Diabetes: Better than hedge funds

Diabetes is where the action is.

While, for virtually all of history, type 2 diabetes was an uncommon condition of adults, the disease has spread so much to all levels of American society that even kids are now developing the adult form. Researchers from the Center for Disease Control and Prevention predict that, by 2050, one in three adults will be diabetic.

The diabetes market is booming, handily surpassing growth of the oil industry, the housing market, even technology. It makes Bernie Madoff’s billions look like small potatoes. In health, few markets are growing as fast as diabetes—-not osteoporosis, not heart disease, not cancer.

Americans are getting fat from carbohydrate consumption, becoming diabetic along with it. While kids hanging around the convenience store gulp down 26 teaspoons of sugar in 32-ounce sodas and 56-grams-of-sugar in 16-ounce frozen ices, health-minded adults are more likely eating two slices of 6-teaspoons sugar-equivalent “healthy whole grain” bread, wondering why last year’s jeans are too tight.

The U.S. is not the only nation affected. Globally, 2.8% of the world’s population are diabetic, a number expected to double over the next 20 years.

Pharmaceutical companies boast double-digit growth for diabetes drugs, growth rates that keep profit-hungry investors happy. Merck’s Januvia, for instance, introduced in 2006, recently catalogued 30% growth in sales, with annual sales approaching $1 billion. Recently FDA-approved Victoza, requiring once-a-day injection, is expected to reap $4 billion in sales per year for manufacturer Novo Nordisk. Such numbers can only warm a drug company CEO’s heart.

Most diabetics don’t just take one medication, but several. A typical regimen for an adult diabetic after a couple of years of treatment and following the dietary advice of the American Diabetes Association includes metformin, Januvia, and Actos, a triple-drug treatment that costs around $420 per month. Two forms of insulin (slow- and fast-acting), along with two or three oral medications, is not at all uncommon.

“Collateral” revenues from the other health conditions that develop from a diet rich in “healthy whole grains,” such as drugs for hypertension, drugs to slow the progression of kidney disease in diabetes, drugs for “high cholesterol,” and drugs for high triglycerides, and you have a pharmaceutical drug bonanza. You, too, would throw all-expenses-paid, fly-the-entire-sales-force-to-the-Caribbean sales meetings.

The global diabetes market has already topped $25 billion and is growing at double-digit rates. Forget the Internet, gold stocks, or solar energy—-diabetes is where the money is. This fact has not been lost on the very market-savvy pharmaceutical industry. As with any successful business, they have devoted substantial resources to develop and grow this booming business.

270 lb man in diapers

Alex is a big guy: 6 ft 4 inches, 273 lbs.

On 10,000 units per day of vitamin D in gelcap form, his 25-hydroxy vitamin D level was 38.4 ng/ml. One year earlier, his 25-hydroxy vitamin D level, prior to any vitamin D supplementation was 9.8 ng/ml.

According to the latest assessment offered by the Institute of Medicine (IOM):

Vitamin D need for a 13-month old infant: 600 units per day

Vitamin D need for a 6 ft 4 in, 273 lb male: 600 units per day

I paint this picture to highlight some of the absurdity built into the smug assumptions of the IOM's report. It would be like trying to fit a large, full-grown man into the diapers of a 13-month old. Few nutrients or hormones (in fact, I can't think of a single one) are required in similar quantity by an infant or toddler and a full grown adult. However, according to the IOM's logic, their vitamin D needs are identical, regardless of age, body size, skin color, genetics, etc. One size fits all.

Just as the original RDA assessment by the Institute of Medicine kept thinking about vitamin D somewhere in the Stone Age, so does this most recent assessment.

90% small LDL: Good news, bad news

Chris has 90% small LDL particles.

On his (NMR) lipoprotein panel, of the total 2432 nmol/L LDL particles ("LDL particle number"), 2157 nmol/L are small, approximately 90% (2157/2432).

Bad news: Having this severe excess of small LDL particles virtually guarantees heart attack and stroke in Chris' future.

Good news: It means that Chris potentially has spectacular control over his lipoprotein and lipid values, achieving statin-like values without statin drugs.

Typically, extravagant quantities of small LDL particles are accompanied by low HDL, high triglycerides, and pre-diabetes or diabetes. Chris' HDL is 26 mg/dl, triglycerides 204 mg/dl; HbA1c 5.9% (a reflection of prior 60-90 days average blood glucose; desirable 4.8% or less), fitting neatly into the expected pattern.

Chris' pattern tells me several things:

1) He overconsumes carbohydrates, since carbohydrates trigger this pattern.
2) He likely has a genetic susceptibility to this effect (e.g., a variant of the gene for cholesteryl ester transfer protein, perhaps hepatic lipase). Only the most gluttonous and overweight carbohydrate consumers can generate this high a percentage small LDL without an underlying genetic susceptibility.
3) Provided he follows the diet advised, i.e., elimination of all wheat, cornstarch, oats, and sugars, he is likely to have an extavagant drop in LDL particle number. Should he achieve the goal I set of small LDL of 300 nmol/L or less, his LDL particle number will likely be around 500 nmol/L. This translates to an LDL cholesterol of 50 mg/dl . . . 50 mg/dl.

In many people, this notion of taking statin drugs for "high cholesterol" is an absurd oversimplification. But it is a situation that, for many, is wonderfully controllable with the right diet.

The American Heart Association has a PR problem

The results of the latest Heart Scan Blog poll are in. The poll was prompted by yet another observation that the American Heart Association diet is a destructive diet that, in this case, made a monkey fat.

Because I am skeptical of "official" organizations that purport to provide health advice, particularly nutritional advice, I thought this poll might provide some interesting feedback.

I asked:

The American Heart Association is an organization that:

The responses:
Tries to maintain the procedural and medication status quo to benefit the medical system and pharmaceutical industry for money
240 (64%)

Doesn't know its ass from a hole in the ground
121 (32%)

Is generally helpful but is misguided in some of its advice
79 (21%)

Accomplishes tremendous good and you people are nuts
6 (1%)


Worrisome. Now, perhaps the people reading this blog are a skeptical bunch. Or perhaps they are better informed.

Nonetheless, one thing is clear: The American Heart Association (and possibly other organizations like the American Diabetes Association and USDA) have a serious PR problem. They are facing an increasingly critical and skeptical public.

Just telling people to "cut the fat and cholesterol" is beginning to fall on deaf ears. After all, the advice to cut fat, cut saturated fat, cut cholesterol and increase consumption of "healthy whole grains" in 1985 began the upward ascent of body weight and diabetes in the American public.

Believe it or not, my vote would be for something between choices 1 and 3. I believe that the American Heart Association achieves a lot of good. But I also believe that there are forces within organizations that are there to serve their own agendas. In this case, I believe there is a substantial push to maintain the procedural and medication status quo, the "treatments" that generate the most generous revenues.

I believe that I will forward these poll results to the marketing people at the American Heart Association. That'll be interesting!

The formula for aortic valve disease?

I've discussed this question before:

Can aortic valve stenosis be stopped or reversed using a regimen of nutritional supplements?

I had a striking experience this past week. Don has coronary plaque and began the Track Your Plaque program. However, discovery of a murmur led to an echocardiogram that measured his effective aortic valve area at 1.5 cm2. (Normal is between 2.5-3.0 cm2.)

Because of his aortic valve issue, I suggested that, in addition to the 10,000 units of vitamin D required to increase his 25-hydroxy vitamin D level to 70 ng/ml, he also add vitamin K2, 1000 mcg per day, along with elimination of all calcium supplements. (I asked Don to use a K2 supplement that contained both forms, short-acting MK-4 and long-acting MK-7.)

One year later, another echocardiogram: aortic valve area 2.6 cm2--an incredible increase.

This is not supposed to happen. By conventional thinking, aortic valve stenosis can only get worse, never get better. But I've now witnessed this in approximately 10% of the people with aortic valve stenosis. The majority just stop getting worse, an occasional person gets worse, while a few, like Don, get better.

Aortic valve stenosis is to the aortic valve as degenerative arthritis is to your knees: A form of wear-and-tear that leads to progressive dysfunction. When the aortic valve becomes stiff enough (i.e., "stenotic"), then it leads to chest pains, lightheadedness or losing consciousness, heart failure, and, eventually, death. Bad problem.

Aortic stenosis typically starts in your 50s with calcification of the valve, getting worse and worse until the calcium makes the valve "leaflets" unable to move. The treatment: a new valve, a major undertaking involving an open heart procedure.

What if taking vitamins D and K2 and avoiding calcium do not just reverse or stop aortic valve stenosis once established, but prevents it in the first place? Tantalizing possibility.

Pressures on my time being what they are, I've not had the freedom to put together a prospective study to further examine this fascinating question. But it is definitely worth pursuing.

Blood glucose 160

What happens when blood glucose hits 160 mg/dl?

A blood glucose at this level is typical after, say, a bowl of slow-cooked oatmeal with no added sugar, a small serving of Cheerios, or even an apple in the ultra carb-sensitive. Normal blood sugar with an empty stomach, i.e., fasting; high blood sugars after eating.

Conventional wisdom is that a blood sugar of 160 mg/dl is okay, since your friendly primary care doctor says that any postprandial glucose of 200 mg/dl or less is fine because you don't "need" medication.

But what sort of phenomena occur when blood sugars are in this range? Here's a list:

--Glycation (i.e., glucose modification of proteins) of various tissues, including the lens of your eyes (cataracts), kidney tissue leading to kidney disease, skin leading to wrinkles, cartilage leading to stiffness, degeneration, and arthritis.
--Glycation of LDL particles. Glycated LDL particles are more prone to oxidation.
--VLDL and triglyceride production by the liver, i.e., de novo lipogenesis.
--Small LDL particle formation--The increased VLDL/triglyceride production leads to the CETP-mediated reaction that creates small LDL particles which are, in turn, more glycation- and oxidation-prone.
--Glucotoxicity--i.e., a direct toxic effect of high blood glucose. This is especially an issue for the vulnerable beta cells of the pancreas that produce insulin. Repeated glucotoxic poundings by high glucose levels lead to fewer functional beta cells.

A blood glucose of 160 mg/dl is definitely not okay. While it is not an immediate threat to your health, repeated exposures will lead you down the same path that diabetics tread with all of its health problems.

Indian buffet

I took my family to a local all-you-can-eat Indian buffet. It was delicious.

I confined my food choices mostly to vegetables and soups. Within about 30 minutes, I started to get that odd buzz in my head that usually signals a high blood sugar.

When I got home, my fingerstick blood glucose: 173 mg/dl. Darn it! Must have been cornstarch or other sugars in the sauces.

I got on my supine stationary bike and pedaled for 40 minutes at a moderate pace while I played Modern Warfare on XBox. (A great way, by the way, to fit in some low- to moderate-intensity exercise while occupying your brain. My wife often has to yell at me to get off, it's so much fun.)

Blood glucose at the conclusion of exercise: 93 mg/dl-- a nice 80 mg/dl drop.

This is a useful strategy to use in a pinch when you've either been inadvertently exposed to more carbohydrate than you can tolerate, or if you'd like to blunt the adverse glucose effects of a bowl of ice cream or other carbohydrate indulgence.

Should we explore the idea of a "morning-after" pill, or actually a "meal-after" pill, a supplement pill or liquid that blunts or eliminates the blood glucose rise after a meal? I've considered such an idea, but have been fearful that people would start to use it habitually. Thoughts?

American Heart Association diet makes a monkey out of you

Heart Scan Blog reader, Roger, brought this New York Times article to my attention.

In an effort to develop a better experimental model for obesity than mice, scientists have turned to monkeys and other primates. The emerging observations are eerily reminiscent of what you and I witness just by going to the local grocery store or fast food outlet:

"'It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,' said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio."

"Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but American Heart Association-recommended diet,” she said."

Yes, indeed: The American Heart Association diet makes monkeys fat. Extrapolate this a little higher on the evolutionary ladder and guess what?

This is one of the many reasons why, when I have a patient who is counseled by the hospital dietitian on the American Heart Association diet, I advise them to 1) ignore everything the dietitian told them, and then 2) follow the wheat-free, cornstarch-free, sugar-free, whole food diet I advocate.

Not unexpectedly, much of this primate research is not being devoted to just manipulating diet to achieve weight loss and health, but to develop new drugs to "treat" obesity.

Would you like a banana?

Construct your glucose curve

In a previous Heart Scan Blog post, I discussed how to make use of postprandial (after-meal) blood sugars to reduce triglycerides, reduce small LDL, increase HDL, reduce blood pressure and inflammatory measures, and accelerate weight loss.

In that post, I suggested checking blood glucose one hour after finishing a meal. However, this is a bit of an oversimplification. Let me explain.

A number of factors influence the magnitude of blood glucose rise after a meal:

--Quantity of carbohydrates
--Digestibility of carbohydrates--The amylopectin A of wheat, for example, is among the most digestible of all, increasing blood sugar higher and faster.
--Fat and protein, both of which blunt the glucose rise (though only modestly).
--Inclusion of foods that slow gastric emptying, such as vinegar and fibers.
--Body weight, age, recent exercise

Just to name a few. Even if 10 people are fed identical meals, each person will have a somewhat different blood glucose pattern.

So it can be helpful to not just assume that 60 minutes will be your peak, but to establish your individual peak. It will vary from meal-to-meal, day-to-day, but you can get a pretty good sense of blood glucose behavior by constructing your own postprandial glucose curve.

Say I have a breakfast of oatmeal: slow-cooked, stoneground oatmeal with skim milk, a few walnuts, blueberries. Blood glucose prior: 95 mg/dl. Blood glucose one-hour postprandial: 160 mg/dl.

Rather than taking a one-hour blood glucose, let's instead take it every 15 minutes after you finish eating your oatmeal:


In this instance, the glucose peak occurred at 90-minutes after eating. 90-minute postprandial checks may therefore better reflect postprandial glucose peaks for this theoretical individual.

