride in fat cells. That's a good thing.

    Postprandial high triglycerides from a high fat diet is a marker of fat intake. Postprandial low triglyceride on a high carb diet is a marker of carbohydrate metabolism. The later increase in triglyceride is the corrective process.

    It's hard to make the case that triglyceride is itself bad when it's one of the body's innate responses to the bad hyperglycemia. If triglyceride is bad, then the body is stuck between a rock and a hard place. It's win-lose, so the low fat diet is worse than the low carb one.

    Given my experience with dieting, I would favour low carb over anything balanced in the way of fat/carb. From dietary intervention trials, I'm unconvinced that high fat is worse (or much better) than a mixed blend of carb and fat from a mortality perspective. But from experience, I favour low carb for general sense of well-being.


    Stan wrote:
    "Hyperglycemia and hyperinsulinemia also happen to coincide with elevated TG and LDL but those are coincidental markers of metabolic syndrome induced by the common high carb (high sugar) diets rather than causing heart disease. That I believe has nothing to do with dietary fat."

    It's tough to isolate lipids as causal as opposed to effects of diet. Smoking and fructose lead to increased LDL. So in this case, high LDL is really a symptom smoking and fructose intake. The latter two likely being causal for anything related to your health. 8 egg yolks a day on a high fat diet and your LDL is a symptom of that. And some people have normal LDL on that even.

    Mark.

  • Dr. William Davis

    1/4/2010 11:33:43 PM |

    Hi, Shel--

    No, absolutely not.

    Quite the opposite: Given what happens after eating, grazing is a destructive practice that likely increases risk for heart disease.

    See the previous Heart Scan Blog post: http://heartscanblog.blogspot.com/2009/11/triglyceride-and-chylomicron-stacking.html

  • shel

    1/4/2010 11:52:20 PM |

    ~hi Dr Davis.

    i agree. and i do much better when i eat two meals within an eight hour window.

    my focus has always been on keeping blood glucose low (i'm not diabetic, but use a glucose meter for my own curiosity), so was a bit floored by the thought that i have to watch every postprandial spike!

    ...so, what's left? huge salads and skinless chicken breasts? ;)

  • vin

    1/5/2010 9:33:36 AM |

    It is pure and simple observation of two parameters after eating a low carb and low fat meal. Nothing more that that.

    After all most of us eat more than just carbs and fat: there are vitamins, enzymes, minerals, fiber and hundreds of other nutrients. I am certain that they more than compensate any damage that glucose or triglycerides can cause to your arteries.

  • Dr. William Davis

    1/5/2010 4:39:02 PM |

    Sorry, Vin.

    You're kidding yourself if you belief that.

    It reminds me of the people I meet who take a list of supplements 30 items long (though lacking the most crucial like vitamin D) prior to their bypass or heart attack. That's called magical thinking.

  • Kurt

    1/5/2010 9:27:14 PM |

    Both diets seem to be extremes, whereas many of us are trying to eat a balanced diet of vegetables, lean meats, nuts, and some legumes and whole grains - call it moderate fat and moderate carbohydrate - but focusing on heart-healthy foods. I'd like to see postprandial data on that.

  • O

    1/5/2010 10:39:05 PM |

    I have been eating a primal low-carb diet for almost 2 years and feel great.  My fasting blood work is : trig = 40, HDL=88, LDL=114 (calculated), total chol=214, testosterone=606.  My heart scan score is 0.  I am physically active muscular male with 4 intense weights + some cardio workouts 2 hours each.  My bodyfat % is about 8-10% (I can see a clear 6-pack), age=43, height=5'7", weight=160 lbs.

    I have made an analysis of my daily intake in a spreadsheet.  My diet on workout days is 3000 kcal, of which 50% fat (167g, out of which 60g saturated), 20% carbs (150g), and 30% protein (200g).  Half the carbs are timed post-workout (workout shake, followed by dinner of meat + sweet potato).  On a non-workout days, I do not have a shake nor sweet potatoes, so the carbs drop to 10% (70g).

    Given the amount of fats I take every day, I am rather alarmed by the postprandial triglycerides.  My breakfast, in particular, has 57g of fat which will cause probably a substantial postprandial triglycerides.  Breaking up my food intake into many smaller meals doesn't seem to be a good thing.   We don't want increasing carbs or protein at expense of fats either.  Therefore, what is the solution here?

  • Dr. William Davis

    1/5/2010 11:21:32 PM |

    O--

    I am afraid there's no quick answer. That question is answered in an exhaustive report on the Track Your Plaque website.

