Track Your Plaque and non-commercialism

29. April 2007 William Davis (6)
If you're a Track Your Plaque Member or viewer, you may know that we have resisted outside commercial involvement. We do not run advertising on the site, we do not allow drug companies to post ads, we do not covertly sponsor supplements. We do this to main the unbiased content of the site.

We've seen too many sites be tempted by the money offered by a drug company only to see content gradually drift towards providing nothing more than cleverly concealed drug advertising. I personally find this deceptive and disgusting. Ads are ads and everyone knows it. But when you subvert content, secretly driven by a commercial agenda, that I find abhorrent.

That said, however, I do wonder if we need the participation of some outside commercial interests to help our members. In other words, many (over half) of the questions and conversations we have with people is about what supplement to take, or what medication to take. While we cannot offer direct medical advice online (nor should we) because of legal and ethical restrictions, I wonder if could facilitate access to products.

Many people struggle, for instance, with trusted sources for l-arginine, vitamin D, fish oil. Other people struggle with finding a heart scan center because of the changing landscape of the CT scanning industry. Could we somehow provide a clear-cut segment of the website that clearly demarcates what is commercial and non-Track Your Plaque-originated, yet at least provides a starting place for more info?

Ideally, we would have personally tried and investigated everything there is out there applicable to the program. But that's simply impossible at this stage.

I feel strongly that we will never run conventional ads on the site. Nor will we ever permit any outside commercial interest to dictate what and how we say something. The internet world is full of places like that. Look at WebMD. I find the site embarassing in the degree of commercial bias there. We will NEVER sell out like that, regardless of the temptation. People with heart disease are all conducting a war with the commercial forces working to profit from them--hospitals, cardiologists, drug companies, medical device companies (yes, even they advertise to the public, e.g., implantable defibrillators--no kidding). Genuine, honest, unbiased information is sorely needed and not from some kook who either knows nothing about real people with real disease, or has a hidden agenda like selling you chelation.

I'd welcome any feedback either through this Blog or through the contact@cureality.com.

The nattokinase scam

28. April 2007 William Davis (179)
A conversation about vitamin K2 commonly leads to confusion. Several people have asked about something called nattokinase.

The scientific data on the potential role of vitamin K2 deficiency in causing both osteoporosis and vascular calcification is fascinating. Along with vitamin D3, vitamin K2 may be an important factor in regulation of calcium metabolism. Supplementation may prove to be a major strategy for inhibition of vascular calcification.

Obtaining K2 in the diet is tricky, since it's present in just a handful of foods: egg yolks, liver, traditional cheeses, and natto. This is where the confusion starts.

Natto is a Japanese fermented soy product. I've had it and it's quite disgusting. Nonetheless, Japanese who eat natto experience less fracture. (A parallel study in heart disease has not been performed.) Natto is also a source of another substance called nattokinase.

Advocates (otherwise often known as supplement distributors) claim that nattokinase is a "fibrinolytic", or blood clot-dissolving, preparation that "improves blood flow, protects from blood clots, and prevents heart attacks and strokes."

Don't you believe it. This is patent nonsense. There are several problems with this rationale:

--Any oral fibrinolytic agent is promptly degraded in the highly acid environment of the stomach. That's why all medically used fibrinolytics are given intravenously. Drug companies have struggled for years to encapsulate, modify, or somehow protect protein (or polypeptide) products taken orally from degrading this way. They've never succeeded. That's why, for instance, growth hormone (a polypeptide) remains an injection, not an oral agent. An oral growth hormone, by the way, would sell like mad, so the drug companies would very much like to figure out how to bypass the degradative effects of stomach acid. One of the "researchers" behind the nattokinase claims boasts that he has single-handedly figured out how to protect the nattokinase molecule in the gastrointestinal tract. However, he won't tell anybody how he does it. Right.

