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.

Synthroid, Armour Thyroid, and the battle for T3

6. July 2008 William Davis (2)
In the last Heart Scan Blog post on thyroid issues, Is normal TSH too high?, the provocative findings of the the HUNT Study were discussed. The text of the study can be found at:

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

Hypothyroidism, or low thyroid that is signaled by high thyroid-stimulating hormone, TSH, is proving far more prevalent an issue than previously thought. While previous estimates put hypothyroidism as affecting only about 3% of younger populations, 10-20% of older populations (women more so), data like the HUNT Study suggest that, if lower and lower TSH levels (higher thyroid) are necessary for perfect heart health, then many more people stand to benefit than we used to think.

But another crucial issue in the world of hypothyroidism: Is T4 (thyroxine) enough? Or should we be supplementing T3 (triiodothyronine) along with T4?

Your friendly neighborhood primary care doctor or endocrinologist would likely argue vehemently that T4 (as Synthroid, Levoxyl, levothyroxine, and others) is adequate and not subject to the impurities and contaminants of natural thyroid extracts. They would also argue that T4 is effectively converted to T3 at the tissue level, and exogenous supplementation is unnecessary.

Others--most of all thyroid patients themselves, along with thyroid advocates like Mary Shomon and Janie Bowthorpe, along with some physicians--argue that supplementing T3 along with T4 can be very important. They argue that people feel better, have more physical energy, lose weight more effectively, and more completely resolve many of the phenomena of hypothryoidism with T3 added. There are also some data that argue the same.

Adding T3 to the mix may address the presumed poor conversion of T4 to T3 that is peculiar to some people. It may overcome the "reverse T3" phenomenon, the production of a useless look-alike T3 that occurs in some people. It may also (anecdotally) exert greater effects on some lipid/lipoprotein parameters, such as Lp(a).

My experiences adding T3 to T4 have been mixed: Some feel better, others do not. Some show objective improvements, others do not.

Nonetheless, hypothyroidism, or incompletely corrected hypothryoidism by way of inadequate T3, is an issue to consider in your plaque-control program.

More on this somewhat complex issue, along with practical solutions to consider, can be found on the Special Report to be released this week on the Track Your Plaque website.

Letter to New York Times

3. July 2008 William Davis (9)
All right. I sent a Letter to the Editor to the New York Times. No word from them; it's no longer news.

So here is what I tried to convey.

While the authors overall did a credible job of talking to my colleagues and laying out the issues, they made the crucial and boneheaded mistake of confusing CT heart scans with CT coronary angiograms. Sadly, many people who may have been considering having a simple screening heart scan may be scared away by the confused authors, Alexn Berenson and Reed Abelson.

They do correctly point out that, while CT coronary angiograms are fascinating examples of technology and a way of visualizing coronary arteries, this test all too often is being subverted into the "let's make money from high-tech testing" medical model. It's also a test that frequently leads to the "real" test, heart catheterization, since the "time bomb" you have in your arteries might "need" a stent.

CT coronary angiograms are also virtually useless for purposes of tracking disease, since they are not longitudinally (along the length of the artery) quantitative, nor should anyone be exposed to this much radiation repeatedly.

A simple heart scan, on the hand, provides a longitudinal summation of coronary plaque volume. Radiation exposure is sufficiently low that repeated scanning can be performed for purposes of tracking . . .yes, track your plaque.

Poorly-informed reporters can do a lot of damage. As always, you and I must dig a little deeper for the truth.




Dear Editor,

Re: Weighing the Costs of a CT Scan’s Look Inside the Heart

The Times featured an article on June 29th that discussed rapidly expanding use of CT scans for the heart:
Weighing the Costs of a CT Scan’s Look Inside the Heart.

The authors, Alex Berenson and Reed Abelson, stated that CT heart scans “expose patients to large doses of radiation, equivalent to at least several hundred X-rays, creating a small but real cancer risk.”

I’d like to offer a clarification.

Though the authors discuss both CT heart scans and CT coronary angiograms, they confuse the two and use the terms interchangeably.

A heart scan is a simple screening test for coronary atherosclerotic plaque. It detects the presence of calcium in the heart’s arteries, provided as a “score.” (Because calcium occupies 20% of total plaque volume, knowing the amount of calcium tells you how much total coronary plaque is present by applying this simple proportion.) Just having a high score should not prompt heart procedures, since people undergoing simple screening heart scans are without symptoms. However, a stress test may yield some useful information.

On present-day CT devices, heart scans expose a patient to 0.4 mSv of radiation on an electron-beam, or EBT, device, and on up to 1.2 mSv on a 64-slice multi-detector, or MDCT, device, compared to 0.1 mSv during a standard chest x-ray. CT heart scans are therefore performed with about the same quantity of radiation as a mammogram done to screen women for breast cancer, or about the equivalent of four chest x-rays on an EBT scanner, up to 12 chest-xrays on a MDCT scanner.

