Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

2. April 2010 William Davis (12)
Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

1. April 2010 William Davis (11)
The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

28. March 2010 William Davis (16)
Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

26. March 2010 William Davis (20)
Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

23. March 2010 William Davis (24)
Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

21. March 2010 William Davis (19)
No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.

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.
Track Your Plaque makes Consumer Reports!

Track Your Plaque makes Consumer Reports!

8. August 2011 William Davis (27)
. . . but not in a good way.

The September, 2011 issue of Consumer Reports showcases their Protect Your Heart discussion. Third paragraph: "The website Track Your Plaque warns, 'The old tests for heart disease were wrong--dead wrong.' It says heart scans are 'the most important health test you can get.'"

They go on to expose the overuse of heart procedures like angioplasty and stent implantation and offer their advice on how to manage heart disease risk: lower BP, reduce LDL cholesterol, lose weight, stop smoking, take aspirin. They quote Dr. Paul Ridker who declares heart scans are not useful because the "deposits cardiologists worry about are the less stable plaques that CT scans routinely miss."

I thought I'd been transported back to 1995. Not only is it clear that the Consumer Report writers never looked beyond the homepage of Track Your Plaque, but somehow saw our heart disease prevention and reversal program as promoting heart procedures. Incredible.

Of course, the Track Your Plaque program does the exact opposite: Advocates an approach that virtually eliminates the need for procedures and returns control over heart disease to the participant. That's a critical difference.

And, as I've had to remind my colleagues time and time again, what we are really after is an index of total coronary atherosclerotic plaque. Even in 2011, that index remains the simple coronary calcium score, a gauge of total plaque, not just of "hard," stable plaque. Perhaps in 10 years we will be using a better tool to gauge progression and regression of all the components of coronary atherosclerotic plaque, but today it remains the simple, accessible, mammogram-like coronary calcium score.

Consumer Reports does for the idea of heart disease prevention what food manufacturers do for health and weight loss: Echo conventional wisdom of the sort that generally makes us fatter, more diabetic, leads us to more heart procedures and needless deaths. I might use Consumer Reports to rate MP-3 devices or toasters, but I certainly would not rely on them for insightful health advice.
Tags :

Comments (27) -

  • Carl

    8/8/2011 1:37:53 PM |

    Actually, I have been unhappy with the some of the consumer products they recommend. Their tests are not as objective as they seem to believe. For example, I bought an inferior, yet expensive, air cleaner which happened to win their blessings just because its lowest fan speed was higher than the lowest fan speed of the competition. Air cleaned to noise ratio would have been the better metric.

  • Frankie

    8/8/2011 2:04:15 PM |

    I am sorry this happened to you and your excellent program. I expected more from Consumer Reports.

  • Dee

    8/8/2011 2:59:16 PM |

    My Dr is worried about the amount of radiation that I would be gettin from a heart scan.  I am 72 and get mammo's every year.  Plus other mri's and x-rays.  He feels they would add up to to much radiation.

    Dee

  • Princess Dieter

    8/8/2011 3:16:46 PM |

    Thanks for the heads up. I bought this CR yesterday, and have been reading some parts of it (smart phones, heart issue).

    I never smoked. I was obese for decades, but am no longer as of Friday, hah! I can't take aspirin due to sensitivity (flares up my asthma). I got my blood pressure normal (off meds), and my sugar is great (finally), but my LDL is up. I gave up wheat/gluten and cut way down on starches, mostly gave up convenience/fast foods and eat fresher, better. HDL is very very good. Triglycerides great. But LDL went up. Lipoproteins are the fluffier kind. I'm a regular exerciser now.

    So, I'm doing a lot to improve things, but obviously, I have some to go. I 've never done this test you recommend, so that goes on the list to ask doc for. Whether she approves it or not, don't know, but it's on my list to request. I just had a bone mineral density (great) and some x-rays (suspected arthritis hip, sacrum/coccyx). So, I don't want to be exposed to more anytime soon....I do mammos every 2 years, not years, due to radiation concerns, but I do want to know what that coronary calcium score says for my heart.  I suppose I can consider it as my "non-mammo year" test. Thank you...

  • chuck

    8/8/2011 4:07:14 PM |

    based on this half assed research on the part on CR, can you trust their reports on simpler things such as toasters and TVs???

  • Gene K

    8/8/2011 5:33:19 PM |

    The next day I received this issue of CR, I sent them a comment saying that I found the way they mentioned trackyourplaque.com uninformed and out of context and an explanation why I thought so. Maybe my comment or somebody else's will appear in the next issue's Letters to the Editor section.

  • Gene K

    8/8/2011 5:40:39 PM |

    The kind of advice CR gives people on health made me discontinue my subscription to CR on Health. Either you read CR on Health, WebMD, etc. or you listen to Dr Davis, Dr Eades, Dr Kruse. Combining both kinds of sources makes no sense to me.