--Fibrinolytic agents are extremely dangerous. In years past, we used to treat heart attacks with intravenous fibrinolytic agents like tissue plasminogen activator, urokinase, streptokinase, and others. They have fallen by the wayside, for the most part, because of limited effectiveness and the unavoidable dangers of their use. Fibrinolytics are "dumb": they dissolve blood clots in both good places and bad. While they might dissolve the blood clot causing your heart attack, they also degrade the tiny clot in your cerebral (brain) circulation that was protective. That's why fatal brain hemorrhages, bleeding stomach ulcers, and blood oozing from strange places can also occur with fibrinolytic administration. Believe me, I've seen it happen, and I've watched people die from them.

The idea that a small dose taken orally is healthy is ridiculous. Even if nattokinase worked, why the heck would you take an agent that has known dangerous and very real consequences?

Don't let this idiocy reflect poorly on the K2 conversation, which, I believe, holds real merit and is backed by legitimate science. This is symptomatic of a larger difficulty with the supplement industry: Insane and unfounded claims about one supplement erodes credibility for the entire industry. It gives regulation-crazed people like the FDA ammunition to go after supplements, something none of us need. You and I have to sift through the nonsense to uncover the real gems in this rockpile, real gems like vitamin D3, omega-3 fatty acids from fish oil, and, perhaps, vitamin K2. But not nattokinase.

Blood pressure with exercise

27. April 2007 William Davis (10)
Here's a frequently neglected cause for an increasing CT heart scan score: High blood pressure with exercise. Let me explain.

Paul's blood pressure at rest, sitting in the office or on arising in the morning, or at other relatively peaceful moments: 110/75 to 130/80--all in the conventional normal range.

We put Paul on the treadmill for a stress test. At 10 mets of effort (on the protocol used, this means 3.4 mph treadmill speed at 14 degree incline), Paul's blood pressure skyrockets to 220/105. That's really high.

Now, blood pressure is expected to increase with exercise. If it doesn't rise, that's abnormal and may, in fact, be a sign of danger. Normally, blood pressure should rise gradually in a stepwise fashion with increasing levels of exercise. But any blood pressure exceeding 170/90 is clearly too high with exercise. (Not to be confused with high blood pressures not involving exercise.) A handful of studies have suggested that a "breakpoint" of 170/90 also predicts heightened risk of heart attack over a long period.)

I see this phenomenon frequently--normal blood pressure at rest, high with exercise. This also suggests that when Paul is stressed, upset, in traffic congestion, under pressure at work, etc., his blood pressure is high during those periods, as well. I wouldn't be surprised to see other phenomena of underappreciated high blood pressure, like abnormally thick heart muscle (left ventricular hypertrophy), an enlarged thoracic aorta (visible on your heart scan), left atrium, perhaps even an abnormal EKG or abnormal kidney function (evidenced by an elevated creatinine on a standard blood panel).

Unfortunately, the treatments that reduce blood pressure are "stupid," i.e., they have no appreciation for what you are doing and they reduce blood pressure all the time, whether or not you're stressed, exercising, or sleeping.

Blood pressure reduction should begin with weight loss, exercise, reduction of saturated fats and processed carbohydrates (esp. wheat), magnesium replacement, vitamin D replacement. Think about CoQ10. After this, blood pressure medication might be necessary.

The message: Watch out for the blood pressures when you have a stress test. Or, if you have a friend who is adept at getting blood pressures, get a blood pressure immediately upon ceasing exercise. It should be no higher than 170/90.

Vitamin D2 vs. vitamin D3

26. April 2007 William Davis (21)
An interesting question came up on the Track Your Plaque Member Forum about vitamin D2 vs. vitamin D3. This often comes up among our patients, as well.

Vitamin D is measured in the blood as 25-OH-vitamin D and is distinct from 1,25-diOH-vitamin D, a kidney measure, a test you do not need unless you have kidney failure.