I previously picked 60-minutes postprandial to approximate the peak. You have the option of going a step better by, at least one time, performing your own every-15-minute glucose check to establish your own curve.

Why is type 1 diabetes on the rise?

Type 1 diabetes, also called "childhood" or "insulin-dependent" diabetes, is on the rise.

Type 2 diabetes, or "adult," diabetes, is also sharply escalating. But the causes for this are easy-to-identify: overconsumption of carbohydrates and resultant weight gain/obesity, inactivity, as well as genetic predisposition. A formerly rare disease is rapidly becoming the scourge of the century, expected to affect 1 in 3 adults within the next several decades.

Type 1 diabetes, on the other hand, generally occurs in young children, not uncommonly age 3 or 4. Type 1 diabetes also shares a genetic basis to some degree. But the genetic predisposition should be a constant. Obviously, lifestyle issues cannot be blamed in young children.
Then why would type 1 diabetes be on the rise?

For instance, this study by Vehik et al from the University of Colorado documents the approximate 3% per year increase in incidence in children with type 1 diabetes between 1978 and 2004:


(From Vehik 2007)

(For an excellent discussion of the increase in type 1 diabetes in the 20th century, see this review.)

This is no small matter. Just ask any parent of a child diagnosed with type 1 diabetes who, after recovering from hearing the devastating diagnosis, then has to stick her child's fingers to check glucose several times per day, mind carefully what he or she eats or doesn't eat, watch carefully for signs of life-threatening hypoglycemic episodes, not to mention worry about her child's long-term health. Type 1 diabetes is a life-changing diagnosis for both child and parents.

Various explanations have been offered to account for this disturbing trend. Some attribute it to the increase in breast feeding since 1980 (highly unlikely), exposure to some unidentified virus, or other exposures.

I'd like to offer another explanation: wheat.

Lest you accuse me of becoming obsessed with this issue, let me point out the four observations that lead me to even consider such an association:

1) Children diagnosed with celiac disease, i.e., the immune disease of wheat gluten exposure, have 10-fold greater likelihood of developing type 1 diabetes.

2) Children diagnosed with type 1 diabetes are 10-fold more likely to have abnormal levels of antibodies (e.g., transglutaminase antibodies) to wheat gluten.

3) Experimental models, such as in these mice genetically susceptible to type 1 diabetes, showed a reduction of type 1 diabetes from 64% to 15% with avoidance of wheat.

4) The increase in type 1 diabetes corresponds to the introduction of new strains of wheat that resulted from the extensive genetics research and hybridizations carried out on this plant in the 1960s. In particular, unique protein antigens (immune-provoking sequences) were introduced with the dwarf variant attributable to alterations in the "D" genome of modern Triticum aestivum.

Proving the point is tough: Would you enroll your newborn in a study of wheat-containing diet versus no wheat, then watch for 10 years to see which group develops more type 1 diabetes? It is a doable study, just a logistical nightmare. Perhaps the point will be settled as more and more people catch onto the fact that modern wheat--or this thing we are being sold called "wheat"--is a corrupt and destructive "foodstuff" and eliminate it from their lives and the lives of their young children from birth onwards. Then a comparison of wheat-consuming versus non-wheat-consuming populations could be made. But it will be many years before this crucial question is settled.

Yet again, however, the footprints in the sand seem to lead back to wheat as potentially underlying an incredible amount of human illness and suffering. Yes, the stuff our USDA puts at the bottom, widest part of the food pyramid.
All posts by william-davis

Lipoprotein(a) Research Foundation

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies


Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.


Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.



Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.




From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

More on ASTEROID

Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:


Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.



Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

LDL cholesterol, statins, and plaque regression

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.


Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.


Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:





The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:





The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.



Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

When is a calorie not a calorie?

One ounce of raw almonds (about 23 nuts) contains:


6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.


(From the USDA Nutrient Database)


Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.


The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).



Copyright 2008 William Davis, MD

Track Your Plaque data abstract

An extraordinary thing happened about 2 1/2 years ago.

While we have been following the Track Your Plaque program for coronary plaque regression for nearly 10 years, about 2 1/2 years ago we witnessed an extraordinary surge in success--bigger, faster, and more frequent drops in heart scan scores.

Up until then, we did witness significant reversal of coronary plaque by heart scan scores. We were planning to publish the data to validate this approach, but then . . .

Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. Why? I attribute the surge in success to the addition of vitamin D.

Unfortunately, it also meant that the preceding 8 or so years of data lacked experience with supplementing vitamin D. The hundreds of participants in the Track Your Plaque program had not, until then, included vitamin D in their program.

So I decided to start from scratch (from the standpoint of data collection, not for the participants). That also meant that the preceding years of experience went unreported, though even that data far exceeded the results of what is achieved in conventional heart disease prevention.

Thus, the data I presented at the Experimental Biology Proceedings (FASEB 2008) in San Diego this week included only experiences in the group of participants that included vitamin D in their program, with data collected until mid-2007. The number of experiences is therefore modest.

However, the Track Your Plaque experience, as reported, far exceeds any prior experience in coronary plaque regression.

The full abstract will be published in the Track Your Plaque website.


Copyright 2008 William Davis, MD

Small fish oil capsules

Many people complain about the size of fish oil capsules. Let's face it: They're usually big and kind of smelly.

Women in particular struggle with big capsules. This becomes a real problem when somebody requires high-dose fish oil for treatment of post-prandial (after-eating) abnormalities, high triglycerides, or lipoprotein(a), when 6 or more--occasionally up to the equivalent of 20--standard fish oil capsules are required.

I came across a small capsule alternative for people who struggle with the big capsules. It's a product called Learn from PharmaOmega, a source of super purified fish oil.

The Learn product is actually made for children, since omega-3 fatty acid supplementation has been linked with improved intellectual performance. But the small capsule size is convenient for women and other people who would like to avoid the big standard-sized capsules.

Each capsule is about 60% of the size of a standard fish oil capsule (the smaller capsule in the photo, next to a standard size fish oil capsule), yet contains 375 mg EPA + DHA per capsule, 25% more than standard capsules (which contain 300 mg per capsule). The ratio of of EPA:DHA is a little more heavily weighted towards EPA with a 5:2 ration, compared to 3:1 of standard capsules. The capsules are also faintly orange flavored and non-fishy.





Disclosure: I receive no compensation for discussing or promoting this product.


Copyright 2008 William Davis, MD

Low-carb eating for diabetes

Jenny provided permission to reprint her very excellent introduction to low-carbohydrate eating for people with diabetes. You can also view the original version on her Diabetes 101 website.

Jenny is a stickler for monitoring the effects of blood sugar. We might take some lessons from her experiences for improving management of people with metabolic syndrome or borderline blood sugars. In other words, monitoring the blood sugar-raising effects of various foods and food portions can provide great feedback on what foods are preferable, what undesirable, given your physiology.

Even if you are not a diabetic, Jenny's discussion is must reading to gain a better understanding of food choices, particularly carbohydrates. Along with seizing control of health, she has also gained deep wisdom in how to best manage this disease and its physiology.


Introduction to low-carb nutrition for diabetics

It's carbohydrates that raise blood sugar.

Sugars and starches, not the fats that dietitians have been warning you about for so long. If you've been testing your blood sugar after meals, you've probably noticed that already and you are starting to understand why a healthy diabetes diet will have to be one that limits carbohydrates to an amount that doesn't push your blood sugar up over the level where you are damaging your body.

But if your previous experience with restricting carbohydrates involved doing a weight loss diet like Atkins or Protein Power, which worked well for you until you crashed off it entirely and gained back all the weight you'd lost, you may be hesitant to embark on another course of dieting that requires some carb restriction.

I've been there myself. I've done the extremely low carb diet Dr. Richard Bernstein recommends for months on end. I did Protein Power for 3 years. And I've gone on the "Eat all the carbs you didn't eat over the past three years all at once" diet, too. The following observations grew out of my 8 years of experience with learning how to make carb restriction work long-term.

Unlike much of what you've read before, there are no scholarly references for this section. It's based entirely on my own observations and the experience of many dozens of people who have participated in online discussion groups devoted to low carb dieting and diabetes.


Weight Loss Diets Usually Fail but Diabetes Diets Can't Afford To Fail

People who adopt a low carb diet to lose weight tend to start out with great enthusiasm, adapt extreme dieting strategies, swear they will never eat another piece of bread or french fry for the rest of their lives, lose some weight, stall out, burn out, and slink back to their old diets, where they gain back all the weight they lost and more.

This is not a surprise. People on any diet, including low calorie and low fat, do the same thing. The body is very resistant to weight loss and deeply buried instincts in our brains do everything they can to maintain our weights, no matter how unhealthy they might be.

But while this pattern of dieting may be tolerable for those who are dieting to shed a few pounds before their class reunion, it spells disaster for those who must change their diet in order to prevent the high blood sugars that result in amputation, blindness, kidney failure and heart attack death.

Low carbing for diabetes means low carbing for life, long after the thrill has worn off of eating that runny brie and steak. Despite the hype in the diet books, it is not easy, simple, and fun. I know only a handful of people who have been able to sustain a low carb lifestyle for more than five years. And that is after years of online participation in low carb groups.

What you'll find below is what I've found works for me. I used a low carb diet to control my blood sugar for more than five years and have gone through the whole cycle, from enthusiasm, to boredom, to burnout, to saying "To hell with it, we've all got to die some time!" to starting all over again determined to avoid the mistakes that sent me round the bend the first time.


How Many Grams of Carbs to Eat? As Many as Allow You to Reach Your Blood Sugar Targets

When people think about adopting a lower carb diet, their first question is almost always, "How many grams of carbs can I eat at each meal?" Most of the diet books will answer that question with a hard and fast number. Atkins, for example, tells you to start out with 20 grams a day. Protein Power starts you at 30 grams. And Dr. Bernstein suggests 6 grams for breakfast and snacks and 12 grams at lunch and dinner.

Adopting these very low carbohydrate limits will control your blood sugar very nicely. But over time, many people find that sticking to a diet this low in carbohydrate becomes impossible. That's why I'm going to ask you to throw away all those diet books and try a new approach to restricting carbs.

What you will do is to try the strategy used by the people from the alt.support-diabetes newsgroup who informally call themselves "The 5% Club" because their A1c test results fall in the 5% range which doctors consider normal: use your blood sugar meter after each meal to determine how many grams of carbs you can eat and still meet a healthy blood sugar target.

You will start out by measuring your blood sugar one and two hours after each meal. Write down what you ate and observe what it did to your blood sugar. If a meal allows you to reach your blood sugar targets, try eating it again on a different day and test it test again, possibly at a later time, to make sure that your good numbers weren't just a result of slow digestion.

If you end up too high after a meal, the next time you eat it, cut back on the portion size of the carbohydrate elements in the meal and test again. Do this until you can hit your targets, or flag the carbohydrate-containing foods in that meal as ones your body can't handle.

What you're doing here is creating what newsgroup activist Alan S. calls, "a low spike diet" rather than a low carb diet. He can achieve normal post meal blood sugars by eating as many as 30 or 40 grams of carbohydrates at a meal. Others will find that they need to eat a lot less than that amount to hit safe post-meal blood sugar targets.

Usually how much carbohydrate you can manage has something to do with your body size. The more you weigh, the less each gram of carbohydrate you eat will raise your blood sugar. Those of us whose weight is less than 150 lbs often find that we can eat between 12 and 20 grams of carbohydrate and still reach normal blood sugar targets without the help of medications, and that we can add perhaps another 10 or 20 grams more, with medications. People who are much heavier can often eat 30 or 40 grams per meal and still reach their blood sugar targets. In general, men can eat more carbohydrates and still reach their targets than can women, again, because of their larger body size.


How to Learn How Much Carbohydrate is in Your Food

To make this system work, it helps if you start to learn how many grams of carbohydrate are in the foods you eat. That way you won't have to test hundreds of foods once you've learned how a representative sample affect you.

The best way to learn how many grams of carbohydrates are in the different foods you eat is to read food labels carefully, invest in a nutritional guide like one of Connie Netzer's books of nutritional information, download nutrition software like LifeForm (http://www.lifeform.com) or use online calculators like Fit Day (http://www.fitday.com). Software and online sites will compute the amount of carbohydrates and other nutrients in your meal for you as long as you know the portion size.


Learn about Portion Sizes!
This brings up an important point: When you estimate how many grams of carbohydrate there are in a portion of food, it is very important to find out if the amount of food on your plate corresponds to the amount in the "one serving" listed on a label, in a book, or in your software.

The best way to do this is to invest in an electronic food scale and to weigh your foods for a few weeks until you get the hang of estimating portion size. You can get a good food scale at a gourmet kitchen shop for $25 to $40 dollars. This food scale may be the best nutritional investment you'll ever make.

Once you start using your scale, you will find that the muffin you bought at the coffee shop weighs 8 ounces, which is fully four times the 2 ounces that most food databases give as "one serving" of a muffin. When you read that a mythical 2 ounce portion of muffin contains 27 grams of carbohydrate you will realize why that 8 ounce coffee shop muffin with its 108 grams of carbohydrates sends your blood sugar into the psycho zone!

With ice cream, when you weigh your ice cream on a food scale, you'll quickly see that the "one portion" listed on the package turns out to be only a few teaspoons' worth. That bowl you've been considering as one portion of ice cream weighs in as four servings or 72 grams of carbohydrate and 600 calories, which may explain its damaging effect on both your blood sugar and your waistline.

This may sound like a lot of work, and when you first start, it is. But after you do it for a few weeks you'll find you have memorized the carbohydrate gram counts and the portion sizes for the foods you usually eat, and once you have tested your blood after eating these portion sizes, you won't have to test every time you eat a favorite meal, because you will know what it is going to do to your blood sugar.


Eating Away from Home

The biggest challenge you'll encounter as you start learning what you can eat will be eating away from home. You aren't going to be able to weigh restaurant foods nor can you look up the nutritional values of many restaurant offerings--though many of the common fast food outlets do provide nutritional information online--though often without listing portion sizes.