    Alternatively, you could conduct your own do-it-yourself postprandial triglyceride test.

  • Anonymous

    1/6/2010 3:17:23 PM |

    This doesn't detract from any of the points you're making about postprandial triglycerides--but it looks like you're reading the chart from the wrong side here for triglycerides, from the left instead of from the right.

  • Catherine

    1/6/2010 4:16:40 PM |

    YIKES!
    I have been experimenting with a gluten-free, low carb, low sugar diet for 5 months and my LDL just shot UP from 220 to 230 and my HDL went DOWN a little from 66 to 61. (tryglicerides and CRP are excellent). This is opposite what's supposed to happen. Serum D level is good at 54.

    Can someone please tell me the name of the test to request from my doctor to tell if I have the small evil-type LDL or the big fluffy okay-type LDL?

    Thanks for your help,
    Warmly, Catherine

  • Lucy

    1/6/2010 4:33:54 PM |

    These results seem completely contradictory to the way Dr. Eades described the breakdown of saturated fat in his blog "The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route."

    Why was there a triglyceride spike after a high fat meal, but not a high carb one?  Were the fats Gretchen consumed not saturated?  It can't be both ways, which metabolic pathway is correct?

  • Catherine

    1/6/2010 9:08:44 PM |

    Oops, sorry i made a mistake.---My LDL went up from 120 to 130 (not 220 to 230)

  • vin

    1/7/2010 11:16:29 AM |

    Thanks for your comment Dr. Davis but for the first time you sound just like my cardiologist. He does not believe in reversal and thinks it is all down to one's genes and there is nothing one can do to change that. Well I think differently having postponed bypass surgery seven years ago. I will continue with 'magical thinking'. Its nice, you should try it sometime.

  • Anonymous

    1/7/2010 4:29:08 PM |

    To eat one extreme one day (low fat) and then eat another extreme (low carb, high fat) the next is a sure-fire way to get whacky blood/lipid results. Also, lipid levels can fluctuate more than 10% within a given day under normal circumstances. Alternating eating radically different extremes in terms of diet is anything but normal in my view.  Stress, exercise, or even one's sex can cause also shifts.  Trying to prevent every potential/alleged problem with postprandial lipids seems like a sure-fire way to increase stress which is also damaging to the heart and body.  I doubt paleo manwoman worried about the spike in his/her triglycerides from gorging on the fat from fatty meat meals.  I think one can micromanage one's self or rather labs, lipids etc to death...

    PS: Forgot to mention lab error.  Before drawing any conclusions from any lab results, have them repeated multiple times and at different labs.  My husband has to communicate with lab techs for his job and was horrified when one kept referring to "esterified" as "stir-fried"! And this was the one of the largest labs in the US...

  • Jim Purdy

    1/18/2010 4:38:41 AM |

    Doctor Davis, have you seen the new PR campaign from manufactured "food" giant Unilever to "Ban butter to save thousands of lives."

    Unilever is the company behind many fake foods, including fake butters Country Crock and  I Can't Believe It's Not Butter!

    I've posted a little about this ban-butter campaign on my blog at blogsthatmakemethink.blogspot.com

  • shoby

    1/28/2010 3:25:55 PM |

    I also have a blog about the diet we can share experiences and exchange links.
    This blog http://just-slim.blogspot.com
    thanks

  • Fran

    2/1/2010 5:51:52 AM |

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

    Please tackle this discussion soon.

  • ET

    2/26/2010 6:52:28 PM |

    I also keep a spreadsheet that details all the different fatty acids and such for every meal.  I've also had three lipid tests this year which were not fasting.  Two were in the afternoon, eight hours after a five-egg omelet with coconut oil, cheese and bacon; 2 hours later I had eight oz of full-fat greek strained yogurt which adds up to over 120 g of fat 6 to 8 hours before the test.  Add another 40 g of fat 2-hours pre-test and according to your theory, my triglycerides should be high.  On each occasion they were 91.  This is on a low-carb (<70g/day) diet.

    There's more to postprandial triglyceride metabolism than is covered here.  My next test will be a non-fasting NMR lipoprotein analysis.  Should be interesting how that stacks up against a fasting NMR test.

  • A. Lanine Pro

    6/21/2010 8:55:09 AM |

    Well I think differently having postponed bypass surgery seven years ago. I will continue with 'magical thinking'. Its nice, you should try it sometime.

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What goes up can't come down

What goes up can't come down

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.