The human form of vitamin D is cholecalciferol and is usually obtained via activation of a precursor molecule in the skin on activation by the sun. You can also take cholecalciferol and it increases blood levels of 25-hydroxy vitamin D reliably.

However, there is a cheap, plant-sourced, alternative to vitamin D3, called vitamin D2, or ergocalciferol. D2 has far less effect in the body. Taking D2 or ergocalciferol orally is an extremely inefficient way to get D. Unfortunately, it's the form often used in milk and many supplements, even the prescription form of D. About half the multivitamins and calcium supplements I've looked at contain ergocalciferol rather than cholecalciferol.

Taking vitamin D2 yields very little conversion to the effective D3. This particular issues is maddening, as the USDA requires dairy farmers to add 100 units of vitamin D to milk, and D2 is often used. In other words, the D in many dairy products barely works at all. There are many children who rely on D from dairy products who are at risk for rickets and are not getting the D they need from dairy products because of this cost-saving switch. Do not rely on milk for vitamin D for your children.

D2 or ergocalciferol is often included in the blood measures of vitamin D along with vitamin D3. The only reason it's checked with blood work is to ensure "compliance,", i.e., see whether or not you're taking a prescribed ergocalciferol. Beyond this, it has no usefulness.

25-OH-vitamin D3, or cholecalciferol, is both the blood measure and the supplement you need. This is the one that packs all the punch. Keep in mind also that it is the oil-based gelcap you want, with more consistent and efficient absorption. Tablets usually barely work at all, even if it contains cholecalciferol. Most people who take calcium tablets with D, or multivitamin with D, not only are getting a powdered form of D, but also in trivial doses. It's the pure vitamin D3, cholecalciferol, in gelcap form you want if you desire all the spectacular benefits of vitamin D.

World record heart disease reversal

26. April 2007 William Davis (0)
A quick but important note.

Track Your Plaque Members:

Keep your eyes on the Track Your Plaque Member website for details and images of our most recent huge success story. Track Your Plaque participant, Neal, dropped his score more than anyone else before.

Although reduction of heart scan score is an everyday event around here, a 51% drop in score deserves to make news!

We will post the images of Neal's heart scans on the www.cureality.com Member website in the coming days.

Dose of fish oil

26. April 2007 William Davis (2)
Dosing for fish oil is a perennial point of confusion. However, it's quite simple.

The active ingredients in fish oil are DHA and EPA, the so-called omega-3 fatty acids. Of course, if there's anything else in your capsules, such as omega-6, omega-9, or linolenic acid, these should not count towards the sum of EPA + DHA, since they do not exert the same benefits as the omega-3s.

The basic suggested starting dose for the Track Your Plaque program is 1200 mg of EPA+DHA. This is usually provided by taking 4 x 1000 mg capsules of fish oil, providing 180 mg EPA, 120 mg DHA per capsules, for a total of 1200 mg EPA+DHA.

About a third of people, however, will require greater doses of omega-3s to reduce triglycerides, VLDL, and/or intermediate-density lipoprotein (IDL). Most people will do fine with an increase to 1800 mg EPA+DHA, usually provided by 6 x 1000 mg standard capsules. A very occasional person (about 1 in 100) will require even higher doses.

If you ever decide to change your fish oil preparation, or if you change to a more concentrated form or another form such as liquid fish oil (e.g., Carlson's), paste (e.g., Coromega), or syrup (e.g., Pharmax Frutol), then you will need to examine the label to determine the dose of EPA+DHA. If, for instance, a teaspoon of liquid fish oil provides 360 mg EPA and 240 mg DHA, that's a total of 600 mg omega-3s per teaspoon. If your EPA+DHA dose is 1200 mg per day, then two teaspoons a day should provide it. Always adding up the EPA+DHA content of whatever preparation you choose will therefore allow you to mix, match, or change your dose whenever you like.

Niacin scams

24. April 2007 William Davis (11)
As most of you know, niacin (vitamin B3) is an important tool for many in the Track Your Plaque program.