CT coronary angiograms, while performed on the same devices as heart scans, require x-ray dye to fill the contours of the coronary arteries. It also requires up to several hundred times more radiation. While new engineering innovations are being introduced that promise to reduce this exposure, the current devices being used today do indeed require a radiation dose equivalent to 100 to 400 chest x-rays (usually in the range of 10-15 mSv), a value that equals or exceeds that obtained during a conventional heart catheterization.

While heart scans are most useful to detect and quantify plaque that can help determine the intensity of a heart disease prevention program, CT coronary angiograms are generally used as prelude to hospital procedures like catheterizations, stents and bypass surgery. That’s because they are performed to look for (or rule out) “severe” blockages.
CT heart scans and CT coronary angiography are therefore two different tests that yield two different kinds of information, and yield two entirely different levels of radiation exposure.

This confusion from a major and respected media outlet like the New York Times is unfortunate, because it could persuade millions of people who otherwise could benefit from simple heart scans to avoid them because of misleading information on radiation exposure of a different test.

Thank you.

William Davis, MD

Red yeast rice alert

2. July 2008 William Davis (9)
While there have been some positive reports in the media lately about the cholesterol-reducing effects of red yeast rice, Consumer Lab has issued a very concerning report.

Because Consumer Lab is a subscription website (incidentally, the $20 per year membership fee is money well spent for insightful tests on many supplements, though new reports only come out a handful of times per year), I won't discuss the results of their red yeast rice in its entirety.

However, Consumer Lab testing uncovered several disturbing findings:

--The lovastatin content varied by a factor of 100, from 0.1 mg per tablet/capsule in one brand up to 10.6 mg in another brand. By FDA regulations, lovastatin is a drug and NO red yeast rice preparation is supposed to contain ANY lovastatin. Nonetheless, despite the marketing of supplement manufacturers, it is probably the lovastatin that is largely responsible for the LDL-reducing effect. The monacolins or mevinolins in red yeast rice add little, if any, further LDL-reducing effect.

--Several preparations contain a potential kidney toxin called citrinin. The Walgreen's product, specifically, contained substantial quantities of this toxin.



Interestingly, the FDA has taken repeated action against red yeast rice manufacturers and distributors because they continue to contain lovastatin. In the FDA's most recent action in August, 2007, for instance, Swanson's product and Sunburst Biorganics' Cholestrix, were both sent letters to stop selling their product because it contained lovastatin.

The Consumer Lab findings would explain the enormous variation in LDL-reducing effect of various red yeast rice products. In my experience, some work and reduce LDL 40 mg/dl or so, some fail to reduce LDL at all, others generate a modest effect, e.g., 5-10 mg/dl LDL reduction.

In effect, red yeast rice IS a statin drug, albeit a highly variable and weak one. Although readers of The Heart Scan Blog know that I am a big fan of nutritional supplements and self-empowerment in health, I am a bigger fan of truth. I despise B--- S---- of the sort that emits from some nutritional supplement manufacturers and drug companies.

I am puzzled by much of the public's readiness to embrace a statin drug if it comes from a supplement company while avoiding it if it comes from a drug manufacturer. Personally, I do not like the drug industry, their questionable (at best) ethics, their aggressive marketing tactics, their sleazy sales people.

But, in this instance, if a statin effect is desired, I'd reach for generic lovastatin before I purchased red yeast rice. The Consumer Lab report tells us that red yeast rice IS essentially a statin drug, an inconsistent one that often contains a potential toxin.

"Average amount of heart disease for age"

2. July 2008 William Davis (4)
A 72-year old woman came to my office after a complicated hospital stay (unrelated to heart disease). She'd undergone a CT coronary angiogram and heart scan as part of a pre-operative evaluation prior to a surgery for a non-heart related condition.

The heart scan portion of the test (I was impressed they even did this) yielded a heart scan score of 212. The CT coronary angiogram portion of the test revealed a 50% blockage in one artery, a lesser blockage in one other artery.

The cardiologist consulting on the case advised her that the amount of coronary disease detected was insufficient to pose risk during her surgical procedure. He also advised her that she had "an average amount of disease for age." He thought that nothing further was necessary since she was "average."

Say what?  

What if I told you that you have an average amount of cancer for your age? After all, cancers become more common the older we get. Who would find that acceptable?

Then why should ANY amount of coronary atherosclerotic plaque be "acceptable for age"? Coronary plaque is a degenerative disease that poses risk for rupture. While it is indeed common, by no means should it be acceptable.

I would bet that this same cardiologist would be from the same school of thought that would be eager to advise heart catheterization, stent, and other procedures--revenue-generating procedures--should she have a heart attack appropriate for age.