That makes it a very good idea to avoid starchy or sugary restaurant foods or, if you do eat them, to eat only a small portion of what you are offered. Measure your blood sugar an hour or two hours after eating if you aren't sure about how a restaurant food will affect you.


Fat and Carbs Eaten Together will Digest Slowly

Foods with a lot of fat in them take longer to digest than those without a lot of fat. This is why pizza and ice cream often give deceptively good readings on your meter. If you test a meal and see a reading that is too good to be true, be sure you test at 3 or four hours after eating.


The Truth About Pasta

Pasta was long recommended to people with diabetes as a food that would not raise blood sugar and you will still see it starring in many cookbooks and magazines intended for people with diabetes.

However, if you test pasta 4 or 5 hours after eating, you may get an unpleasant surprise. This is true with the so-called "low carb" pastas, too. These foods give you excellent readings at one and two hours because they are resistant to digestion so they don't turn into glucose right away. But five hours later, they do break down into glucose and when they do, the 52 grams of carbohydrates found in each 2 ounce serving of pasta will hit your blood stream with a nasty wallop. (Not to mention that you almost need a microscope to see a 2 ounce portion of pasta. Most people's idea of a portion of pasta is closer to 6 ounces--and 156 grams of carbohydrate!)

If you have pasta for dinner and don't see a peak 3 hours later, be sure to check your fasting blood sugar the next morning. You may see the blood sugar rise there, too.


Sugar Alcohol and "Sugar Free" Foods

The sugar alcohol used in so-called "sugar free" foods can also show up in your blood sugar an hour or two after you'd expect to see them, especially the maltitol used in "sugar-free" candy. At least half of the sugar in Maltitol does turn into glucose in your blood stream and it can raise your blood sugar, but the rise is delayed so you may miss it on testing. So if a "sugar free" food seems to be kind to your blood sugar, try testing it an hour or two after your first tests. Erythritol is the one sugar alcohol that usually does not show up in your blood sugar.


Dealing with Limited Blood Testing Supplies

In in ideal world, we'd all have all the testing supplies we needed to control our blood sugar, but in real life blood sugar test strips are very expensive and many insurers sharply limit the number of strips people with Type 2 diabetes can get each month.

Here are some strategies that can help you if your access to strips is limited.

If you only have 50 strips to get you through a month, plan out what you are going to test ahead of time. Pick one of your favorite meals, and test at 1 hour after eating the first time you eat it and 2 hours after eating the second. Do this with a couple different meals and see if there's a pattern as to when you see the highest reading--whether it is at one hour or two. Then choose another meal and test it at the time when you saw the highest reading in the earlier meal. If you ever get a surprisingly low reading, try testing an hour later or earlier, to make sure you aren't missing the peak.

Make the goal of your testing be learning how many grams of carbs you can tolerate in one meal. If you learn that 30 grams is your upper limit, use software and your scale to find portions of other foods that will also clock in at 30 grams or less. Test one or two of these, and if you see the result you expect, you don't have to test every time you eat these foods again.

Wal-mart sells a cheap and effective blood sugar meter with strips that cost one half as much as other vendors. Some drug stores also sell store brand meters with cheaper strips. If you need more strips, consider the $50 you pay for another 100 strips an investment in your health. It's far better to spend that $50 now, than to spend it on expensive doctor bills caused by complications you don't need to develop!


Keep the focus on Achieving your Blood Sugar Goals

By testing after meals, you'll learn how many grams of carbohydrate your own, unique, body can handle. And more importantly, you'll also be able to decide if you are going to be able to control through diet alone, of whether it is time to talk to your doctor about supplementing dietary control with drugs.

Many people are so excited to learn that they can achieve normal blood sugars by cutting way back on carbohydrates that they become zealots for low carb dieting. I've been there and I've done that. But it's important not to get too carried away with a "Carbs are Evil" mentality which makes it a matter of religious zeal never to let evil carbs cross your lips again. Like all conversions this one tends to fade out in time. And as we said at the start of this chapter, your ultimate goal is to maintain your blood sugar targets for the rest of your life. So the safest approach is to get the most blood sugar benefit you can out of restricting carbohydrates, but restrict them to a level you can maintain year in and year out.

Most importantly, I have learned it is best to treat carb restriction as a strategy, one of many, which used in combination with other strategies including medications if needed, can give you normal blood sugars, rather than the One and Only True Way. If you can be flexible and find more than one tool to help you meet your blood sugar targets, you are more likely to be able to maintain those excellent blood sugars for years to come.


Eliminate "Habit Carbs" and Concentrate on "Value Carbs"
When people think about restricting their carb intake they assume this means never eating any of their favorite foods again.

But for many of us, this doesn't have to be true. Why? Because a quick look at your daily carb intake will often reveal that the bulk of the carbohydrates you are eating are what I call "habit carbs." These are the carbs you eat without a second thought because they are there. Not because they taste good. Not because you couldn't live without them. Just because you're in the habit of eating them.

Here is a list of some prime "habit carbs."

Steam table mashed potatoes

Limp french fries

Squashy hamburger buns

Cardboard toast

Cold home fries

Stale boxed cookies


How many of these flavorless, starchy foods are you consuming everyday just because they're there? Probably more than you realize. So before you lift that fork-full to your mouth, ask yourself, "Is this food thrilling me?" If not, put it down. This should go a long way towards getting your carb intake down.

What I'd call "value carbs" are those carb-rich foods that really do mean something to you. I'm not going to lie to you. You are not going to be able to make them the mainstays of your diabetes diet. But by using the strategies describe below, you should be able to eat enough of these foods to keep yourself from feeling deprived--without destroying your health.


Don't Create "Forbidden Foods!"

If you are one of those people who could live happily on Purina People Chow, you can skip what follows. But if food has been important to you, and if you have hitherto had a long and emotionally satisfying relationship with food, or if, like me, baking from scratch was one of your favorite ways to show love and express creativity, restricting your carbohydrate input will mean that a whole lot of what you've been eating (and baking) up until now is suddenly, completely, off limits. I can't eat cake and get a healthy blood sugar level. Even with two different diabetes drugs in my system. I can't eat cake even with an insulin shot before I eat it. I love cake but there is no way I can eat more than a bite or two without seeing very high blood sugars and there is no way I can eat two bites of cake and be happy. The same goes for french fries and Thai noodles.

During the first enthusiastic weeks of exploring carb restriction most people deal with this kind of discovery by coming up with new recipes and finding new, delicious and healthy things they can substitute for old, high carb standards. They appreciate the way cutting way back on carbohydrates curbs their hunger and makes food much more manageable. This is good and it is why long term low carbing is possible. But our old favorite foods do not go away that easily.

If you decide that some food you have been eating and enjoying all your life will never again cross your lips, it is almost 100% guaranteed that you'll end up pigging out on that very same food at some time in the future, hating yourself, and even beginning a binge that can throw you completely off your diet for months.

It might not happen the first month you are restricting your carb intake or even the first year. It took me three years of low carbing to get to where I crashed off my stringent low carb diet. But eventually it happens, and because after almost a decade of counting my carbs I've learned that I will never lose my love for certain foods that don't love me, I've put a lot of time into finding a way of restricting my carbohydrate intake in a way that avoids the buildup those feelings of deprivation that eventually lead to long periods of unwise eating.

The key, for me, is to build safety valves into my diet. I don't call them "cheats" or "bad foods" for reasons I'll get into later. I call them "off plan" foods because they are not food I can make an ongoing part of my daily food plan. Because my goal is life-long blood sugar control, I accept that I will occasional eat "off plan" and that this is okay as long as I am meeting my blood sugar targets most of the time. "Good enough" control that I can adhere to year in and year out beats a few months of perfection followed by crashing off the diet entirely and ruining my health. Here is one way to approach doing this:

Do the Diet Straight for a Month or Two Before You Try Off-Plan Goodies

As you learn what foods raise your blood sugar and what foods don't, you will almost certainly find that there are a lot of foods you used to love that don't work for you anymore. Waffles for breakfast, coffee cake at coffee break, three slices of pizza with crust, a burger with a bun and a side of fries are just a few of the foods that it is almost certain will not allow you to meet your post-meal blood sugar targets.

As you keep using your meter to test what you eat, if you are like most people with diabetes you'll also learn that some of the so-called "low glycemic" foods and the supposedly "healthy" whole grains that nutritionists recommend for people with diabetes won't work either. Oatmeal and whole wheat bagels raise my blood sugar far too high, so does cracked whole wheat, whole wheat bread, and brown rice.

If the dietician tells you a food is good for you, but your meter tells you it is raising your blood sugar to a level that is high enough to cause complications, you will have to listen to your meter. Your meter will tell you what is safe to eat and for the first couple of months while you are learning how to get your blood sugar under control and how bring those high blood sugars down to normal levels you will have to accept that you can only eat those foods that don't cause spikes.

If you attempt to add in off-plan foods before you are solidly on-plan you may never really get into the swing of eating a diet that controls your blood sugars and you may not get to where your body learns to enjoy the lower carb foods that don't give you blood sugar swings.

But after you've gotten your blood sugar under control, nothing horrible will happen if you make room for a small portion of some high carb treat every now and then.


How to Add Off-Plan Foods to the Plan

If you've avoided bread for a couple months, the humble roll in that restaurant bread basket may start to call out to you with an irresistible siren song. If you give in and eat it, with each bite you may find yourself feeling as if you are doing something incredibly sinful--the way you might have felt if you had eaten a whole box of chocolates in the past.

That feeling is the sign that you're heading for trouble. You've created a "forbidden fruit" and sooner or later that forbidden fruit is going to get you. You may find yourself thinking about that roll, craving another, sneaking off to eat one where nobody knows you, or, alternatively, you may declare that you will never again eat a roll ever--and then ruin your Thanksgiving holiday when you go to Aunt Glenda's and refuse to eat even a single one of those wonderful rolls of hers you've eaten every year of your life which say, "This is the family Thanksgiving" to you.

It is far better to make a bit of room in your diet for high carb treats so that they don't build up a charge. If you do this, you'll find that they almost never taste as good as you remembered, and you'll be able to leave them behind without turning them into an object of obsession.

Just knowing that you can eat some specific off-plan food at some future time, when it is scheduled, makes it that much easier to say, "No thanks" to it, and maintain your healthy blood sugar the rest of the time.


How Often Can You Eat Off-Plan?
How often you have an off-plan food depends a lot on your dietary goals, how high your blood sugar is before you eat carbs, and whether you are willing to exercise after eating. It also depends greatly on what medications you are taking for your diabetes. Whatever I eat, I try to keep my blood sugar below 120 mg/dl (6.7 mmol/l) at 2 hours after any meal.

Forty minutes of cardiovascular exercise will burn off a lot of extra carbs, so if you exercise regularly, try to eat your high carb treat before you head for the gym.

If you're trying to lose weight, you may have to keep off plan treats few and far between. When I was actively losing weight on a low carb diet without medications I ate one off-plan meal about once every two weeks.

Once I reached my weight loss goal I loosened up a bit but I found it best to cycle between weeks of eating a strict very low carb diet, and then a week of eating slightly more carbs--but I tried very hard not to ever anything that would cause my blood sugar to be over 120 mg/dl (6.7 mmol/L) at 2 hours after a meal because doing so makes me feel rotten.


Throw Away the Vocabulary of Self-Destructive Dieting

When you eat something with carbs in it, don't think of it as a "cheat." Cheating is what you do when faced with an authority figure--your 9th grade math teacher or the IRS. But you are the one in control of what you eat. So when you eat something that is off-plan, you should stop thinking of it as "getting away with something" and treat it instead as something you've decided to do--for a reason that should be clear to you while you do it.

If you keep eating things that were not what you had intended, rather than beating yourself up, it's time to reconsider your food plan and figure out why it isn't working. Are you having trouble finding foods in restaurants that don't raise your blood sugar? Maybe it's time to bring your lunch along to work for a while, or to find new place to dine.

Are you bored with what you have been eating? Google for good low carb recipes you can try at home. There are thousands of them. If you use the Google Groups search and look for messages in alt.support.diet.low-carb that start with "REC" you'll find a treasure trove of ideas to try.

Keep the vocabulary of sin and guilt for the confessional. You're going to eat a lot of things in the years to come that will mess up your blood sugar. But if you are kind to yourself and dust yourself off after you mess up and keep on going, doing the best you can to hit your blood sugar targets, you may very well end up healthier than many people who do not have diabetes. The important thing is to keep at it, doing the best you can and forgiving yourself when the best you can do isn't as good as you wish it was.


Know Your Limits
I've learned the hard way I can't eat half a blueberry muffin, so I don't even try portion control for that particular food. I know blueberry muffins are trouble and I also know that I will eventually eat one. That's just how it is, so every blue moon or so I eat a blueberry muffin, experience the miserable high blood sugars that follow, and then remember why I don't eat muffins every day any more. What I don't do is fool myself that I can buy a muffin and only eat half. Everyone has a few foods that fall into this category. Treat them with caution!


Eat Off-Plan Foods Out of the House
I've learned the hard way that if a big box of something full of carbs is in the fridge, bad things are going to happen. So I try to eat my off-plan foods away from home. I eat my muffins or cookies at a coffee house. I have a slice of pizza at a pizzeria. I don't buy a box of muffins or a whole pizza and bring them home.

Getting this strategy to work requires that your whole family understand what's at stake. It took me a couple years of harping on what "complications" means, but by now, my family understands that if my blood sugar is too high, I'm damaging my body. They want to keep me around for a while, so they understand that there are some foods that shouldn't be brought into the house--ever.

When other family members want to have treats at home, they are kind enough to buy things I don't like. For example, if someone wants Ben & Jerry's they buy the Chunky Monkey flavor that I find revolting, not the New York Fudge. By the same token, when my kids lived at home, I didn't buy them the brands of cookies I can't resist. There are plenty of others cookies they liked that don't tempt me at all, and those were the ones in the cupboard.