Comments (13) -

  • karl

    11/28/2009 8:01:01 PM |

    Where is this published?

  • Nigel Kinbrum BSc(Hons)Eng

    11/28/2009 9:09:40 PM |

    Has anyone investigated the effect of Vitamin K2 on CCS?

  • Dr. William Davis

    11/28/2009 9:23:30 PM |

    Karl--

    In the American Journal of Therpeutics 2009 Jul-Aug;16(4):326-32.

    For abstract, go to Pubmed and enter "Davis + Rockway" into the search.

  • Dr. William Davis

    11/28/2009 9:24:14 PM |

    Hi, Nigel--

    There are no studies in which K2 vs. placebo have been administered, only observations studies in which lower K2 intake has been related to greater risk for cardiovascular events.

  • David

    11/29/2009 2:17:29 AM |

    Hi Dr. Davis,

    Do you have any insight into what separated those that had reversal from that those that had slow and rapid progression?

    Thanks,
    David

  • drake

    11/29/2009 2:24:04 AM |

    My cardiologist said essentially the very point of your first sentence.  I had pestered my PCP to order a heart scan a month ago.  He relented only by stating that I should then go see a cardiologist.  

    The cardio stated that scores can't be decreased unless "they change the software reading the scan."  He further stated, "calcium is calcium; where's it going to go?"  Needless to say, he placed very little value on heart scans but it made for some lively discussion between he and I.

  • Paul Smith

    11/29/2009 2:36:20 AM |

    Dr. Davis - I'm 36YO in Australia with a 50% blockage on my LAD (vulnerable plaque). I have 1 tiny spec of calcium on a branch of my LAD so not much of a calcium score. I realise this is a serious problem.
    I guess 'track you plaque' would be harder for my with such a low calcium score so I haven't joined up.
    I've been using your techniques for 3months now - I'm sugar and carb free and I'm very close to 60/60/60 as you have recommend.
    With reference to your most recent posting, what is your experience with Vulnerable Plaque reduction in people with low or no calcium score? Its a bit harder to track I would have thought? PS - TIP for new bloggers - don't take 500mg of Niacin if its the first time your doing it! Ouch.

  • Red Sphynx

    11/29/2009 2:59:29 AM |

    Wow.

    Any general insight as to why this worked so markedly well for some of your patients, less well for others, and not at all for 3?  Obesity?  Tobacco?  Stress? Not taking their meds? Diabetes? Working in a refinery?  Or is It more about choosing the right ancestors?

  • Anonymous

    11/29/2009 4:48:45 AM |

    A major question remains: "Why are some patients NOT responsive to the TYP protocol"?

    Is their coronary artery disease being driven by a different cause?

  • billye

    11/29/2009 6:12:09 PM |

    Hi Dr. Davis,
    As usual you always provide great information.  I have been following a life style change that features the diet of our ancient ancestors, with great results for the last 12 month.  I use saturated fats exclusively, including MCT and coconut oil, Weight loss 55 pounds, Diabetes type 2 cured (A1c's of 4.7,4.8,and 5.0 all without medication). My doctor stopped all Staten's. I recently received the results of a VAP test 11/16/09.
    Some of the pertinent results are:
    Tot. LDL-C Direct 154 mg/dl
    Tot. HDL-C Direct  63 mg/dl
    Tot. TG    Direct  63 mg/dl
    Sum Tot. Cholesterol 233
    Real-LDL sz. Pat. A large buoyant
    Remnant Lipo (IDL+VLDL3) 26
    HDL-2(large,buoyant) 18
    HDL-3(small, dense)  45
    VLDL-3 (remnant lipo)9
    Recommendation: Consider lowering LDL-C goal.

    Because I am not a doctor, I am having trouble analyzing this VAP test.  I have started a course of Usher Smith 500mg SLO NIACIN.  Any other suggestions?  Is this  enough to  
    lower my LDL? I very much value your opinion, any input will be greatly appreciated.  Thanks in advance.
    Bill Eisenberg

  • Dr. William Davis

    11/29/2009 6:35:07 PM |

    Paul--

    I believe you may be misinterpreting what Track Your Plaque is intended to do. It is NOT  a program to reduce the amount of calcium in the coronary arteries; it is a program that uses the surrogate marker of coronary calcium as a means of reducing plaque.

    All the strategies we use in the program still apply, regardless of the proportion of calcium to non-calcified elements.

  • Anonymous

    12/8/2009 3:09:48 AM |

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    11/3/2010 10:05:27 PM |

    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.)

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