I wish that I could tell you that this silly comment was provided by some peculiar, "everyone-knows-he's-crazy" doctor. But it was not. It was a solidly mainstream physician. He pooh-poohs nutrition, laughs when asked about nutritional supplements, thinks anyone complaining about symptoms less than a full-blown heart attack is a baby. He is respected by the primary care physicians, lectures on the advantages of prescription medications. In short, he is your typical conventional cardiologist.

This is the way they think. I know, because I was one of them. Thankfully, something banged me upside my head one day (my Mother's sudden cardiac death) and tipped me off to the painful irony of the conventional approach to heart disease.

There is NO amount of coronary disease appropriate for age. This notion is a remnant of the paternalistic, "I-know-better-than-you" attitude of the last century of medicine.

The 21st century promises a new age.

Quantum leaps

29. June 2008 William Davis (6)
A reader of The Heart Scan Blog and member of the Track Your Plaque program posted this comment on The Heart.org:

*The facts speak for themselves.*

Dr. William Davis and Dr. William Blanchet, your patients thank you for the low cost PREVENTIVE care you prescribe. The published facts speak for themselves. It is indeed a sad state of affairs, that the larger cardiology community does not take the time to research the data and results you have been reporting. Unfortunately it is the patients who are the victims of the mainstream, inappropriate, treatment protocols, as evidenced with the ongoing high rate of CV death rate.

I am dumbfounded by the lack of open-minded inquisitive curiosity to thoroughly research your claims by many/most cardiologists. Understood, we are all busy, but that is no excuse to stick with practices that do not result in major breakthrough improvements in patient outcomes.

Then again, we are all humans, and when "we" are convinced that "our" approach is correct, "we" tend to conveniently ignore any evidence to the contrary. "We" like to believe "we" have been right all along.

A very insightful book, recently published, says it all in its title: "Mistakes were made (but not by me)."

From the intensity of the comments on this topic, it is clear that we are in the middle of a battlefield. It is to be hoped that the facts will become visible before too much smoke obscures the field, and before the patients are all dead.

George Orwell said it correctly, back in 1946:

“We are all capable of believing things which we know to be untrue, and then, when we are finally proved wrong, imprudently twisting the facts so as to show that we were right. Intellectually, it is possible to carry on this process for an indefinite time: the only check on it is that sooner or later a false belief bumps up against solid reality usually on a battlefield.”

And, after several posts that preventive care with EBT would be too costly.....

*Heroic*

Prevention is what matters, but it is not very heroic. A hospital that advertises the highest volumes in heart bypasses and other heart "repair" procedures, sounds to many like a go-to place when one gets into trouble with one's heart.

Cardiologists who perform impressive surgical procedures are heroes. Not unlike fire-fighters. We celebrate them (deservedly!) for rescues and life saving heroic actions.

We tend to not pay much attention to the folks that work hard to minimize risk of calamities in the first place.

Similarly, we recently learned that it is too costly to build schools that are earthquake resistant in China. Parents had to look at their children's bodies, crushed.

Is it too graphic to imagine 20,000 American bodies, who died of heart disease, piled up on a field?

What will it take before we make prevention our first priority?

AL, Ann Arbor, Michigan


The reader also tells me that, prompted by his father's death from heart attack while following conventional advice after heart catheterization, he has lost 50 lbs and corrected his lipid patterns on the Track Your Plaque program. The reader is currently struggling with full correction of his severe small LDL pattern and is following some of the advice we discussed on our webinar recently.

Another Heart Scan Blog reader, Stan the Heretic, posted this quote from scientist, Max Planck, in his comment:


"A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it." - M. Planck

(Max Planck was a German physicist who developed quantum theory, a disruptive set of ideas that supplanted other explanations of energy mechanics of the day.)


I fear that may prove to be the case for heart disease. The revenue-generating formula for heart disease management that dominates practice in cardiovascular medicine today is so deeply ingrained into the thinking and revenue expectations of practicing cardiologists that a preventive or reversal approach just won't cut it--even if it is vastly superior.

That's why it is important for you to take control yourself. You will be the one who obtains and applies the information that saves your life or the lives of those around you. It is, in all likelihood, NOT your doctor who will save your life, but YOU.

Body count

28. June 2008 William Davis (7)
Imagine the following headline:

War in Iraq a growing success: 20,000 Americans now dead!


If a newspaper ran that headline, we would all be outraged, and rightly so. Deaths in war are a tragedy. They are not something we celebrate.

Then why do we hear hospitals boasting about the number of bypass operations performed every year, number of heart catheterizations performed, number of heart attacks treated?


"_______ Hospital breaks 1000-heart bypass per year milestone"

"We treat more heart attacks than other other hospital in the state!"

"More people come to ________ Hospital than any other in the region!"



I hear this stuff on the radio, on TV, see it in newspapers and magazines, even on highway billboards every single day in Milwaukee.