Over the years the nondiabetic members of my family learned that no one is doing themselves a favor scarfing down 300 grams of fast acting carbohydrate every day--particularly not people with a family history of diabetes and heart disease!


Medications Can Help

I'm not a big fan of medications because I've learned the hard way that drug companies lie about side effects and some of these side effects are permanent and can ruin your life. But I learned the hard way, too, that some of us (like, say me) can't get normal blood sugars no matter how low our carb intake. For us, adding a diabetic drug or two to our daily regimen may be the only way we can get normal blood sugars without a life of tormenting self-denial.

Drugs I have found useful over the years include metformin, precose, and post-meal insulin shots. The new incretin drugs, Januvia and Byetta help some people make dramatic improvements in their blood sugar, but the way that they work makes it necessary to eat a slightly higher amount of carbohydrates with them because they only work when your blood sugar rises over a certain threshold. Even with these drugs (including Januvia) I've never been able to eat more than 120 grams of carbohydrates a day, but after many years of eating an extremely low carb diet--which was the only diet that would control my blood sugars--120 grams of carbs a day feels like a completely normal diet!


Be Aware of Rising Insulin Resistance

Some people may find that eating a low carb diet is not enough to control their blood sugar because they are very insulin resistant. Perhaps they have been diagnosed with PCOS, or have to take a drug, like Prednisone that increases insulin resistance. The book, Dr. Bernstein's Diabetes Solution by Dr. Richard K. Bernstein, the distinguished diabetes doctor, recommends Metformin as an appropriate drug for patients on a low carb diet whose blood sugars are still not completely controlled. It isn't a cure by any means, just one more tool you can use to keep blood sugars under control, and if you limit your insulin resistance you may solve both weight and hunger problems that otherwise can derail your diet.

You can read more about the different drugs available to help control blood sugars HERE. Just remember that all these diabetes drugs work best when you combine them with some level of carbohydrate restriction. How much restriction? Test your meals one and two hours after eating, and your blood sugar meter will tell you exactly how much.


Top Medical Journal Publishes Landmark Study Showing Very Low Carb Diet Most Effective and Safest for Lipids etc.

In case you are still being given out-of-date medical or nutritional advice by people who tell you that a low carb/high fat diet will give you a heart attack, take a look at this recently published study, which appeared in the Journal of the American Medical Association.

This study found that an Atkins style low carb diet not only caused double the weight loss of the low fat diet at the end of one year, but it did not adversely affect cholesterol levels.

This finding, added to the Women's Health Initiative finding (after $40 million dollars of research) that low fat dieting does NOT prevent heart disease, should lay to rest any last fears you might have about the impact of cutting carbs on your health.

The findings of this study, are not news to anyone who has tried a low carb diet and stuck with it for any period of time, but they appear to amaze the entire medical community who continue to cling to their to the "Fat is Bad" religious belief long no matter what evidenced-based medical studies might come up with.

Bottom line: You can cut your carbs way down, replace carbs with fat, and await the better health this kind of eating will provide.

Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial.Christopher D. Gardner, PhD; Alexandre Kiazand, MD; Sofiya Alhassan, PhD; Soowon Kim, PhD; Randall S. Stafford, MD, PhD; Raymond R. Balise, PhD; Helena C. Kraemer, PhD; Abby C. King, PhD


Here's the summary of the WHI findings:

NIH News: News from the Women?s Health Initiative: Reducing Total Fat Intake May Have Small Effect on Risk of Breast Cancer, No Effect on Risk of Colorectal Cancer, Heart Disease, or Stroke


Here's a study that documents the effectiveness of lowering carbs and increasing fat and protein consumption for the control of blood sugar in the absense of weight loss:

Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutrition & Metabolism 2006, 3:16.


To Get More Help with Making a Low Carbohydrate Diet Work

My "Low Carb Facts and Figures" site, which now shares this server, has more information I collected back in the days when I used a low carb diet for both weight loss and blood sugar control.

You'll find articles there that address a few of the issues people run into while eating a very low carb diet,which are not answered in a completely honest fashion by the people who sell diet books promising you can lose weight easily while gorging on all your favorite foods--which, sadly, is 99% of all authors writing diet books.

Interview with an outspoken advocate of truth in diabetes

I stumbled onto Jenny Ruhl's Diabetes Update blog after I received several very insightful comments to this blog whenever I posted a discussion on diabetes or pre-diabetes/metabolic syndrome.

Who the heck was this commenter who clearly had deep insight into diabetic issues?

It turned out to be Jenny Ruhl, a woman who learned her lessons the hard way: by receiving a belated diagnosis of (an unusual form of) diabetes, then receiving plenty of mis-guided advice from physicians on diet and treatment. Reading her many blog posts and websites, you get the clear sense of how hard this individual worked to gain the depth of knowledge she's acquired, on a par or superior to most diabetes specialists.

And she minces no words in expressing her heartfelt and carefully considered opinions. But that's what I look for: people who are unafraid to voice opinions that may not be consistent with the flow of conventional thought, but ring true and prove effective.


Dr. Davis: From your blog and websites on diabetes, it is clear that you exceptionally knowledgeable in the world of diabetes, metabolic syndrome, and related disorders. Can you give us a little background on how you came to this quest?

Jenny: Though I was told I was a "classic type 2" [diabetic] by my doctors, nothing I read about diabetes corresponded to my own experience. I knew my diabetes had not been caused by obesity because I'd been a normal weight all my life until my blood sugars went out of control at which point I developed ravenous hunger and gained a lot of weight very quickly.

I also wondered at the huge gap between what Dr. Bernstein said was a normal blood sugar and what my doctors told me was a safe blood sugar for a person with diabetes. The people I met who followed Bernstein's very low carb diet had much better blood sugars and far fewer complications, but my doctors dismissed this as irrelevant. So I decided to do some research to find out who to believe. I plunged into the medical journal articles that had recently been made available on the web to see if I could answer two questions: What causes diabetes? and "What does science actually know about what blood sugar levels damage organs?"

The result was the information that became the basis for the Blood Sugar 101 site. Initially, I attempted to sell it as a book, but editors told me that though what I'd learned was "fascinating" it would be "over the head" of the typical health book buyer who wanted simple explanations and if possible, a simplistic slant towards "cure." Fortunately, the very strong response and high traffic volume to the web site proved that, as I had thought, there are a lot of people who do want more than an oversimplified overview and who, given the information they needed, were able to make huge positive changes in their health.


Dr. Davis: What do you think your life would be like if you hadn't pursued this unique course?

Jenny: Possibly a lot shorter.

People in my family die of heart attacks in their 50s, probably from undiagnosed high blood sugars. The pattern of the type of diabetes I have is to have a normal fasting blood sugar and an extremely high post-meal blood sugar after consuming very few grams of carbohydrate. When doctors diagnose using only the fasting blood test, they miss those highs, which research is now finding to be a primary cause of heart disease.

I also would have been a lot fatter. My doctors told me that I was packing on 20 lbs a year due to "normal menopausal changes" and that there was nothing I could do about it. Lowering my carbs significantly dropped all the weight I had gained and I still weigh a lot less now than I did in 1998.


Dr. Davis: You've been a keen observer of the diabetes scene for some years. Have you discerned any important trends in both the public's perception of diabetes as well as how diabetes is managed in the conventional world?

Jenny: The huge difference I see is that, over the last decade, the online diabetes community has learned the value of cutting back on carbohydrates and shooting for truly normal blood sugar levels. So people who put some time into researching diabetes online and talking with those of us who have succeeded in avoiding complications will learn that they do not have to settle for very high blood sugars and deterioration their doctors think inevitable.

Unfortunately, the media have put most of their energy into promoting the discredited idea that diabetes is caused by gluttony and sloth and to promoting the equally discredited idea that people with diabetes should eat a high carbohydrate diet and avoid fat.

So for now there is a huge divide in the quality of life of those people with diabetes who educated enough to go out on the web and educate themselves and those who get their diabetes information from doctors. Sadly most doctors still encourage patients to eat low fat/ high carb diets, and counter the very high blood sugars this diet produces with oral drugs of questionable efficacy, while assuring patients they will be safe if they maintain blood sugar levels that meet the American Diabetes Association's recommendations, though a mass of research shows these are high enough to produce every single diabetic complication possible.


Dr. Davis: I understand that you've released a new book, Blood Sugar 101. How is your book unique in the world of diabetes books? Who should read Blood Sugar 101?

Jenny: Blood Sugar 101: What They Don't Tell You About Diabetes differs from other books in that it gives the reader a much deeper understanding of what is really going on in their bodies as their blood sugar control breaks down and what sciences knows about how abnormal blood sugars cause complications. Then it gives the reader the tools they need to find what diet and/or drug regimen will brings their own, unique, blood sugars down to a truly safe level.

Unlike some books, this one does not present a one-size-fits-all solution, but recognizes that Type 2 diabetes is really a catch-all diagnosis that covers a lot of disorders that behave quite differently. That is why what works for one person with diabetes may not work for another.

Because this book provides details available nowhere else about the physiology of diabetes and the drugs available to treat it, readers will find the information they need to work with their doctors to craft a regimen that brings their blood sugar into the range that preserves and improves their health.


Dr. Davis: Before we close, tell us a little about yourself outside of your diabetes advocate role.

Jenny: I live in rural New England and am a passionate gardener. I've been online since 1980 when I was part of the team at IBM that developed the first commercial email program, PROFS. I got involved in online discussion groups in 1987 and have been messaging on bulletin boards ever since.

I was a professional singer/songwriter in Nashville in my youth and spent my middle years as a bestselling author of books about consulting. Right now a lot of my energy goes into managing the financial and software side of a family business that makes hand made pocket tools for collectors.


Dr. Davis: Thank you for your great insights, Jenny!

The Marshall Protocol and other fairy tales

True to form, Dr. John Cannell has published yet another wonderfully insightful Vitamin D Newsletter.

One item caught my eye, a response to a question about the Marshall Protocol. I, like Dr. Cannell, was inundated with questions about this so-called protocol, which amounts to little more than the unfounded speculations of a non-physician, actually someone not even involved in health care.

In all honesty, I blew the whole issue off after I read Dr. Marshall's rants. They smack of pure quackery, though from somebody who clearly has a command of scientific lingo. To Dr. Cannell's credit, he took the time and effort to construct a rational response in the latest issue of the newsletter. I reproduce his response here:



Dear Dr. Cannell:

I understand Dr. Marshall conducted a study and found vitamin D is bad for you. What kind of study did he do?

Mary, Minneapolis, Minnesota


Dear Mary:

I have been inundated with letters asking about Professor Marshall's recent "discovery." Some have written that to say they have stopped their vitamin D and are going to avoid the sun in order to begin the "Marshall protocol." The immediate cause of this angst is two publications, a press article in Science Daily about Professor Marshall's "study" (which is no study but simply an opinion) in BioEssays. Dr. Trevor Marshall has two degrees, both in electrical engineering. Before I begin, I want to again remind you that I am a psychiatrist who works at a state mental hospital. In my duty to full disclosure, I must say that I have known a lot of psychiatrists in my life and a few electrical engineers. If I knew nothing else of a disagreement between two people but their professions, I would believe the electrical engineer, not the psychiatrist.

In reading his two articles, Dr. Marshall's main hypotheses are simple. (1) Vitamin D from sunlight is different than vitamin D from supplements. (2) Vitamin D is immunosuppressive and the low blood levels of vitamin D found in many chronic diseases are the result of the disease and not the cause. (3) Taking vitamin D will harm you, that is, vitamin D will make many diseases worse, not better. If you read his blog, you discover that the essence of the Marshall protocol is: "An angiotensin II receptor blocker medication, Benicar, is taken, and sunlight, bright lights and foods and supplements with vitamin D are diligently avoided. This enables the body's immune system, with the help of small doses of antibiotics, to destroy the intracellular bacteria. It can take approximately one to three years to destroy all the bacteria." That is, Dr. Marshall has his "patients" become very vitamin D deficient.

Again, Dr. Marshall conducted no experiment and published no study. He wrote an essay. He presented no evidence for his first hypothesis (sunlight's vitamin D is different than supplements). From all that we know, cholecalciferol is cholecalciferol, regardless if it is made in the skin or put in the mouth. His second hypothesis is certainly possible and that is why all scientists who do association studies warn readers that they don't know what is causing what. Certainly, when low levels of vitamin D are found in certain disease states, it is possible that the low levels are the result, and not the cause, of the disease. Take patients with severe dementia bedridden in a nursing home. At least some of their low 25(OH)D levels are likely the result of confinement and lack of outdoor activity. However, did dementia cause the low vitamin D levels or did low 25 (OH)D contribute to the dementia? One way to look at that question is to look at early dementia, before the patient is placed in a nursing home. On the first day an older patient walks into a neurology clinic, before being confined to a nursing home, what is the relationship between vitamin D levels and dementia? The answer is clear, the lower your 25(OH)D levels the worse your cognition.

Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Apr 15;460(2):202-5. Epub 2007 Jan 8.


These studies suggest that the low 25(OH)D levels are contributing to the dementia but do not prove it. Only a randomized controlled trial will definitively answer the question, a trial that has not been done. So you will have to decide if vitamin D is good for your brain or not. Dr. Marshall seems to be saying demented patients should lower their 25(OH)D levels. Keep in mind, an entire chapter in Feldman's textbook is devoted to the ill effects low vitamin D levels have on brain function.

Brachet P, et al. Vitamin D, a neuroactive hormone: from brain development to pathological disorders. In Feldman D., Pike JW, Glorieux FH, eds. Vitamin D. San Diego : Elsevier, 2005.