  • Dr. William Davis

    8/8/2011 5:57:40 PM |

    You need either to educate your doctor or get a new doctor.
    A standard CT heart scan yields the equivalent of 2 mammograms. He is confusing a heart scan to generate a coronary calcium score with a CT coronary angiogram, which can expose you to plenty more.
    Sorry, but your doctor is confused.

  • Dr. William Davis

    8/8/2011 10:06:09 PM |

    I'm wondering the same thing. I do believe that, with this analysis, they bit off more than they can chew.

  • Dr. William Davis

    8/8/2011 10:07:31 PM |

    Hi, Princess--
    I think that would be a very good compromise, especially in view of the fact that heart disease afflicts far more women than breast cancer.

  • Terrence

    8/8/2011 11:00:27 PM |

    I am not at all surprised that CR gave Dr Davis such an uniformed, silly "review/comment". I used to read them all the time. But they slowly (early 1990's on) became politically correct, and published more and more uninformed nonsense - not reviews, simply uninformed opinion pieces.

  • Gene K

    8/9/2011 2:52:44 AM |

    Dr Davis,

    I suggest that you comment on the CR article. They always publish these comments with disagreements. Go to http://custhelp.consumerreports.org/cgi-bin/consumerreports.cfg/php/enduser/ask.php, select Consumer Reports Magazine from their product list and choose Comment on a Report or Letter to the Editor. The more people will see it, the more people will visit your site.

  • Gene K

    8/9/2011 2:56:48 AM |

    I still trust their reports on physical goods, because they actually test them instead of just publishing an opinion. They have never lost a lawsuit filed by a manufacturer, according to what they say.

  • Ed Terry

    8/9/2011 2:01:01 PM |

    Most of the health and nutrition information provided by Consumer Reports parrots the information from the AHA and the ADA.  In other words, it's just plain wrong.

    I can sum it up best by relaying the conversation I had with my latest cardiologist (I fired my first one.)  When he saw that my calcium score had decreased since my initial scan, he was puzzled.  I then explained my diet, and all he could say was "That's not what we were taught in school."  My response was "I understand."

    Keep up the good work.

  • Might-o'chondri-AL

    8/9/2011 7:35:29 PM |

    Hi Renfrew,
    Was "SERVER" blocked responding in previous post, so trying here:
    It is not my place to make dietary suggestions on anyone's blog. The reason I just wrote out that specific data of a Japanese report was to indicate that individual fatty acids can have different affects. There is a link above  which goes to one Drs. discussion of Arachidonic Acid (AA) and how although  many think AA is only pro-inflammatory that AA also performs worthwhile functions. I find it interesting that although insulin increases the synthesis of AA from other n-6 polyunsaturated fatty acids the Japanese find AA itself does not worsen insulin resistance; but again tissue specifics are complex.


    Let's look at the vascular role of AA in tissue cell lipid membranes as it responds with cascades of both pro & aniti-inflammatory responses by  AA converting into prostaglandins . When AA from the lipid membrane  interacts with the notorious COX1 & COX2 cyclo-oxygenase enzymes found in blood vessels Prostanoid series 2 can form (prostanoids = both prostacyclin and prostaglandin molecules). Normally the 1/2 life of prostanoids is just a duration of minutes.  
    What is important to grasp is that when prostanoid 2 is at work in vascular tissue  it can  prolong any local inflammation reaction. AA (with COX catalysis)  generated pro-inflammatory prostanoid 2s are what  lets the circulating leucocytes (neutorophils) drifting across blood vessels previously irritated by cytokines  (ex: TNF alpha the tumor necrosis factor also now called cadexin). Prostaglandin 2 is part of the immune response loop and also has it's own receptor inside of the leukocyte itself; this becomes involved in signalling that makes a risk laden leukocyte physically reorganize it's own actin cyto-skeleton enough so that it (the leucocyte) can move across the endothelium layer of a vessel into the inside of a vascular tissue cell made permiable due to cytokine inflammation.

    The poly-unsaturated fatty acid EPA  generates it's own prostaglandin, the Prostaglandin  D3, which blocks  a lot of the relatively short lived risky Prostaglandin D2s. EPA in people is not always in high enough concentration to counteract the pro-inflammatory reaction, and in that case a person's AA level may be so high that it negates the helpful level of  prostaglandin D3 being put out (by EPA). The trick is to get high EPA levels which can  use the COX enzymatic pathway to make prostaglandin D3 and  allay prostaglandin 2 signal ; for if there is sparse prostaglandin 2 then it isn't binding to it's receptor inside a leukocyte , and  thus no leukocyte tarries long enough to be tethered by an adhesion molecule to the wall of that blood vessel. Without EPA supplementation blood levels of EPA average +/- 1 uM and with supplementation can average +/- 5 uM, while the levels of AA  needing off setting in terms of vascular risk will vary greatly depending on which substrate PUFA n-6 fats are ingested.