Heart procedures, like deaths in war, are casualties of health.

They are not successes (though, of course, you can have a "successful" bypass). I see most procedures as a failure of prevention.

Death from heart attack is a failure of prevention. Tim Russert's death was a (unnecessary) failure of prevention. But so are bypass surgery, stents, and the like.

Such is the perverse state of affairs in hospitals and health: They celebrate illness. They glamorize it with ads displaying high-tech equipment, efficient staff in scrubs, "caring and friendly staff." But it is illness they are celebrating. Why? Because it has become a business necessity, a necessary strategy to remain competitive and profitable in the business called "healthcare" that makes money from treating people. The biggest return is from major procedures like bypass operations.

Every success in prevention denies the hospital an $80,000+ opportunity. You'll never hear that advertised.

Dr. Bill Blanchet: A ray of sunshine

26. June 2008 William Davis (4)
Another heated discussion is ongoing at The Heart.org, this one about Tim Russert's untimely death: Media mulls Russert's death as cardiologists weigh in

Although I posted a couple of brief comments there, I quickly lost patience with the tone of many of the other respondents. Should you choose to read the comments, you will see that many still cling to old notions like heart attack is inevitable, defibrillators should be more widely available, "vulnerable" plaques cannot be identified before heart attacks, etc.

I quickly lose patience with this sort of outdated rhetoric. However, our good friend, Dr. Bill Blanchet of Boulder, Colorado, has a far stronger stomach for this than I do.

Here, a sample of his wonderfully persuasive comments:


Heart disease cannot be stopped but we can certainly do better!

Goals we must achieve if we hope to solve the Rube Goldberg of coronary disease:

1. Find something more reliable than Framingham risk factors to determine who is at risk. Framingham risk factors are wrong more often than they are right. If you are comfortable treating 40% of the patients destined to have heart attacks, continue to rely on “traditional” risk factors only.

2. Treat to new standards beyond NCEP/ATP-III. These accepted standards prevent at best 40% of heart attacks in patients treated. This is unacceptable, and arguably why Tim is dead today! Why prevention protocols emphasize LDL and more or less ignore HDL, triglycerides and underemphasize blood pressure eludes me.

3. Motivate patients to participate in coronary prevention. Saying “you need to get exercise and lose weight” is not adequate motivation, it hasn't worked to date and probably won't work tomorrow. If you are satisfied saying it is "the patient's fault for not listening to me" so be it, that excuse doesn't work for me!

Currently “good results” consist of being able to convince 50% of patients at risk by traditional risk factors to participate in prevention and hopefully 30% will be treated to goal. Of those treated to goal, 60% of the heart attacks will still happen anyway. Mathematically we can hope to prevent <10% of heart attacks with this approach!

I have personally found a solution to this dilemma. It goes like this:

1. EBT-CAC [electron-beam tomography coronary artery calcium] is the most reliable predictor of coronary events period, the end! Anyone who disagrees has not objectively read the literature. The only test more predictive than the initial calcium score is the follow up score 12 to 36 months later. EBT predicted Tim Russert’s event 10 years before it happened; passing his stress test gave him inappropriate reassurance 2 months before he died. If only Tim had the benefit of a second EBT sometime over the last 10 years he and his doctor would have known that what they were doing was insufficient and improvements could have been made.

2. I treat to the standard of stable calcified plaque by EBT (<15% annualized progression, preferably <1% annualized progression). This correlates with a very low incidence of coronary events. Even the ACC/AHA 2007 position paper agrees with this. This is accomplished with aspirin, omega-3 fatty acids, diet, exercise, weight control, smoking cessation, treatment of sleep apnea, stress reduction, control of HDL, triglycerides and LDL cholesterol and excellent control of BP and insulin resistance plus the recent addition of vit D-3. Meeting an LDL goal of 70 is easy but prevents only a minority of events, treating to the goal of stable CAC by EBT is a challenge but when achieved, the reward is near elimination of heart attacks and ischemic strokes. This has indeed been my personal experience!

3. A picture of plaque in the coronary artery is a monumental motivator for patients to get on board to make things better. The demonstration of progression of that plaque despite our initial therapies gets all but a few suicidal patients interested in doing a better job. I think that similar motivational results can be had with carotid imaging; the difference is that CAC by EBT is clinically validated as being a much stronger predictor of events with progression and non-events with stability than any ultrasound test including IVUS.



Wow! I couldn't have said it better.

Sadly, I doubt even Dr. Blanchet's persuasive words will do much to convince my colleagues on this forum. And the cardiologists on this forum are likely among the more inquisitive and open-minded. The ones stuck in the cath lab day and night, or implanting defibrillators, are even less inclined to entertain such conversations.