It is true that in some diseases, high doses of vitamin D may be harmful. For example, in the early part of last century, the AMA specifically excluded pulmonary TB from the list of TB infections that ultraviolet light helps. They did so because many of the early pioneers of solariums reported that acutely high doses of sunlight caused some patients with severe pulmonary TB to bleed to death. Thus, these pioneers developed very conservative sun exposure regimes for pulmonary TB patients in which small areas of the skin were progressively exposed to longer and longer periods of sunlight. Using this method, sunlight helped pulmonary TB, often to the point of a cure. Furthermore, it is well known that sunlight can cause high blood calcium in patients with sarcoidosis. In fact, sarcoidosis is one of several granulomatous diseases with vitamin D hypersensitivity where the body loses its ability to regulate activated vitamin D production, causing hypercalcemia.

Cronin CC, et al. Precipitation of hypercalcaemia in sarcoidosis by foreign sun holidays: report of four cases. Postgrad Med J. 1990 Apr;66(774):307-9.

Furthermore, although medical science is not yet convinced, some common autoimmune diseases may have an infectious etiology. I recently spoke at length with a rheumatologist who suffers from swollen and painful joints whenever he sunbathes or takes high doses of vitamin D. As long as he limits his vitamin D input his joints are better. To the extent vitamin D upregulates naturally occurring antibiotics of innate immunity, sunlight or vitamin D supplements may cause the battlefield (the joints) to become hot spots. I know of no evidence this is the case but it is certainly possible.

However, If Dr. Marshall's principal hypothesis is correct, that low vitamin D levels are the result of disease, then he is saying that cancer causes low vitamin D levels, not the other way around. The problem is that Professor Joanne Lappe directly disproved that theory in a randomized controlled trial when she found that baseline vitamin D levels were strong and independent predictors of who would get cancer in the future. The lower your levels, the higher the risk. Furthermore, increasing baseline levels from 31 to 38 ng/ml reduced incident cancers by more than 60% over a four year period. Therefore, advising patients to become vitamin D deficient, as the Marshall protocol clearly does, will cause some patients to die from cancer.

Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.

I will not write again about Dr. Marshall's theories. No one in the vitamin D field takes him seriously. Personally, I admire anyone willing to swim against the tide and raise alternative theories. I have done the same with influenza and autism. However, I agree with the New York Times, An Oldie Vies for Nutrient of the Decade and Jane Brody's conclusion, "In the end, you will have to decide for yourself how much of this vital nutrient to consume each and every day and how to obtain it." I agree. You will have to decide for yourself.

John Cannell, MD
The Vitamin D Council

Breaking news from the American College of Cardiology meetings

The American Heart Association (AHA) was kind enough to send me an e-mail headlining the breaking news from the American College of Cardiology (ACC) meetings underway in Chicago:


ISAR-REACT 3
A Randomized, Double-Blind, Active-Controlled, Multi-Center Trial (ISAR-REACT 3) of Bivalirudin Versus Unfractionated Heparin in Troponin-Negative Patients Undergoing Percutaneous Coronary Interventions After Pre-Treatment With 600 mg of Clopidogrel

TRITON - TIMI 38 Stent Analysis
Prasugrel Compared to Clopidogrel in Patients With Acute Coronary Syndromes Undergoing PCI With Stenting: The TRITON - TIMI 38 Stent Analysis

Percutaneous Coronary Interventions in Facilities without On-Site Cardiac Surgery (NCDR)

(And four other similar reports)


Let's meld the ACC headlines with the financial headlines:

July 2, 2007
The Medicines Company announces reacquisition of all marketing rights to bivalirudin, anticoagulant growing in use for coronary angioplasty and related procedures. 2008 sales anticipated to be in the $15-20 million range, to grow to $90-110 million, a growth rate of 50% per year.


November 20, 2007
Drug manufacturing giant, Eli Lilly, vies for a portion of the $5 billion (annual revenues) oral anti-platelet market, now occupied by Plavix, with its newer, but questionably better, agent, prasugrel.


Growth of the coronary angioplasty (percutaneous coronary intervention, or PCI) doesn't ordinarily make headlines, but the performance of specific companies within the industry does. Angioplasty and cardiac device maker (inc. the drug-coated stent, Taxus), Boston Scientific, for instance, announced record sales of $8.537 billion for 2007, an increase of $536 million. How to grow this market? We could always hope for more people with heart attacks or other unstable symptoms. Or, we could . . . increase the number of hospitals capable of PCI! Brilliant.


The money behind this push for procedures is staggering. It drives enormous marketing efforts, pays Washington lobbyists, pays for many nice dinners and trips for doctors who engage in the system, and pays for very costly research.

And the AHA and ACC are kind enough to let us know about these great pieces of news.

Cholesterol effects of carbohydrates

Let's take a hypothetical person, say, a 50-year old male. 5 ft 10 inches, 160 lbs, BMI 23.0. He's slender and in good health.

Our hypothetical man eats a simple diet of vegetables, some fruit, nuts, and meats but avoids processed industrial foods. By macronutrient composition, his diet is approximately 30% protein, 40-50% fat, 20-30% carbohydrate. His starting lipid panel:

Total cholesterol 149 mg/dl
LDL cholesterol 80 mg/dl
HDL 60 mg/dl
Triglycerides 45 mg/dl

His starting lipids are quite favorable (though I don't often see this kind of starting panel nowadays except in athletes). We begin here because this hypothetical man is going to serve as our test subject.

We ask our hypothetical man to load his diet up on "healthy whole grains." He complies by eating whole grain cereals for breakfast, whole wheat toast; sandwiches made with whole grain bread; dinners of whole wheat pasta; snacks of granola bars, whole wheat pretzels and crackers.

Three months later, his lipids show:

Total cholesterol 175 mg/dl
LDL cholesterol 130 mg/dl
HDL 45 mg/dl
Triglycerides 150 mg/dl


You can see that LDL cholesterol has increased, HDL has dropped, and triglycerides have increased. This wave of change is the hallmark of carbohydrate excess, but more specifically of overreliance on wheat products. Beyond his lipid panel, the man has gained 10 lbs, all concentrated in a soft roll around his abdomen, his blood sugar is now in the "borderline range" of between 110 and 126 mg/dl, i.e., pre-diabetic.

If we were to examine this man's advanced lipoproteins (e.g., NMR from Liposcience, or VAP from Atherotech), we would see that there has been an explosive increase in small LDL particles, along with a shift of large HDL to small, and the appearance of multiple abnormal classes of particles called VLDL and IDL (signalling abnormally slowed clearance of dietary by-products from the blood).

Familiar scenario? The "after-carbohydrate" situation is the rule among the people who I first meet who claim to be eating a "healthy" diet, though their patterns are usually much worse, with higher LDL, lower HDL, and much higher triglycerides, an exaggeration of our hypothetical man's abnormalities.

What if our hypothetical man now goes to his conventionally thinking (read "taught medicine by the pharmaceutical industry") physician? What will likely be the advice he receives? Reduce his saturated fat intake, eat plenty of healthy whole grains, take a statin drug.

Although my illustrative man is hypothetical, I've seen this scenario play out many thousands of times. It happens in real life all the time. It is predictable, it is highly manipulable. Sadly, it is rarely recognized for what it is: the result of excess carbohydrates, or what I call "Carbohydrate Intolerance Syndrome."

The misinterpretation of this condition has created 1) an epidemic of diabetes and pre-diabetes, 2) a nation of frustrated obese Americans, 3) a $27 billion per year statin industry, 4) another growth opportunity for the drug industry in diabetes drugs.

Wheat Belly Revisited

Do you have a wheat belly?

When I first coined this phrase back in July, 2007, I had witnessed the phenomenal health effects of wheat elimination in several hundred patients.

In the nearly two years that have passed since my original post, I have witnessed hundreds more people who have done the same: eliminate pretzels, crackers, breads of all sorts, bagels, pasta, muffins, waffles, pancakes, etc.

If anything, I am convinced now more than ever that wheat is among the most destructive foods in the human diet. At least 70% of people who eliminate wheat from their diet obtain at least one, if not several, substantial health benefits.

Now, if I were trying to sell you something, say, an alternative to wheat, then you should be skeptical. If I tell you that drug or nutritional supplement X is great and you should take it, only to follow it with a sales pitch, you should be skeptical.

What am I selling? Nothing. I gain nothing by telling everyone to avoid wheat. In fact, I wish it wasn't true. Wheat foods taste good. Wheat flour makes great comfort foods. In years past, I spent many hours sitting at the bagel shop reviewing papers over a cup of coffee and a bagel. No longer.

So here, back by popular demand, the original Wheat Belly post:



Wheat Belly

You've heard of "beer bellies," the protuberant, sagging abdomen of someone who drinks excessive quantities of beer.

How about "wheat belly"?

That's the same protuberant, sagging abdomen that develops when you overindulge in processed wheat products like pretzels, crackers, breads, waffles, pancakes, breakfast cereals and pasta.



(By the way, this image, borrowed from the wonderful people at Wikipedia, is that of a teenager, who supplied a photo of himself.)

It represents the excessive visceral fat that laces the intestines and triggers a drop in HDL, rise in triglycerides, inflames small LDL particles, C-reactive protein, raises blood sugar, raises blood pressure, creates poor insulin responsiveness, etc.

How common is it? Just look around you and you'll quickly recognize it in dozens or hundreds of people in the next few minutes. It's everywhere.

Wheat bellies are created and propagated by the sea of mis-information that is delivered to your door every day by food manufacturers. It's the same campaign of mis-information that caused the wife of a patient of mine who was in the hospital (one of my rare hospitalizations) to balk in disbelief when I told her that her husband's 18 lb weight gain over the past 6 months was due to the Shredded Wheat Cereal for breakfast, turkey sandwiches for lunch, and whole wheat pasta for dinner.

"But that's what they told us to eat after Dan left the hospital after his last stent!"

Dan, at 260 lbs with a typical wheat belly, had small LDL, low HDL, high triglycerides, etc.

I hold the food companies responsible for this state of affairs, selling foods that are clearly causing enormous weight gain nationwide. Unfortunately, the idiocy that emits from Nabisco, Kraft, and Post (AKA Philip Morris); General Mills; Kelloggs; and their kind is aided and abetted by organizations like the American Heart Association, with the AHA stamp of approval on Cocoa Puffs, Cookie Crisp Cereal, and Berry Kix; and the American Diabetes Association, whose number one corporate sponsor is Cadbury Schweppes, the biggest soft drink and candy manufacturer in the world.

As I've said many times before, if you don't believe it, try this experiment: Eliminate all forms of wheat for a 4 week period--no breakfast cereals, no breads of any sort, no pasta, no crackers, no pretzels, etc. Instead, increase your vegetables, healthy oils, lean proteins (raw nuts, seeds, lean red meats, chicken, fish, turkey, eggs, Egg Beaters, low-fat yogurt and cottage cheese), fruits. Of course, avoid fruit drinks, candy, and other garbage foods, even if they're wheat-free.

Most people will report that a cloud has been lifted from their brains. Thinking is clearer, you have more energy, you don't poop out in the afternoon, you sleep more deeply, some rashes disappear. You will also notice that hunger ratchets down substantially. Most people lose the insatiable hunger pangs that occur 2-3 hours after a wheat-containing meal. Instead, hunger is a soft signal that gently prods you that it's time to consider eating again.

You will also make considerable gains towards gaining control over your risk for heart disease and your heart scan score, a crucial step in the Track Your Plaque program.

Thank you, Crestor

I'm sure everyone by now has seen the Crestor ads run by drugmaker, AstraZeneca. TV ads, magazine ads, and the Crestor website all echoing the same message:

"While I was busy building my life, something else was busy building in my arteries: dangerous plaque."

While previous drug trials with Mevacor, Pravachol, Zocor, and Lipitor have focused mostly on examining whether the drugs reduced incidence of cardiovascular events, Crestor studies have also focused on effects on atherosclerotic plaque volume. The best example is the ASTEROID trial that demonstrated approximately 7% reduction in plaque volume by intracoronary ultrasound.

So the AstraZeneca decision makers took the leap from cholesterol reduction to plaque reduction.

I'm sure this switch wasn't taken lightly, but was the topic of discussion at many meetings before the decision to make plaque reduction the focus of hundreds of millions of dollars of advertising. After all, billions of dollars are at stake in this bloated statin market.

Ordinarily, I couldn't care less about how the drug manufacturers conduct their advertising campaigns. But this one I paid attention to because the Crestor ads are helping fuel a new way of thinking about coronary heart disease: It's not about the cholesterol; it's about the atherosclerotic plaque that accumulates in arteries.

It's not cholesterol that grows, limits coronary blood flow, and causes angina. It's not cholesterol that "ruptures" its internal contents to the surface within the interior of the blood vessel and causes blood clot and heart attack. It's not cholesterol that fragments from the carotid arteries and showers debris to the brain, causing stroke. It's all plaque.

I took the same leap years ago, though not backed by hundreds of millions of dollars of marketing money. When I first called my book Track Your Plaque, some of the feedback I got from editors included comments like "I thought this was a book about teeth!" Even now, the word "plaque" in the book title and website is responsible for confusion.

But AstraZeneca is helping me clear up the confusion. As the word plaque gains hold in public consciousness, it will become increasingly clear that cholesterol reduction is not what we're after. We are looking for reduction of plaque.

If you are trying to develop an effective means to reduce or reverse coronary heart disease, then there are two simple equations to keep in mind:


Plaque = coronary heart disease

Cholesterol ? coronary heart disease


Plaque is the disease, cholesterol is not. Cholesterol is simply a crude risk for plaque.

While I'm no friend to the drug industry nor to AstraZeneca, some good will come of their efforts.

Supermarkets and buggy whips

Will supermarkets eventually phase out, joining the history books as a phenomenon of the past? Or are supermarkets here to stay, an emblem of the industrialization of our food--easy access to foods that are convenient, suit the undiscriminating masses, stripped of nutritional value despite the prominent health claim on the package front?