Niacin:

--raises HDL cholesterol
--reduces small LDL
--reduces lipoprotein(a)

And it's the most potent agent we have for all three patterns, despite just being a vitamin. Niacin also reduces LDL cholesterol, VLDL, IDL, triglycerides; reduces heart attack risk dramatically either alone or in combination with other agents.

Unfortunately, some people who are either afraid of the "hot flush" side effect, or experience excessive degrees of it, have resorted to two preparations sold in stores that have none of these effects.

Most notorious is "No-flush" niacin, also known as inositol hexaniacinate. This compound is an inositol sugar molecule complexed with 6 ("hexa-") niacin molecules. Unfortunately, it exerts none of niacin's effects in the human body. No-flush niacin has no effect on HDL, small LDL, or Lp(a), nor on LDL or heart attack.

In short, no-flush niacin is a scam. It's also not cheap. I've met people who have spent hundreds of dollars on this agent before they realize that nothing is happening, including a flush.

Likewise, nicotinamide does not work. It sounds awfully close to the other name for niacin, nicotinic acid. But they are two different things. Like no-flush niacin, nicotinamide has no effect on HDL, small LDL, Lp(a), etc.

Though I've discussed this issue in past, somehow these two "supplements" seem to sneak back into people's consciousness. You walk down the health food store aisle and spy that bottle of X-brand No-flush niacin, promising all the benefits of niacin with none of the bother. Then you remember that rough night you spent a few months back when the hot flush lasted longer than usual. That's when some people end up buying this agent making extravagant--and false--promises.

For now, for all its imperfections, niacin is still a pretty darn good agent for these patterns. Remember that the best strategy to minimize the hot flush effect is to drink plenty of water. We generally recommend taking the dose at dinner along with water. If the hot flush occurs, drink two large glasses of water (total volume 16-24 oz). Nine times out of ten, the flush is gone. It also dissipates the longer you take niacin.

Media mis-information

21. April 2007 William Davis (2)
This is an excerpt from a popular health website, EverydayHealth.com:


A Cholesterol-Busting Vitamin?
Did you know that niacin, one of the B vitamins, is also a potent cholesterol fighter? Find out how niacin can help reduce cholesterol…

Niacin is safe — except in people with chronic liver disease or certain other conditions, including diabetes and peptic ulcer. It is also inexpensive. However, it has numerous side effects. It can cause rashes and aggravate gout, diabetes, or peptic ulcers. Early in therapy, it can cause facial flushing for several minutes soon after a dose, although this response often stops after about two weeks of therapy and can be reduced by taking aspirin or ibuprofen half an hour before taking the niacin. A sustained-release preparation of niacin (Niaspan) appears to have fewer side effects, but may cause more liver function abnormalities, especially when combined with a statin.

Many people begin treatment at low doses (250 mg twice a day, for example) and, over six weeks or so, gradually build up to an amount that lowers lipid levels, anywhere from 1,000 to 2,500 mg split between two doses during the day. This gradual approach may help build tolerance to side effects such as facial flushing. Although niacin is available over the counter, you should not use it in quantities sufficient to lower cholesterol without a physician’s supervision. It is important to test liver function and levels of blood sugar and uric acid before beginning niacin therapy and during the course of treatment.

(Bold emphasis mine.)

At http://www.everydayhealth.com/publicsite/index.aspx?puid=548e8630-32d6-41dd-91a7-48e1cbac65ad&p=4




After an enticing headline, the article goes on to scare the pants off you. It also sounds like accurate information, delivered in an unbiased way, cold and straight.

If we were to use niacin this way, it would indeed be intolerable for most. Do not follow the above nonsensical advice. But that may have been the intention from the start.


Very telling are the fact that, both above and below the article were colorful advertisements for Lipitor, complete with Dr. Robert Jarvik’s (inventor of an implantable mechanical heart) soothing, professorial image.