While I admire Dr. Blanchet's energy for continuing to argue with my colleagues, the lesson I take is: Take charge of health yourself. If you wait for your doctor to do it for you, you could be in the same situation as poor Tim Russert. This is an age when your physician should facilitate your success, not prevent it or leave you wallowing in ignorance.

The Russert Protocol at work

25. June 2008 William Davis (6)
Without a concerted effort at prevention, heart scan scores (coronary calcium scores) grow like weeds. The average rate of growth is 30% per year.

Keith is an illustrative case. At age 39, Keith's heart scan score was 29, in the 99th percentile due to his young age. (In other words, young people before age 40 have no business having plaque. If they do, it's bad.)

True to conventional practice, Keith's doctor prescribed a cholesterol drug (Zocor), asked him to take a baby aspirin, and prescribed a blood pressure medicine. He asked Keith to cut the fat in his diet. His doctor even exceeded conventional (ATP-III) LDL cholesterol treatment targets.

Keith, an intelligent and motivated businessman, happily complied with his doctor's instructions. Eighteen months later, a 2nd heart scan showed a score of 68, representing an increase of 135%, or 76% per year.

This is the very same approach that the late Mr. Tim Russert's doctors employed: treat (calculated) LDL cholesterol with a statin drug, treat high blood pressure, reduce saturated fat, take aspirin. It was a miserable failure in Keith, whose plaque continued to grow at a frightening rate of 76% per year. It was also an obvious failure in poor Tim Russert.

Further investigation in Keith uncovered:

--Severe small LDL--80% of all LDL was small (despite a favorable HDL of 58 mg/dl)
--Measured LDL particle number (NMR) showed that "true" LDL was actually about 60 mg/dl higher than suggested by the crude calculated LDL
--An after-eating (postprandial) disorder (IDL)
--A pre-diabetic blood sugar and insulin
--Severe vitamin D deficiency
--Very low testosterone

All these patterns were present despite the steps Keith and his doctor had instituted. It's no wonder his plaque was undergoing explosive growth.

The conventional approach to coronary disease prevention is inadequate, more often than not a mindless adherence to one-size-fits-all template crafted to a great degree by drug industry interests and "experts" who often stand at arm's length from real live patients.

Keith's "residual" abnormalities are all readily correctable. He has since made dramatic improvements in all parameters. Among the strategies used is a wheat- and cornstarch-free diet that resulted in 12 lbs lost within the first few weeks of effort.

If you are on the "Russert Protocol," have a serious conversation with your doctor about the continued advisability of remaining on this half-assed approach to heart disease. Or, consider finding another doctor.

Petition to the National Institutes of Health

24. June 2008 William Davis (2)
A petition to the National Institutes of Health (NIH) is being circulated in response to the mis-statement made in an NIH-sponsored study, ACCORD.

The ACCORD Trial included over 10,000 type II diabetics and compared an intensive, multiple-medication group to achieve a target HbA1c of <6.0%, with a less intensively treated group with a target HbA1c of 7-7.9%. (HBA1c is a long-term measure of glucose, averaging approximately the last 3 months glucose levels.) To the lead investigators' surprise, the intensively treated group experienced more death and heart attack than the less intensive group. The conclusion suggested that intensive management of diabetes may not be a desirable endpoint and may result in greater risk for adverse events.

The petitioners argue that the problem was not with intensive glucose control per se, but the use of multiple side-effect-generating medications. Unfortunately, the ACCORD conclusions give the impression that loose control over blood sugar may be desirable.

The petition originates from the Nutrition and Metabolism Society, a non-profit organization seeking to promote carbohydrate restriction.


The petition reads:

National Institute of Health re: the ACCORD Diabetes Study: "Intensively targeting blood sugar to near-normal levels ... increases risk of death. "

This statement is untrue. This study lowered blood glucose levels only by aggressive drug treatment.

Preventative measures and proven non-drug treatments are being ignored by the NIH, ADA and many other governing agencies.

There is abundant scientific evidence proving a carbohydrate restricted diet can be as effective as drugs in lowering blood glucose levels safely. Many times diet is more effective than medication in controlling diabetes - all without side effects or increased risk of death.

I ask that the NIH publicly retract the above statement. It is misleading the public.

I also request that the NIH acknowledge the existing science and fund more research by the experts who have experience with carbohydrate restriction as a means of treatment for diabetes.

For more info, or to help people with diabetes, please e-mail info@nmsociety.org .

Thank you.



I added my comment:

In my preventive cardiology practice, I have been employing strict carbohydrate restriction in both diabetics and non-diabetics. This results in dramatic improvement in lipids and lipoprotein abnormalities, substantial weight loss, and improved insulin sensitivity. This experience has been entirely different from the heart disease-causing and diabetes-causing low-fat diets that I used for years.

I have a substantial number of diabetics who have been to reduce their reliance on prescription medication for diabetes or even eliminate them. In my experience, the power of carbohydrate-restricted diets is profound.