Anna left an insightful comment on the last Heart Scan Blog post, Sterols should be outlawed, along with some useful advice on how to avoid this trap for poor health called a supermarket:


I rarely shop in regular supermarkets anymore (farm subscription for veggies, meat bought in bulk for the freezer, eggs from a local individual, fish from a fish market, freshly roasted coffee from a local coffee place, etc.). What little else I need comes from quirky Trader Joe's (dark chocolate!), the fish market, farmer's markets, a small natural foods store, or mail order.

When I do need to go into one of the many huge supermarkets near me, not being a regular shopper there, I never know where anything is, so I have to ramble a bit around the aisles before I find what I'm looking for (and I almost always can grab a hand basket, instead of a trolley cart).

It's almost like being on another planet! There's always so many new products (most of them I hesitate to even call food). It's really a shock to the senses now to see how much stuff supermarkets sell that I wouldn't even pick up to read the label, let alone put in a cart or want to taste. I'm not even tempted by 99% of the tasting samples handed out by the sweet senior ladies in at Costco anymore (only thing I remember tasting at Costco in at least 6 mos was the Kerrygold Irish cheese, because I know their cows have pasture access and it's real food).

What's really shocking to me is how large some sections of the markets have become in recent years. While Americans got larger, so did some sections of the supermarket (hint - good idea to limit the consumption of products from those areas). Meat and seafood counters have shrunk, though. Produce areas seem to be about the same size as always (but more of it is pre-prepped and RTE in packaging.

But the chilled juice section is h-u-g-e! And no, I don't think there is a Florida orange grove behind the cases. Come on, how much juice do people need? Juice glasses used to be teeny tiny, for a good reason. To me it looks like a long wall stocked full of sugar water. Avoiding that section will put a nice dent in the grocery expenses.

The yogurt case is also e-n-o-r-m-o-u-s! Your 115 yo Bulgarian "grandmother" wouldn't know what to make of all these "pseudo-yogurts"! Chock full of every possible variety, but very little fit to eat. The only yogurts I'll look at are made with plain whole milk, without added gums, emulsifiers, or non-fat milk solids, and live cultures (I mostly buy yogurt now and then to refresh my starter culture at home). I can flavor them at home if needed. The sterols are showing up in processed yogurts, too, along with patented new strains of probiotic cultures (I'll stick to my old fashioned, but time-proven homemade lacto-cultured veggies and yogurt instead).

I found the same "cooler spread" in the butter & "spread" section. The spread options were just grotesque sounding. Actually, the butter options weren't much better, as many were blended with other ingredients to increase spreadability, reduce calories or cholesterol/saturated fat, etc. A few plain butters were enhanced with "butter flavor" - say what? And on no package could it be determined if the butter came from cows that were naturally fed on pasture or on grain in confined pens.



Well said, Anna.

There's a huge supermarket about 1 mile away from my house similar to the one Anna describes with aisle after aisle of eye-catching cellophane-wrapped foods. I go there about every 3 or 4 months, and then I only go to get something I need in a pinch. Every time I go, I too am reminded just how many products there are that look more like junk food than real food.

But there's no real money in real food. Who gets rich off of selling green peppers, tomatoes, and eggs?

Supermarkets sell these modern industrial foods because people buy it: Look around you. You don't get to be a 250 lb 5 ft 2 inch-woman by eating too many cucumbers.

Like Anna, I drive an additional several miles to Trader Joes', buy at farmers' markets whenever possible, buy some odds and ends like wine and cheese and raw nuts at specialty stores. I grow my own basil in a big pot I keep in the kitchen and we are just about to start turning over the soil in the back yard for our vegetable garden. I don't need nor do I miss having the choice among 40 different chips, 25 brands of ready-made microwavable dinners, an entire aisle of breakfast cereasl (all of which are virtually the same with different names and labels), or 75 varieties of salad dressing.

The supermarket for me--and I hope for many of you--has become a place rarely frequented, and only for the odd forgotten item. Oh, I forgot the dog chewies the grocery does have--my dogs love them. So perhaps they are good for something after all.

Sterols should be outlawed

While sterols occur naturally in small quantities in food (nuts, vegetables, oils), food manufacturers are adding them to processed foods in order to earn a "heart healthy" claim.

The FDA approved a cholesterol-reducing indication for sterols , the American Heart Association recommends 200 mg per day as part of its Therapeutic Lifestyle Change diet, and WebMD gushes about the LDL-reducing benefits of sterols added to foods.


Sterols--the same substance that, when absorbed to high levels into the blood in a genetic disorder called "sitosterolemia"--causes extravagant atherosclerosis in young people.

The case against sterols, studies documenting its coronary disease- and valve disease-promoting effects, is building:

Higher blood levels of sterols increase cardiovascular events:
Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study.

Sterols can be recovered from diseased aortic valves:
Accumulation of cholesterol precursors and plant sterols in human stenotic aortic valves.

Sterols are incorporated into carotid atherosclerotic plaque:
Plant sterols in serum and in atherosclerotic plaques of patients undergoing carotid endarterectomy.




Though the data are mixed:

Moderately elevated plant sterol levels are associated with reduced cardiovascular risk--the LASA study.

No association between plasma levels of plant sterols and atherosclerosis in mice and men.




The food industry has vigorously pursued the sterol-as-heart-healthy strategy, based on studies conclusively demonstrating LDL-reducing effects. But do sterols that gain entry into the blood increase atherosclerosis regardless of LDL reduction? That's the huge unanswered question.

Despite the uncertainties, the list of sterol-supplemented foods is expanding rapidly:




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












HeartWise orange juice contains 1000 mg sterols per 8 oz serving.













Promise SuperShots contains 400 mg sterols per container.














Corozonas has an entire line of chips that contain added sterols, 400 mg per 1 oz serving.














MonaVie Acai juice, "Pulse," contains 400 mg sterols per 2 oz serving.














Kardea olive oil has 500 mg sterols per 14 gram serving.










WebMD has a table that they say can help you choose "foods" that are sterol-rich.

In my view, sterols should not have been approved without more extensive safety data. Just as Vioxx's potential for increasing heart attack did not become apparent until after FDA approval and widespread use, I fear the same may be ahead for sterols: dissemination throughout the processed food supply, people using large, unnatural quantities from multiple products, eventually . . . increased heart attacks, strokes, aortic valve disease.

Until there is clarification on this issue, I would urge everyone to avoid sterol-added "heart healthy" products.


Some more info on sterols in a previous Heart Scan Blog post: Are sterols the new trans fat? .

Texas today, tomorrow . . . the world?

Texas state representative, Rene Oliveira, has introduced legislation that mandates heart scans for adults in the state of Texas.

Rep. Oliveira

A press release from the SHAPE Society ( Society for Heart Attack Prevention and Eradication) reads:

Assessment of heart attack risk on the basis of traditional risk factors alone such as high cholesterol and high blood pressure and so forth, while useful, misses many who are at high risk and also incorrectly flags some for high risk who are in fact at very low risk of near term heart attack; on the other hand detection of atherosclerosis by non-invasive imaging, as suggested by the SHAPE group, accurately identifies plaque and improves the ability to identify at-risk individuals who could benefit from aggressive preventive intervention while sparing low-risk subjects from unnecessary aggressive medical therapy," said Dr. P.K. Shah, Director of Cardiology at Cedars Sinai Heart Institute in Los Angeles, a leading member of the SHAPE Task Force who is also an active member of the American Heart Association. "Sadly, these vulnerable patients go undetected until struck by a heart attack, because insurance companies don't cover the newer heart attack screening imaging tests."


Rep. Oliveira, whose coronary disease was first uncovered by a heart scan and prompted a bypass operation, states:

"It is about time that we cover preventive screening for the number one killer in Texas, and take action to reduce healthcare costs through preventive healthcare. Right now, we are extending the lives of those who can afford the procedure while hundreds of thousands of Texans with hidden heart disease go undetected because of antiquated thinking. The time has come for this change."


Is this what we've come to? Since practicing physicians are either so entranced by the drug and procedural solutions to heart disease, do we need to resort to heart scan by legislation?

It does indeed appear that we've come to this point. Should this trend catch on, it will surely mean an upfront increase in healthcare costs to cover the expense of heart scans. But in the long run, it will mean reduction in healthcare costs--dramatic reduction--if heart scans prompt effective preventive action.

What your doctor doesn't know about heart disease

What causes coronary heart disease or coronary atherosclerotic plaque, this thing that we track with heart scans?

Well, here are a few little-publicized facts about heart disease that you are unlikely to hear from your When's-the-next-stent? cardiologist or the What is there besides statins? primary care doctor.

(Since everybody knows that smoking is a modifiable risk for heart disease that can be readily identified, let's focus on the blood tests that reveal heart disease causes.)


What's the number one most common cause for heart disease?

Small LDL particles. The proliferation and popularity of the snack food/processed food culture, compounded with the "eat more healthy whole grain " propaganda has launched small LDL solidly to first place as the most common reason to have heart attacks, stents, and bypass. All that advice to increase your "healthy whole grain" intake? It increases heart attack risk.


What's the number one most aggressive cause for heart disease?

That's lipoprotein(a), or Lp(a). It's certainly not high cholesterol, though the drug industry loves that you think that. We could argue over whether smoking is more aggressive, but the two are pretty darned close. Combine the two--Lp(a) in a smoker--and the combination is an explosively powerful trigger for heart disease and stroke.


What's the number two cause for heart disease?

After small LDL comes low HDL cholesterol. Ask anyone who has had a heart attack: What was your cholesterol panel like? 9 out of 10 will say "My LDL cholesterol was 135 mg/dl" while knowing little or nothing about HDL, which is commonly in the 30-42 mg/dl range--sufficient to contribute to heart disease risk considerably.


Can "normal" thyroid hormone tests still contribute to heart disease?

Yes. Hypothyroidism is an exceptionally powerful risk factor for heart disease. Many people have been told that their thyroid tests are "normal," when in reality risk for heart disease may be as much as tripled from low thyroid with thyroid blood tests in the "normal" range.


Does a "balanced, healthy diet" prevent heart disease?

No, it does not. In fact, the modern notion of a "balanced, healthy diet" increases risk for heart disease. Of course, the dangers of such diets vary, depending on how you define it. If it's the diet advocated by the USDA Food Pyramid, then it is an enormously destructive diet that causes your health to careen towards both diabetes and heart disease. The American Heart Association TLC diet is little better.


Does eating fish twice a month reduce heart attack risk?

Yes, it does--but just barely. Unfortunately, large studies that show that eating fish as infrequently as twice per month reduce risk for dying from heart attack have led some authorities to suggest that's all you need to do. What they fail to understand is that the benefit is dose-dependent--the greater the intake of omega-3 fatty acids, the greater the benefit (within reason, of course). So, while the effect can be detected by eating fish twice per month, it doesn't mean that full benefits are achieved with this "dose." Full benefits are obtained by mimicking the omega-3 intake of the Japanese.


Do nutritional supplements reduce risk for heart attack?

If you are referring to vitamin D, then, yes, nutritional supplements reduce risk for heart attack . . . enormously. We need more data to validate this phenomenon, though epidemiologic observations strongly bear this out, including the Health Professionals Follow-up Study, the Framingham Heart Study and NHANES, all of which demonstrate a graded effect: the lower the vitamin D blood level, the greater the risk for heart attack.

Over the years, we've experienced more than our share of disappointments in nutritional supplements for heart disease, including vitamin E and B vitamins to reduce homocysteine. But I believe that nothing approaches the solid feel of vitamin D--no other nutritional supplement raises HDL, reduces triglycerides, reduces blood sugar, enhances insulin responses, reduces the inflammatory C-reactive protein, reduces blood pressure like vitamin D. Vitamin D is here to stay--and I'm very grateful.

And don't forget omega-3 fatty acids from fish oil, yet another supplement with unquestioned benefits for reduction of heart attack and death from heart attack.


Why didn't your doctor counsel you on the importance of these issues?

The primary reasons your doctor didn't tell you any of the above:

1) He/she has been persuaded that only drugs are of any real use in health. Nutritional supplements? Hah!

2) Neither the number one cause of heart disease in the U.S.--small LDL particles--nor the most aggressive cause for heart disease--Lp(a)--are corrected by patent-protectable, high profit pharmaceutical agents promoted to your doctor. Instead, these abnormalities can be corrected inexpensively, without prescription. That means no expensive commercials, no media spots, no write-ups in magazines.

3) Your doctor's business is to treat crisis: sore throat, broken ankle, lung tumor, heart attack. Prevent heart disease 10 or 20 years before it shows itself? Heck, no (unless the marketing pull of the drug industry is involved, of course).


It's best that you bear in mind: What your doctor doesn't know can kill you.

Thank you, Dr. Eades


Thanks to some readers of The Heart Scan Blog, I've become acquainted with Dr. Michael Eades' wonderful blog, Health and Nutrition by Dr. Michael R. Eades, MD.

Dr. Eades is co-author (with his wife, Mary Dan Eades, MD) of Protein Power

In one of his conversations, I stumbled on this exchange between Dr. Eades and one of his readers:



Reader: Regarding EBT scans, I looked up the topic on Google and read an informative 5-page article: EBT (Ultrafast CT) Scans - Godsend, or Scam? Dr. Fogoros says that false positives (where the EBT shows the presence of calcium, but the patient has little coronary artery blockage) occur about 50 percent of the time. The next step, if the EBT is positive, is to do a heart catherterization to find out whether there actually is coronary artery blockage. So the odds are that I’d have to worry!

Dr. Michael Eades: The info you got from Google is one of the reasons one shouldn’t get medical information online. As far as I’m concerned the EBT is the BEST way to determine the presence of plaque. If you have a positive calcium score, you have plaque, and there’s an end on’t (as Samuel Johnson would say). Now you may have a low calcium score for your age or you may have a calcium score that doesn’t change, which means you have stable plaque, but if you have a positive calcium score, you have some amount of plaque in your coronary arteries.

And whoever says that the next step to take if you receive a positive calcium score is a coronary artery cath is a real moron. That’s probably the last thing you would want to do if you are asymptomatic. All the cath procedure does is shows whether or not you have a blockage - you can have huge amounts of plaque (which are a disaster waiting to happen) and have a normal cardiac cath.