Did they want to bait us with promising information about cholesterol and niacin, only to throw water on our fire and steer us towards something else?

That would be typical drug company marketing.

All in all, I’m grateful for the attention the media provides for health issues. Perhaps many people wouldn’t even be aware of niacin and other healthy strategies if some website, newspaper, or magazine article hadn’t talked about it.

But I do worry about bias. Was this an unbiased report? Or was it more like much of the physician-directed mail I receive, cleverly concealed propaganda from the drug manufacturers? Who wrote it? No author is listed. Could it have been ghost written by someone in the drug company itself, or an arm of the drug company? That’s a very common practice for the literature physicians receive, glossy, high-class materials paid for by drug companies, written by drug company-owned companies, but no company logo or name listed.

My point: Be skeptical of what the media tells us. There’s usually a good deal of truth in the reporting, but there’s also often just enough mis-information or slanting of content to make you behave or believe a certain way. “If niacin is this dangerous, maybe I really should take the Lipitor.”

A dirty little secret

21. April 2007 William Davis (0)
Here's a dirty little secret many people don't know about.

If I implant a stent, I might get paid somewhere around $2000 for the heart catheterization, stent implantation, femoral artery closure device, hospitalization charges. That's not too bad.

But what if I'd like more? What if I'd like to squeeze this unsuspecting patient for more, or actually his/her insurance company?

Easy: Add on complex procedures to the basic procedure that yield more professional charges. For instance, I could perform laser angioplasty, a procedure that adds another couple thousand dollars. I might pull out the old rotational atherectomy device, a high-speed diamond tipped drill that also adds substantial professional charges. I might also use the intracoronary ultrasound device, an otherwise helpful device, but I might pull it out to use on everybody.

With the exception of ultrasound, all the "add-on" procedures were more popular in the early and mid-1990s--before they were shown in clinical studies to provide no advantage, perhaps even add to procedural risks.

Thus, a patient might undergo a heart catheterization, balloon angioplasty with stent implantation into the proximal left anterior descending coronary artery (LAD), followed by laser angioplasty of the mid-LAD, followed by intracoronary ultrasound of the vessel. Next, rotational atherectomy of the circumflex, followed by stent and ultrasound. Total charges for this 2-3 hour procedure? Somewhere around $8000 to the cardiologist. Of course, hospital charges are far more.

Ironically, patients are invariably impressed. Hearing that they went through all sort of high-tech procedures makes them grateful for receiving the benefits of the skills of their cardiologist. Of course, they would like have done as well with a far simpler procedure. Perhaps they didn't need the procedure at all.

If the excessive use of procedures and devices fails to benefit patients, why don't hospitals discourage it? Two reasons: 1) It's difficult to legislate or regulate decisions made on judgement, which can be a tough issue with many fuzzy edges, and 2) hospitals made oodles more money from the practice.

If you have a salesman in your new car lot and he outsells all his colleagues by 30-50% and makes you a couple hundred thousand a month more in sales. You've watched him at work and he's clearly good at it. But you suspect that he pushes the envelope of propriety frequently--badgering customers, add rustproofing to a little grandmother's car that will be driven 3000 miles a year, selling cars for prices far above what they would have sold for had the customer bargained more vigorously.
do you put a stop to it at the risk of pushing your star salesman away? Few would.

Only a minority of my colleagues are guilty of this despicable practice. I only know of a few who openly do it. Hopefully, you're not among their patients.

The party’s over

21. April 2007 William Davis (0)
A good number of cardiology colleagues are vigorously bashing the outcome of the COURAGE Trial. Recall that COURAGE is the large clinical trial recently released that showed that, in people with stable angina (chest pains), people did equally well with “optimal medical therapy” as with stents.