However, better clinical data to further validate this approach is needed, particularly as diabetes and pre-diabetes is surging in prevalence. I ask that more funding to further explore and validate this research be made available if we are to have greater success on a broader basis.



If you are interested in adding your voice, you can also electronically sign the petition. It is optional, but you can also add your own comments regarding your own views or experiences.

Wheat withdrawal

24. June 2008 William Davis (16)
It happens in the hospital every so often: A clean-cut, law-abiding person is hospitalized for, say, pneumonia, kidney stones, knee surgery, etc.

Everything's fine until . . . they're running down the hospital hallway stark naked, screaming about snakes on the wall, accusing nurses of trying to kill him, all while yanking out IV's and monitor patches.

It's called alcohol withdrawal. Alcohol withdrawal can range from tremulousness and sweatiness, all the way to delirium tremens, the full-blown form that leads to disorientation, seizures, fever, even death. Withdrawal can also be associated with a number of chronically used agents, such as sedatives/sleeping pills, pain medication/opiates, among others.

How about wheat?

I wouldn't have believed it, but after witnessing this effect countless times, I am convinced there is such a phenomenon: Wheat withdrawal.

You'll recognize it in someone who previously ate bread and other wheat flour-containing products freely, then eliminates them. This is followed by extreme cravings, usually for bread, cookies, or cake; profound fatigue; shakiness; mental fogginess; blue moods. The syndrome can last for up to one week.

Then, bam! Sufferers of wheat withdrawal report mental clarity superior to their wheat-crazed days, improved energy, decreased appetite and cravings, heightened mood, and, of course, fantastic drops in weight.

Why would removal of wheat from the diet trigger a withdrawal phenomenon? I can only speculate, but I believe that at least part of this response is due to a physical conversion from a glycogen (sugar)-burning metabolism to that of a fatty acid (fat mobilizing) metabolism. People who lived in the up-and-down cycle of craving and eating wheat constantly fed the sugar furnace for years and are enzymatically impaired in fat burning; they've been growing fat stores. Eliminating wheat deprives the body of this easy source of glycogen, forcing it to mobilize fatty acids in the fatty tissues. Sluggish at first, people feel fatigue, mental fogginess, etc. Once the enzymatic capacity for fat mobilization revs up, then these feelings dissipate.

Could it also relate to the opioid sequences apparently present in wheat? I wasn't even aware of this fact until a reader of The Heart Scan Blog, Anne, left this comment:

Wheat protein contains a number of opiod peptides which can be released during digestion. Some of these are thought to affect the central and peripheral nervous systems.

When I gave up gluten, I felt much worse for a few days. This is a very common reaction in those who stop eating gluten cold turkey.

Dr. BG provides a fascinating commentary on the addictive/opioid aspect of wheat addictions in her Animal Pharm Blog.

Whatever the mechanism, I believe it is a real phenomenon. It can, at times, be so overwhelming that about 20% of people who try to eliminate wheat find they are simply unable to do it without being incapacitated. Of course, that might be a lesson in itself: If withdrawal is so profound, it hints that there must be something very peculiar going on in the first place.
This is your brain on wheat II

This is your brain on wheat II

29. July 2010 William Davis (24)
In the original Heart Scan Blog post, This is your brain on wheat, I discussed how opioid peptides (i.e., small proteins that act like opiates such as heroine or morphine) that result from digestion of wheat cause unique effects on the human brain, particularly addictive behaviors. I also briefly reviewed how elimination of wheat has been shown to reduce auditory hallucinations and other psychotic behaviors in a subset of people with paranoid schizophrenia.

These two phenomena, addictions and schizophrenia, are most likely the result of exorphins that cross the blood-brain barrier. Exorphins--exogenous morphine-like compounds--can be blocked by opiate-blocking drugs like naloxone and naltrexone. Naloxone is used in hospitals to reverse morphine or heroine overdoses; naltrexone is being repackaged into a weight loss drug, since blocking wheat-derived exorphins reduces appetite. (Yes: The USDA tells us to eat more wheat, the drug industry sells us the antidote.)

There's another way that wheat can affect the brain and nervous system: immune-activated damage.

This is similar to the effect seen in celiac. There's even overlap with some of the antibody markers used to diagnose celiac, like the anti-gliadin antibodies and the anti-endomysium antibodies.

The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia, a condition in which an immune response causes damage to the Purkinje cells of the cerebellum, the portion of the brain responsible for balance and coordination. This results in stumbling, incoordination, incontinence, and eventually leads to reliance on a cane or walker and wearing a diaper. Average age of onset: 53 years. A shrunken, atrophied cerebellum can be seen on an MRI of the brain.