If you want to get a little more information on the validity of EBT than what you find on Google, take a look at Dr. Davis’ blog or get a copy of his book: Track Your Plaque. I’m not crazy about all of Dr. Davis’ dietary recommendations because he comes to diet from a different perspective than I, but the EBT info in his book is terrific.

Cheers–


Dr. Eades "gets" it. He understands that quantification of coronary plaque is a tool for prevention, not something to be subverted into the service of procedures for the financial benefit of my colleagues.

And I think that he is absolutely correct on the diet discussed in Track Your Plaque--it's due for a revision. I wrote the book in 2003, while we were still locked into the low-fat mindset. Much has changed.

Since then, our enormous experience in metabolic manipulation and lipoprotein analysis has shown that there is a far better way to correct the causes of coronary plaque and seizing hold of heart scan scores. In particular, the explosion of small LDL has prompted major changes in the diet, specifically removal of wheat and cornstarch, the foods that trigger small LDL particles.

(I am still in the midst of negotiations for release of a bigger and better Track Your Plaque II. In the meantime, Track Your Plaque Members can refer to the New Track Your Plaque Diet, Parts I, II, and III.)

Can millet make you diabetic?
















If wheat is so bad, what about all the other grains?

First of all, I demonize wheat because of its top-of-the-list role in triggering:

--Appetite--Wheat increases hunger dramatically
--Insulin
--Blood sugar--Wheat is worse than table sugar in triggering a rapid, large rise in blood sugar
--Triglycerides
--Small LDL particles--the number one cause for heart disease in the U.S.
--Reduced HDL
--Diabetes
--Autoimmune diseases--Most notably celiac disease and thyroiditis.

Most other "healthy, whole grains" aren't quite as bad. It's a matter of degree.

Millet, quinoa, oats, sorghum, bulghur, spelt, barley, cornmeal--While they don't trigger appetite nor autoimmune diseases like wheat does (oat can in some people), they still pose a significant carbohydrate load sufficient to generate the other phenomena like excessive insulin and blood sugar responses. The grams of carbohydrate of these grains are virtually identical to wheat: 43.5 grams per 1/2 cup (uncooked). The exceptions are barley, which is especially loaded with carbohydrates: 104 grams per 1/2 cup, while oats are lower: 33 g per 1/2 cup.

It's all a matter of degree. Some people who are exceptionally carbohydrate-sensitive (like me) can have diabetic blood sugars with just slow-cooked oatmeal or quinoa. Others aren't quite so sensitive and can get away with eating them.

People with high blood sugars (100 mg/dl or greater) can be very sensitive to the blood sugar effects of these grain carbohydrates. The best marker of all are small LDL particles measured on a lipoprotein panel, such as NMR. Small LDL particles are exquisitely sensitive to your carbohydrate intake: small LDL gets worse with excessive sensitivity to grain carbohydrates, gets better with reduction or elimination.

Flagrant small LDL, in combination with low HDL, high triglycerides, and pre-diabetic or diabetic patterns all develop from carbohydrate indulgence, along with "wheat belly."

Don't believe it? The prove it to yourself: Go to Walmart and buy an inexpensive glucose meter and check your blood sugar one hour after eating. You can gauge the health of these foods by observing the blood sugar increases. (Small LDL closely parallels blood sugar rises.)

The grain that fails to trigger any of these abnormal patterns? Flaxseed. Flaxseed is entirely protein, fiber, and healthy oils, with virtually no digestible starches. In fact, flaxseed is one of the few foods that reduces the quantity of small LDL particles.

Are you a tree?

I assume you answered no. Then why would you consider taking the plant form of vitamin D (ergocalciferol)? That's the prescription form of vitamin D, often dispensed as 50,000 unit tablets.

There's nothing wrong with plants. Some of my favorite foods are plants, full of nutritional value.

Then why shouldn't vitamin D2 from plants be every bit as good as the human form of vitamin D?

I believe the issue boils down to taking hormones from non-human sources. (Remember: Vitamin D is a hormone, a very powerful one at that.) Plants can be wonderful sources of flavonoids, fibers, protein, fats, vitamins, minerals, and other healthy components. But hormones?

There are other examples of non-human hormones being given to humans with undesirable or unpredictable effects:

--Xenoestrogens, phytoestrogens, and non-human mammalian estrogens--While non-human estrogens may partially mimic human estrogens, they can also block estrogen effects, or exert altogether novel effects. Non-human mammalian estrogens like Premarin can exert very peculiar (side-)effects, despite their role as prescription estrogen supplementation in humans.

--Progestins--The synthetic versions of human progesterone, like their non-human estrogen counterparts, exert weird effects that are a world apart from real progesterone.

--Sterols--Similar in structure to human cholesterol (while not a hormone, a building block for hormones), sterols have been used to reduce intestinal cholesterol absorption. However, if sterols are absorbed into the blood, they can enormously accelerate growth of atherosclerotic plaque.

--Anabolic steroids--These modifications of the testosterone molecule build muscle, but also cause liver cancer, kidney failure, violent behavior, suicide and homicidal behavior. That's not normal.

Outside of a pharmacologic effect (e.g., prednisone in place of human cortisol), there is no reason to take a non-human hormone in place of a human hormone. For that same reason, there is NO reason to take plant vitamin D2 (prescription or over-the-counter) in place of human vitamin D3.

If the non-human hormone is identical to the human form, then there is no difficulty. The best example of this are thyroid hormones from pigs. That's what Armour Thyroid is, a thyroid hormone replacement that works wonderfully well.

You will notice that virtually all of the examples of non-human hormones substituted for human hormones share one common motivation: profit. Synthetic or modified versions are more readily patent-protectable, unlike their natural counterparts which are not.

Vitamin D2 is an anemic facsimile of the real human hormone, vitamin D3 (cholecalciferol). Stay away from it.

Protecting the right to use bio-identical hormones in your heart disease prevention program

If you've been following the Track Your Plaque program, you know that we are advocates of "bio-identical hormones", i.e., hormone replacement using forms that are identical to the naturally-occuring human form.

In other words, we find it criminal that pharmaceutical manufacturers continue to promote use of non-identical hormones despite a probable increased side-effect and complication profile (a la Premarin). This unhappy situation persists because bio-identical hormones cannot be patent protected, meaning profits cannot be protected. Synthetic hormones can be patented and profits protected, thus their popularity among drug companies.

If that's not bad enough, Wyeth Pharmaceuticals--maker of synthetic hormone preparations, Premarin and Prempro--has filed an FDA petition to disallow the use of bio-identical hormones as prepared and dispensed by "compounding pharmacies". These are specialty pharmacies that mix and dispense hormones like estrogens (human estradiol, estriol, and estrione) and testosterone. They do so only with a doctor's prescription. Most are members of the Professional Compounding Centers of America (www.pccarx.com), a professional organization devoted to promoting quality-control over compounding practices.

Compounding pharmacies are occasionally guilty of compounding some suspect preparations. Witness the Fentanyl lollipops of 2002 in which the pain medication, Fentanyl, was put into lollipops for patients with chronic pain. This posed obvious dangers to any children who unsuspectingly ate the lollipops.

But the majority of compounding pharmacies are not guilty of such exotic practices. Most are simply pharmacies who might, for instance, mix a specific dermatologic preparation according to the orders of a dermatologist. Likewise with bio-identical hormones.

We have extensive experience with such a pharmacy in Madison, Wisconsin, the Women's International Pharmacy. They have filled hundreds of hormone prescription for us. They are responsible in their dispensing practices, in our experience. In fact, they have been at least as good, if not better, than other pharmacies we've dealt with.

We believe in protecting our rights to prescribe and you to use the choice of hormone preparations you and your doctor desire. This should include bio-identical hormones. The transparent profit motive from Wyeth should raise the hairs on your neck.

If you would like to post your comment to the FDA, there's a little time left. The folks at Womens' International Pharmacy have made it easy by posting links on their website. Go to http://www.womensinternational.com and just follow the instructions.



Here's a sample of some of the objections citizens have raised to Wyeth's petition:


I have been taking bioidentical hormones for two years. Bioidentical Hormones have been a great relief to me without the risk. I consult with my Physician who prescribes bio-identical hormones specifically for me, and my pharmacist prepares them. Without this medication and I would not be able to sleep; I would not be able to work due to the constant hot flashes. Without this medication, I find that I have less tolerance and I am considerably disagreeable. I also have problem with my memory without them. I want the bioidentcial hormones for the health benefits they provide. I urge you to not be swayed by Wyeth's petition. The product Premarin made by Wyeth, is made from pregnant horses not natural sources. Wyeth's hormones have been shown to cause cancer. I would not expect my government and its officials to submit to the highly funded petitioning of a pharmaceutical company who product is threatened by bioidentcial hormones. I do not expect my government to approved Wyeth's petition and leave me no choice of bioidentcial hormones and only the choice of Wyeth's cancer causing drugs Preamrin and Prempro. I ask that the FDA reject Wyeth's petition Docket #2005P-0411.

Another petitioner writes:

As a woman I take exception to Wyeth accusing the Compounding Pharmacy industry of unsafe practices. As a citizen of the United States I expect the FDA to stand up for my rights and the rights of all women who have found or in the future may seek consistent, safe and effective treatment with bioidentical hormones. Eliminating options by bowing to a large pharmaceutical company like Wyeth is not in the public interest and would deprive hundreds of thousands of American women from access to bioidentical hormones. Synthetic hormone replacement has been proven unequivocally unsafe in a government sponsored study and should not be forced as the sole treatment option for women. I hereby request the FDA rule against Wyeth's request. The FDA should not close down the bioidentical option of healthcare. I welcome studies of bioidentical hormones even though they are already FDA-approved and have been working effectively for decades. We already have the proof - hundreds of thousands of women, who over the past two decades have chosen bioidentical hormones based on their physicians' assessments. They are living proof that bioidentical hormones are safer and more effective and reliable than synthetic hormone drugs.

A physician and user of bio-identical hormones writes:

Wyeth, the filer of this complaint, is trying to prevent women from being able to choose less expensive compounded options for hormone replacement. There is medical evidence that in modifying the structure of their drugs (such as Premarin and Prempro) so that they could be patented, they may have introduced factors that cause the health risks identified in the Women's Health Initiative. This complaint appears to be filed for commercial purposes because of the market share that has shifted from Wyeth's products to bio-identical products from compounding pharmacies. If the complaint were upheld, patients and their doctors would not have a choice in hormone treatments. Wythe's commercial strategy of trying to eliminate the 'competition' from compounding pharmacies is against the public interest and in the interest of its own corporate profits. Women and their doctors should be able to choose between patented formulations such as those offered by Wyeth, bioidentical formulas available from compounding pharmacies, and no hormone treatment. I have been taking bio-identical hormones for several years and have had excellent results in improving my symptoms. I have been unable to take other synthetic hormones in the past, and am very concerned that my best treatment option will be taken away.

If you get a 64-slice CT coronary angiogram

With new 64-slice CT scanners popping up everywhere nowadays, be sure to get your heart scan with it.

The new scanners do indeed provide wonderful images of the coronary arteries. But, say you have a 20% blockage in one artery by a coronary angiogram generated on one of these devices. What will you do in 1, 2, or 3 years when you want to know if you have progressed? Should you have the CT angiogram repeated?

Well, if you did you'll be exposed to a large dose of radiation--appropriate for a diagnostic test, but not for a screening test. The radiation exposure is not that different from undergoing a full conventional cardiac catheterization, or up to 100 chest x-rays.

"20% blockage" is also, contrary to popular opinion, not a quantitative measure. It is just an estimate of the diameter reduction at one spot. That number says nothing about the lengthwise extent of plaque. It also says nothing about the potential for "remodeling", the phenomenon of artery enlargement that occurs as plaque grows. In other words, if you had another CT coronary angiogram a year later and was told that your blockag was still 20%, in reality you could have had substantial plaque growth but it would not be reflected in that value.

People will come to me after having a CT angiogram for an opinion. Unfortunately, I send them back to their scan center to get a simple coronary calcium score. That measure is easy, quantitative, precise, and can be repeated yearly if necessary to track progression. (Track Your Plaque--I hope most of you get this by now.) Some physicians poke fun at the heart scan, or calcium, score--it's old, boring, only a measure of hard plaque. None of that's true. The coronary calcium score is a measure of total plaque (hard and soft). And when you are empowered to learn how to control and reduce your score, then it's the most exciting number in your entire health program!

Don't fall for the hype. If you go to a scan center and they insist on a 64-slice CT scanner, or if your doctor orders one, you should insist on getting a calcium score out of the test. Just ask. If they refuse, go somewhere else. Centers that refuse to generate a score have one thing on their mind: identifying people with severe blockages sufficient to obtain the downstream financial bonanza--angioplasty, stents, and bypass surgery.

If you have hypertension, think Lp(a)

Clair has coronary disease.

Clair first came to attention at age 57 when she suffered a large heart attack involving the front of her heart (the "anterior wall") two years ago. Her cardiologist implanted a drug-coated stent. Her doctors advised her to "cut the fat" in her diet, exercise, and take Lipitor.

One year later, she required a stent to another artery (circumflex). At this point, Clair was thoroughly demoralized and terrified for her future. Her first heart attack left her heart muscle with only 50% of normal strength.

She came to my office for another opinion. Of course, one of the first things we did was to identify all causes of her heart disease. No surprise, Clair had 7 new causes not previously identified, including low HDL (37 mg/dl), a severe small LDL particle pattern (75% of all particles were small), and Lp(a).

Her blood pressure was also 190/88, despite her relatively slender build and 3 medications that reduced blood pressure. That's a Lp(a) effect: Exagerrated coronary risk along with unexpected hypertension that often seems inappropriate.

In fact, I saw several patients just this week with lipoprotein(a), Lp(a), and exagerrated high blood pressure (hypertension). It's not that uncommon.