The problem is that many of my colleagues wouldn’t know what to do in a world deprived of implanting 10 stents a day. Giving people nitroglycerin/statin drug/aspirin/beta-blocker day after day, week after week, would be an awfully dull world. All the excitement of the cath lab would be a lot more rare. We’d actually have to wait for a heart attack from some dumb smoker! All the money would disappear, too. After all, seeing a patient in the office pays, at best, $200 (and has to be stretched to cover overhead expenses like staff, malpractice insurance, and rent). Putting a stent in can pay $2000, $3000, $4000, often more. Put in several a day and—Wow! Now we’re talking money.

You can understand how upsetting it is to my colleagues who feel like the rug may be pulled out from underneath their practices and lives. Feel as sorry for them as you do for people who lose their jobs on an assembly line because of robotic technology. Or travel agents because everyone makes travel arrangements over the internet. Technology, in this information technology, marches on.

Cardiologists, cath labs, stent manufacturers, and the huge industry built around heart disease had their party. Now it’s time to clean the room and sober up. The party’s over.

The broader acceptance of “optimal medical therapy,” as lame as it is, will eventually open the door for many to demand for something even better. Ever hear of Track Your Plaque?
All posts by william-davis

Statin stupid

19. March 2010 William Davis (0)
If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

19. March 2010 William Davis (83)
In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

18. March 2010 William Davis (0)
If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

18. March 2010 William Davis (74)
No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.

Fat Head: Tom Naughton's manifesto for low-carb eating

12. March 2010 William Davis (16)
I just got back from Jimmy Moore's low-carb cruise to the Bahamas.

Among the many interesting people I met on the cruise was the creator of the documentary film, Fat Head, Tom Naughton.

Tom brings both creative insights into low-carbohydrate eating as well as humor. Low-carb eating can be a pretty contentious issue, but Tom made it fun. He will make you laugh about many of the odd notions we have about diet.

Among the best parts of Fat Head is Tom's portrayal of the effects of carbohydrates on insulin and fat metabolism:






Fat Head joins the ranks of films like Food, Inc, that make nutrition information entertaining. For anyone interested in a unvarnished look at diet, weight loss, along with a few laughs along the way, Tom Naughton's Fat Head is worth viewing.

Oatmeal: Good or bad?

11. March 2010 William Davis (67)

You've heard it before: oatmeal reduces cholesterol. Oatmeal producers have obtained permission from the FDA to use a cholesterol-reducing claim. The American Heart Association provides a (paid) endorsement of Quaker Oats.

I've lost count of the times I've asked someone whether they ate a healthy breakfast and the answer was "Sure. I had oatmeal."

Is this true? Is oatmeal heart healthy because it reduces LDL cholesterol?

I don't think so. Try this: Have a serving of slow-cooked (e.g., steel-cut, Irish, etc.) oatmeal. Most people will consume oatmeal with skim or 1% milk and some dried or fresh fruit. Wait an hour, then check your blood sugar.

If you are not diabetic and have a fasting blood sugar in the "normal" range (<100 mg/dl), you will typically have a 1-hour blood glucose of 150-180 mg/dl--very high. If you have mildly increased fasting blood sugars between 100 and 126 mg/dl, postprandial (after-eating) blood sugars will easily exceed 180 mg/dl. If you have diabetes, hold onto your hat because, even if you take medications, blood sugar one hour after oatmeal will usually be between 200 and 300 mg/dl.

This is because oatmeal is converted rapidly to sugar, and a lot of it. Even if you were to repeat the experiment with no dried or fresh fruit, you will still witness high blood sugars in these ranges. Do like some people and pile on the raisins, dried cranberries, or brown sugar, and you will see blood sugars go even higher.

Blood sugars this high, experienced repetitively, will damage the delicate insulin-producing beta cells of your pancreas (glucose toxicity). It also glycates proteins of the eyes and vascular walls. The blood glucose effects of oatmeal really don't differ much from a large Snickers bar or bowl of jelly beans.

If you are like most people, you too will show high blood sugars after oatmeal. It's easy to find out . . . check your postprandial blood sugar.