Problem: Most people with central nervous system damage caused by wheat do not have any intestinal symptoms, like diarrhea and abdominal pain, the sort of symptoms usually associated with celiac disease. It means the first sign of wheat-induced brain damage may be bumping into walls and wetting your pants.
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Comments (24) -

  • LeonRover

    7/28/2010 9:18:57 PM |

    Being Irish an' all, my jeans will only allow me to thrive on a few spuds served with lashin's of butter an' onions and o' course sides of bacon and eggs washed down with Whiskey Go Leor, sometimes called The Juice o' the Barley.

    Minimal wheat.

  • Thrasymachus

    7/28/2010 10:35:34 PM |

    It only makes sense that there are vast numbers of people actually addicted to food, not metaphorically, but in the same way people are addicted to drugs and nicotine. A good start would be stop subsidizing this addiction, but since we have a government of the grain farmers, by the grain farmers, and for the grain farmers, that's not likely.

  • Anonymous

    7/29/2010 4:26:28 AM |

    Is wheat induced brain damage reversible, if one goes off wheat say at 50.?

  • Anonymous

    7/29/2010 5:34:31 AM |

    I would bet good money that this post will get more people off wheat than all your posts about wheat and heart disease combined!

  • Hans Keer

    7/29/2010 6:35:47 AM |

    You are totally right the devastating effects of wheat and its palls goes from gut to brain http://bit.ly/cAbZry VBR

  • Anonymous

    7/29/2010 10:22:18 AM |

    Dr. Davis

    As usual you are SPOT ON. exactly right with the symptoms and age. Just amazing all clinical symptoms described were seen by me in my father from 53 (stumbling and falling) to 58 (requiring help walking) to 60 (epilepsy hallucinations and fears)to 61 (bedridden) to 64 (last year November) death.

    Come to think, it was so simple to save him. It is just unreal.

  • Yogi Sinzapatos

    7/29/2010 3:55:16 PM |

    Sprouted wheat however is I believe extremely good for health.

  • Anonymous

    7/29/2010 3:59:26 PM |

    YOU HAVE DEFINITELY MADE YOUR POINT QUITE CLEAR.  NO NO MORE WHEAT.

    Does anyone how tequila is made?

  • lisa32989

    7/29/2010 6:16:37 PM |

    No wheat in tequila Smile

  • stop smoking help

    7/29/2010 9:05:39 PM |

    Is it time to join the bandwagon? No more drinking, no more smoking, no more wheat? Really, did I just write that? I have to say, I really enjoy my PB&J on whole grain wheat bread, as do my kids.

    Eating wheat is like apple pie and July 4th fireworks. How can we possibly do without and find a relatively cheap substitute? Is rice any good or is that a bad carb too?

    To eat healthy, is it just you need to eat organic and nonwheat foods and watch your carb-mix?

    Does it have to be this complicated? Has anyone written a book with easy to find, cheap/healthy ingredients that is easy to prepare in 30 minutes or less and feeds a family of 4?

    Right now, we're basically down to grilled chicken/fish/pork with steamed fresh brocolli/green beans and long-grain rice. That's pretty much all we eat anymore, with the occassional cheeseburger/steak indulgence.

  • Anonymous

    7/29/2010 9:38:25 PM |

    I started Low Dose Naltrexone 2 months ago to help with Autoimmune Disease.  I started at 1.5 and now am at 3.0
    I will increase to 4.5 in 2 weeks.

    I eliminated grains and dairy 1 month ago.

    I have lost 10 pounds.

    I could be as simple as the diet changes but I think more is going on.

    I have less pain which allows me to sleep through the night.
    I have more energy.
    I am more active and actually exercising.
    I am supplementing Vit. D and getting daily sun exposure (my Vit. D level was 41).
    My moods have greatly improved.

    Ironically, any time I have been prescribed an opiate pain medication, I have had severe allergic reactions.

    As far as the Neuro symptoms, I do have Meniere's complete with dizziness and vertigo.  So far I have not noticed any positive impact but still hopeful.

    Thanks Dr. Davis for all your information.

    J9

  • Anne

    7/30/2010 2:36:19 AM |

    "This results in stumbling, incoordination, incontinence, "

    I know you are right on. I was having mild ataxia and stress incontinence. Off gluten for 7 years and balance is better and no stress incontinence.

    This also affects dogs. My 12 year old cairn terrier was stumbling, falling over and urinating in her sleep. Got her off grains 2 years ago and she improved immediately.

  • Anonymous

    7/30/2010 4:35:39 AM |

    I can not say it enough times..............  Be healthy, not Paranoid.

    Dr. D emphasizes extremes for effect.  Do not fall into either side of the trap. Complacency nor paranoia.  informed decisions are critical for you and your family's well being

    Trevor

  • Anonymous

    7/30/2010 7:28:00 AM |

    i'd agree with Trevor as well.

    sourdough wheat (traditional preparation) and boiled raw milk go together.

    sourdoughing helps breakdown anti nutrients in wheat making the nutrients more bio available. Further Raw milk takes care of the rest by providing necessary enzymes (phystase etc) to digest wheat completely.

    pasteurized milk and wheat consumed without sourdoughing give both milk and wheat a bad name and will improve health when stopped simultaneously.

    traditional preparations eliminate such problems to a large extent.