  • Sifter

    8/9/2011 11:01:28 PM |

    I have that copy of CR. My 93 year old mother is suffering from CHF, and its a terrible thing to see, oxygen, Oxyfast, Adavan (sp) Seems like some days are fairly well, than others are just frightful. I think CR has slipped quite a bit over the past decade. They generally take a mainstream approach, while pretending to find 'hidden truths' that mainstreamers won't disclose. Utter nonsense. Separately, I've found them to be rather biased towards any Toyota vs American made vehicles as well. I find this blog to be an excellent source of info and constructive applications to better heart health. Thank you.

  • PHK

    8/10/2011 1:28:09 AM |

    I subscribed Consumer Report's monthly health letter in late 90's.
    it was the same old stuff, not much different from what mainstream (TV/AHA/ADA).
    so i did not renew.
    regards,

  • Cardiac Test

    8/10/2011 9:28:10 AM |

    The best part about this program is that it ddvocates an approach that virtually eliminates the need for procedures and returns control over heart disease to the participant.

  • Dr. William Davis

    8/11/2011 12:25:49 AM |

    Wow, Ed. You manage to reverse an important marker of heart disease that most of my colleagues regard as impossible and all your doctor can say is "That's not what we were taught in school?" "Good riddens!" was the right response! You are better off without this sort of incredible ignorance and disinterest.

  • indium

    8/11/2011 5:44:51 AM |

    me too, what can  i do

  • Dee

    8/11/2011 3:11:50 PM |

    I looked up the 64 slice CT scan and indeed you are right.  My Doc is very open to suggestion and I'm sure he will go along with that.  He is a primary care Dr and would have to send me to a Cardio dr.
    Thanks for your reply.  Dee

  • Doug

    8/23/2011 2:59:41 AM |

    Dr. Davis,

    I used to work as a researcher for a consumer products company testing automatic dish washing machine detergents.  Consumer Reports once reported on one of my products in a comparison study with our major competitors.  I do not know how they achieved their results, but their results were virtually the opposite of the ones I got when I ran the very same tests every day.  

    In  our tests, our main product was so good, that we used it as the reference to a perfect 10 in our grading scale, yet to CR, we were mid range. The product ranked #1 by CR usually was graded a 6 in our tests,  but somehow it was ranked the best in their whacky experiment.

    Since that time, I have learned not to trust Consumer Reports' ratings.

  • Dr. William Davis

    8/23/2011 11:55:10 AM |

    Hi, Doug--
    That's priceless! Thanks for the insight.

  • Barkeater

    8/30/2011 1:35:06 PM |

    I am a long-time TYP member and have read the CR article.  I would stress these points:  

    (1)  As Dr. D says, the article takes a swipe at coronary artery calcium score CT scans if used as a tool for selling interventions that are not beneficial.  It is true that CAC  scans have been used like this, but absolutely false that TYP does this.  Most TYP members want nothing more than to avoid bypass, angioplasty and stents, recognizing (as did the CR article) that, except in acute circumstances, there is a better approach to managing heart disease and heart disease risk.

    (2)  The CR article confuses CT angiography and CT CAC scans.  In CT angiography, the patient has a dye injected, but not in CT CAC scans.  The dose of radiation from CT angiography is very high, vs. a very low dose from CT CAC scans.  Supposely, CT angiography identifies soft plaque as well as calcified plaque, but the information is not too useful to measure the effects of preventative steps on plaque.  The CAC scan gives a measurement of the calcified portion of plaque.  It is not a perfect measure of plaque, but it is very informative.  The TYP program looks in particular at the rate of progression of the calcified plaque (or, we hope, regression), so it shows whether preventative measures are working.  People with stable or regressing calcified plaque are very safe from heart attack.

    (3)  One of the conventional wisdom complaints about CT CAC testing is this:  If it were recommended for the population at large, it would not identify a lot of people at risk or change the recommendations as to what to do about the risk, as compared to existing tests and guidelines.  While this is highly debatable (I don't buy it), it is irrelevant to any motivated individual.   Whenever testing is dismissed by experts, you need to assess whether they are saying the test is useless to me as an individual or whether the test would not be helpful if given to the population at large.  The latter point is irrelevant to any person who wants to seize control of his or her health.  I grant that many people are passive about their health, and their doctors have very limited knowledge of how to reduce heart risk in any event.  If you are in control of your health, then CT scans can be massively informative (with little radiation exposure), and a program like TYP can save you from heart disease and invasive procedures.

  • Dr. William Davis

    8/30/2011 6:32:31 PM |

    Wow, Bark. Elegantly said!

    I find it odd that the conventional answer tries to pigeonhole a fairly detailed preventive approach like Track Your Plaque and compare it to, say, advertising for bypass surgery. Despite the years that have passed with people like you and me fighting this battle to get the real truth out, we still have incredibly silly comments like those in Consumer Reports.

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