In past, I recommended oat products, specifically oat bran, to reduce LDL, especially small LDL. I've changed my mind: I now no longer recommend any oat product due to its blood sugar-increasing effects.

Better choices: eggs, ground flaxseed as a hot cereal, cheese (the one dairy product that does not excessively trigger insulin), raw nuts, salads, leftovers from last evening's dinner.

Mustard: Super health food?

6. March 2010 William Davis (32)
Could mustard--yes, the yellow condiment you smear on hot dogs--be a super heart healthy food in disguise?

Consider that mustard contains:

Vinegar

Turmeric

No appreciable sugar


The vinegar slows gastric emptying, resulting in slower absorption of any carbohydrates and a reduced glucose area-under-the-curve. Of the little fats contained (about 3 grams per 1/4 cup), most are desirable monounsaturates. Mustards are relatively rich in selenium, with 20 mcg per 1/4 cup, helpful for protection against cancer and thyroid disease, and magnesium, 31 mg per 1/4 cup.

Turmeric is added to most mustards. One of the constituents of turmeric, curcumin, the substance that confers the bright yellow color, has been a focus of interest for its anti-inflammatory effects. Curcumin has been documented to reduce activity of the inflammatory enzymes cyclooxygenase-2 (COX-2), lipoxygenase, and reduce activity of inflammatory signal molecules, tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1,2,6,8, and 12, and monocyte chemoattractant protein (MCP). Curcumin also has been shown to reduce LDL oxidation, a potentially important step in atherosclerotic plaque formation. Turmeric is used as a tea by Okinawans. (Hmmmm . . . )

Turmeric content of mustard can vary, of course. Likewise, sugar content. Look for mustards that are not sweetened, so avoid honey mustard in particular. Look for hot, brown, horseradish, Dijon, etc. If there is a downside to mustard, it's sodium content, though the 709 mg per 1/4 cup should only be a problem for those who are sodium-sensitive (African Americans, in particular).

So perhaps mustard isn't exactly a super health food. But it may have some bona fide health effects and should be used generously especially if you are concerned about blood sugar and inflammatory phenomena.

Exercise and blood sugar

5. March 2010 William Davis (30)
There is no doubt that exercise yields benefits across a spectrum of health: reduced blood pressure,  reduced inflammation, reduced blood coagulation, better weight control, stronger bones, less depression, reduced risk for heart attack.

Exercise also influences blood sugar. Diabetics understand this best: Exercise reduces blood sugar 20, 30, 50 or more milligrams. A starting blood sugar, for instance, of 160 mg/dl can be reduced to 80 mg/dl by jogging or riding a bicycle. (I recently had brunch at an Indian restaurant with my family. Blood sugar one-hour postprandial: 134 mg/dl. I was sleepy and foggy. I got on my stationary bike and pedalled at a moderate clip for 60 minutes. Blood sugar: 90 mg/dl.)

Could the reduction of blood sugar with exercise be THE reason that exercise and physical activity provide such substantial benefits?

Think about it. Reduced blood sugar:

1) Reduces risk for future cardiovascular events.
2) Reduces glycation of proteins, i.e., reduced glucose binding to proteins like the ones in artery walls and the lenses of your eyes.
3) Reduces blood coagulation
4) Reduces endothelial dysfunction (abnormal artery constriction that leads to atherosclerosis)

This might explain why it doesn't require high levels of aerobic activity to derive benefit from exercise, since even modest efforts (e.g., a 15-minute walk after eating) reduce blood sugar substantially.

The incredible 33-year, 18,000-participant Whitehall study tells us that a postprandial (after-eating) blood sugar of an impossibly-difficult 83 mg/dl is required to erase the excess cardiovascular risk of blood sugar. Could this simply be telling us that physical activity or exercise is required to suppress blood sugars to these low levels?

It makes me wonder if an index of the adequacy of exercise is your post-exercise blood glucose.

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.