  • Parag

    7/30/2010 9:55:55 AM |

    Celiac disease is a digestive disease that damages the small intestine and interferes with absorption of nutrients from food.  Is an inherited, autoimmune disease in which the lining of the small intestine is damaged from eating gluten and other proteins found in wheat, barley, rye, and possibly oats.
    celiac disease symptoms

  • Alex

    7/30/2010 10:48:56 AM |

    Sprouting wheat begins the process of breaking down gluten, but it is not a complete process. Same goes for fermenting. Making a suboptimal food less bad for you does not mean that food is now good for you.

    As for boiled raw milk, taking raw milk to a boil heats it to an even higher temperature than is done during regular, non-UHT pasteurization, and it keeps it at that high temperature for a much longer time than any commercial pasteurization process. Raw milk that's been pasteurized at home at a higher temperature for a much longer time is not somehow magically superior to commercially pasteurized milk.

  • Anonymous

    7/30/2010 2:51:05 PM |

    I'd personally like to see an experiment on sourdough whole wheat combined with boiled raw milk to see what Dr Davis notes. That should settle it.

    Alex share your experience rather than float around in clouds.

  • Anonymous

    7/30/2010 5:08:37 PM |

    Just out of curiosity, I would like to know what is the point of buying something raw (supposedly because "raw" holds more benefits) only to then get it home and cook it. Boiling raw milk, in my estimation, defeats the purpose of consuming raw milk. Boiling kills everything. I buy raw milk weekly and I drink it "raw." That's why I buy it.  
    Am I missing something? (serious question).

  • Alex

    7/30/2010 5:33:10 PM |

    Anonymous, I don't have acute gluten sensitivity, but I've read enough about gluten sensitivity to know that sprouting and fermentation are not 100% effective at making wheat a tolerable food for people with gluten sensitivity.

    Why cling desperately to consumption of a crap quality food when it's so much easier and simpler to just not eat it at all? One personal experience I can draw on is the addictive nature of wheat. I've been addicted to both tobacco and alcohol, but the most addiction-triggering image I can visualize in my mind is a loaf of locally made, crusty Italian bread. I think people cling to wheat consumption because it's addictive, plus it's deeply embedded in human culture.

  • Anonymous

    7/30/2010 5:45:51 PM |

    raw milk is a relatively new fad in usa while india is the highest wheat and milk consumer since hundreds of years. The way they consume raw milk, is, after boiling it and the way they consume whole wheat is after making sourdough.

    I personally consume raw milk without boiling but whats important is to understand the effects of consuming wheat and milk traditionally on health viz a viz consuming it in modern style.

  • Anonymous

    7/30/2010 6:15:05 PM |

    Alex wheat is sub optimal as are many other foods. the only complete food is milk, everything else is had in combination with a complementary food.

    Wheat is also not easy to avoid while its consumed traditionally  daily in the east, it is everywhere in its modern avatar in the west.

    its not a bad idea to figure out wheats' complement and how it works than declare wheat suboptimal and write it off.

  • Tommy

    7/30/2010 8:13:55 PM |

    I think that more than the problems wheat may cause for some, the problem is the amount of wheat we consume. Consuming the bulk of your calories from wheat (or grain) is a problem, even for those who don't have any existing conditions. Drinking beer all day or more than you should isn't good either but that doesn't mean that a beer here and there or even one per day is a big deal. For an alcoholic one beer is a bad thing but for the average person 1 or 2 isn't. For someone with a problem, wheat is bad; for the average person a little here and there in moderation isn't. There are a lot of things modern man eats that he didn't eat at one time. But then again, there are many things in life in general that modern man does that we didn't do years ago. We will always look to make things easier and in doing so compromise ourselves in some way. The best thing is to be educated enough to make good decisions but not get too carried away in either direction.
    Eating store bought chicken and meat tainted and chemically enhanced isn't good either. What does that do to us long term? What about our children. Eat less wheat and grains and avoid one illness but get another from mystery meat. So I guess we can't win no matter what we do. We can't get crazy, we just have to make good decisions.
    Middle of the road always seems like a good starting point.

  • Anonymous

    8/3/2010 2:59:12 AM |

    "The most common immune neurological syndrome consequent to wheat consumption is cerebellar ataxia"

    Where is the study or other reference that supports this statement? How common is this neurological syndrome in the American general population?

    Thank you.

  • elwiemo

    8/18/2010 10:43:52 PM |

    How exactly are the Purkinje cells damaged, and how specific is the effect to gluten/wheat?  What is your source for this?

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