Though it has not been described in the medical literature, our experience is that hypertension is a prominent part of the entire Lp(a) "syndrome".

Lp(a) is responsible for much-increased potential for coronary disease (coronary plaque). It increases in importance as estrogen recedes in a woman (pre-menopause and menopause) and testosterone in a man, since both hormones powerful suppress Lp(a) expression (though why and how nobody knows).

I believe that Lp(a) is also responsible for hypertension that most commonly develops in a persons mid-50s and onwards, often with a vengeance. 3 or 4 anti-hypertensive medications and still not controlled.



Role of l-arginine

L-arginine may be more helpful in this situation than others. L-arginine, recall, is the supply for your body's nitric oxide, a powerful dilator of the body's arteries and thereby reduces blood pressure. We use 6000 mg twice a day, a large dose that requires use of powder preparations rather than capsules.

More reading about l-arginine and nitric oxide is available through Nobel laureate, Dr. Louis Ignarro's book, NO More Heart Disease : How Nitric Oxide Can Prevent--Even Reverse--Heart Disease and Stroke, available at Amazon.com ( http://www.amazon.com/gp/product/0312335814/104-1247258-6443909?v=glance&n=283155).




Will l-arginine truly reverse heart disease on its own? No, I don't believe so. Contrary to Dr. Ignarro's extravagant claims, I find l-arginine a facilitator of plaque regression, i.e, it helps other strategies achieve regression, but it does not achieve regression or reversal by itself. (Note that Dr. Ignarro is a lab researcher who studies rats and has never treated a human being.)

But l-arginine may have special application in the person with lp(a), particularly if hypertension is part of the syndrome.


Note: As always, please note that I talk frankly about l-arginine and other supplements and medications but have no hidden agenda: I am not selling anything, nor am I affiliated with any source/website/store etc. that sells these products. If I advocate something, I do so because I truly believe it, not because I'm trying to sell something. I make this point because so much nonsense is propagated in the media because of profit-motive. That's not true here.

Dr. Ornish: Get with the program!


In the era up until the 1980s, most Americans indulged in excessive quantities of saturated fats: fried chickem, spare ribs, French fries, gravy, bacon, Crisco, butter, etc.

Along came people like Nathan Pritikin and Dr. Dean Ornish, both of whom were vocal advocates of a low-fat nutritional approach. In their programs, fat composed no more than 10% of calories. This represented a dramatic improvement--at the time.


In 2006, a low-fat diet is a perversion of health. It means over-reliance on breads, breakfast cereals, pasta, crackers, cookies, pretzels, etc., the foods that pack supermarket shelves and that now constitute 70-80% of most Americans' diet.

Dr. Ornish still carries great name recognition. As a result, his outdated concepts still gain media attention. The June, 2006 issue of Reader's Digest, in their RDHealth column, carried an interview with Dr. Ornish in which he reiterates his fat-phobia.

However, on this occasion he takes a different tack. This time he rails against the "dangers" of fish oil and omega-3 fatty acids. "I've recently learned that omega-3s are a double-edged sword...In some cases, omega-3s could be fatal."

He goes on to say that, while he believes that fish oil may prevent heart attacks, it has fatal effect if you already have heart disease.

Does this make sense to you?

He's basing his views on a single, obscure study published in 2003 conducted in rural England that showed an increase in death and heart attack on fish oil. Most authorities have not taken these findings seriously, since they are wildly contrary to all other observations and because the study had some design flaws.

Despite the fact that this isolated study runs counter to all other, better-conducted studies seems not to matter to Dr. Ornish.

Clinging to the low-fat concept is like hoping 8-track tapes will make a comeback. It's not going to happen. We enjoyed the benefits while they lasted, appropriate for the era. But now, they're woefully outdated.

The overwhelming evidence is that fish oil provides tremendous benefits with little or no downside. In the Track Your Plaque program, fish oil remains a crucial supplement to gain control over your coronary plaque and stop or reduce your heart scan score. Ignore the doomsday preachings of Dr. Ornish.

(Watch for an article I wrote updating the benefits of fish oil for Life Extension magazine.)

The cholesterol fallacy

Evan spotted the kiosk set up in the middle of the local mall. "Free cholesterol screenings. Know your heart health!" the sign declared.

It was a free cholesterol screening being offered by a local hospital.

The friendly nurse behind the kiosk had Evan fill out a form, then pricked his finger. Five minutes later, she reported to him with a smile, "Sir, your cholesterol is 177--your heart's fine! We get concerned when cholesterol is over 200. So you're in a safe range."

What the nurse failed to recognize is that Evan's HDL was 30 mg, a low value that actually places him at high risk for heart disease. Low HDL also signifies high likelihood of the small LDL particle pattern, a marked predisposition towards pre-diabetes and diabetes, a probable over-reliance on processed carbohydrates in his diet, a dramatically increased probability of hidden inflammation (e.g., elevated C-reactive protein), increased tendency for high blood pressure. . .

In other words, Evan's "favorable" total cholesterol is, in truth, nonsense. It's misleading, falsely reassuring, and provided none of the insight that a real effort might have yielded. Like hippies, tie-dye, other relics of the 1960s, total cholesterol needs to be put to rest. It has served many people poorly and been responsible for countless deaths.

When you see a kiosk or other service like this, even if it's free, run the other way.

"Heart disease a growth business"





So announced a Boston newspaper recently, featuring a story about new heart program at a local hospital.

They were announcing how a hospital had entered the cardiovasculare procedure game and how it would boost their bottom line. The article discussed how the hospital administration was anticipating "a surge in patients from the baby boom generation."

To justify this new program, the article quoted an administrator from another hospital: "Cardiovascular issues is [sic] the number one cause people sought treatment at our hospital."

The hospital featured in the story had spent $13.5 million dollars to develop their program.

Do you think they'll make it back?

You bet they will--many times over. Hospitals are businesses, complete with a bottom line, an expectation of profit and an eye towards growth.

The hospitals in the city where I live (Milwaukee, Wisconsin) are, as in Boston and elsewhere, very aggressive--expanding into new territories, hiring new "salesmen" (physicians), all to capture more marketshare and produce more "product" (your coronary angioplasty, stent, bypass surgery, defibrillator, etc.).

The equation for hospital profits is tried and true. Ignore your heart disese risk and you can help your local hospital grow its business. Neglect to get your heart scan and you can help your hospital pay down its debt. Get a heart scan, then do nothing about it, and you may even justify a pay raise for the hospital administrators for record revenue growth and profit.

Hospitals are a growth business because of the failure of most people and their doctors to 1) identify hidden coronary disease (CT heart scan to obtain your heart scan score), then 2) seize control over it (the Track Your Plaque program or, at least, your doctor's guidance along with your efforts at prevention).

Unless you do so, you are highly likely to help your hospital boost its annual goal for procedures.

The myth of small LDL

Annie's doctor was puzzled.

Despite an HDL cholesterol of 76 mg (spectacular!) and LDL of 82 mg, her CT heart scan showed a score of 135. At age 51, this placed her in the 90th percentile.

Not as bad, perhaps, as her Dad might have had, since he died at age 54 of a heart attack.

So we submitted blood for lipoprotein testing. Surprise! over 90% of all her LDL particles were small. (By NMR, they're called "small". By gel electropheresis, or the Berkeley Lab test, or VAP (Atherotech) technique, they're called "HDL3".)

What gives? Traditional teaching in the lipid world is that if HDL equals or exceeds 40 mg/dl, then small LDL will simply not be present.

Well, as you can see from Annie's experience, this is plain wrong. Yes, there is a graded, population-based effect--the lower your HDL, the greater the likelihood of small LDL. But small LDL is remarkably persistent and prevalent--regardless of your HDL.

We've seen small LDL even with HDLs in the 90's! I call small LDL the "cockroach" of lipids. If you think you have it, you probably do. Getting rid of small LDL requires a specific bug killer. (Track Your Plaque Members: Read Dr. Tara Dall's interview on small LDL.)

Don't let anybody blow off your request for lipoprotein testing just because your HDL is high. That's just not acceptable. Loads can be wrong even with a favorable HDL.

My stress test was normal. I don't need a heart scan!

Katy had undergone a stress test while being seen in an emergency room, where she'd gone one weekend because of a dull pain on the right side of her chest. After her stress test proved normal, she was diagnosed (I believe correctly) with esophageal reflux, or regurgitation of stomach acid up the esophagus. She was prescrbed an acid-suppressing medication with complete relief.

But Katy also had coronary plaque. Three years ago, her CT heart scan score was 157. She'd made efforts to correct the multiple causes, though she still struggled with keeping weight down to gain full control over her small LDL particle pattern.

I felt it was time for a reassessment: another heart scan. After three years, without any preventive efforts, Katy's score would be expected to have reached 345! (That's 30% per year plaque growth.) It's a good idea to get feedback on just how much slowing you've accomplished.

But Katy declared, "But I didn't think another heart scan was necessary. My stress test was normal!"

What Katy was struggling to understand was that even at the time of her first scan, a stress test would have been normal. Plaque can be present with a normal stress test.

Plaque can even show explosive growth all while stress tests remain normal. Just ask former President, Bill Clinton, how much he should have relied on stress tests. (Mr. Clinton underwent annual stress nuclear tests. All were normal and he had no symptoms--all the way up 'til the time he needed urgent bypass surgery!)

Of course, at some point even a crude stress test will reveal abnormal results. But that's years into your disease and a lot closer to needing procedures and experiencing heart attack.

So, yes, Katy would benefit from another heart scan despite her normal stress test.

The message: Don't rely on stress tests to gauge whether or not plaque has grown, stabilized, or reversed. Stress tests can be used to gauge the safety of exercise, blood pressure response, and the potential for abnormal heart rhythms. Stress tests can be used as a method to determine whether blood flow in your coronary arteries is normal through an area with plaque.

But a stress test cannot be used to gauge whether plaque has grown. It's as simple as that. Gauging plaque growth requires a heart scan.

Patient-napping: Yet another reason to stay clear of hospitals!

When I started practicing medicine around 20 years ago, it was common practice to alert a physician when their patient was seen in an emergency room.

If John Smith, for example, went to the emergency room with chest pain, the physician who had an established relationship with the patient--knew their history, had managed their health and illnesses, etc.--was notified, even if the hospital ER had no relationship with the physician. It was not uncommon for the patient to then be transferred to the hospital where their own doctor practiced.

Though cumbersome at times, it preserved the relationship of the patient with their doctor.

Over the past few years, this practice has crumbled. Nowadays, hospitals and their employed physicians (and other unscrupulous physicians acting in the name of profit) "fail" to notify the physician with an established relationship.

Guess what happens? The patient all too often ends up being put through the gamut of testing and procedures.

Why? For hospital profit, of course. If failure to notify a doctor who's had a 10-year long relationship with the patient is "overlooked" or, even more commonly, it's "unsafe" to transfer the patient because the patient is too "unstable" to be transferred, then this patient becomes ripe for picking--heart catheterization, stents, bypass surgery, etc. Ten's, if not hundreds, of thousands of dollars can be reaped by this deception. I call it "patient-napping".

I see this at least several times every month. As hospitals are becoming increasingly competitive, and as they put pressure on their physicians to churn patients for revenues, you're going to see more and more of this.

As always, what is your protection from this expanding influence of hospitals and the doctors too meek to stand up to them? Education and information. Arm yourself with an understanding of what is accomplished in hospitals, when you truly need them, and when you don't.

Take it one step further. At least from a heart disease standpoint--the #1 profit-maker for hospitals--aim to 1)identify your coronary plaque, then 2) seize control over your coronary plaque and reduce your risk for heart attack and heart procedures as much as humanly possible. That's the goal of the Track Your Plaque program.

Don't believe the negative press on fish oil



A British Medical Journal study released in March, 2006 has prompted a media flurry of reports on the worthlessness of fish oil. (Hooper L, Thompson RL, Harrison RA et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: a systematic review. BMJ March,2006)

Don't believe it for a second.

First of all, the study was a re-analysis of the existing published scientific literature. It was not a new study. It included a wild conglomeration of different clinical observations, as the studies examining fish oil over the years have been extraordinarily heterogeneous--in populations examined, omega-3 supplement (e.g., fish vs. capsule), period of observation, endpoints measured.

The results were skewed by inclusion of a moderate-sized British study by Burr et al in men with angina. In this study, no benefit was demonstrated and, in fact, a negative effect--more heart attack and death--was observed with fish oil. This was not news, since the study was published in 2003. It's results have been a mystery to everyone, since its unexpected negative result for fish oil was so starkly different from virtually every other study that preceded it (suggesting a study flaw or statistical fluke).

Nonetheless, the Burr study served to throw off the overall analysis. It diluted the dramatic and persuasive outcome of the GISSI-Prevenzione Study of 11,000 people in which a 28% reduction in heart attack and 45% reduction in cardiovascular death was observed. Note that the substantial numbers of the GISSI make the study's outcome nearly unassailable.

Another important fact: fish oil is among the most powerful tools available to correct elevated triglycerides. Drops of 50% are common. Recall that triglycerides are a necessary ingredient to create the nasty LDL, as well as VLDL, Intermediate-density lipoprotein, and an undesirable shift from large to ineffective small HDL. Reducing triglycerides is therefore crucial for your plaque control program.

This re-analysis serves to prove nothing. Such analyses can only pose questions for further study in a real study like GISSI: a randomized (random participant assignment), controlled (treatment vs. placebo or other treatment) study.

The weight of evidence remains heavily in favor of fish oil, not only as helpful, but fabulously beneficial, particularly for anyone aiming to reduce coronary plaque.
All posts by william-davis

Genetic vs. lifestyle small LDL

Let me explain what I mean by "genetic small LDL." I think it helps to illustrate with two common examples.

Ollie is 50 years old, 5 ft 10 inches tall, and weighs 253 lbs. BMI = 36.4 (obese). Starting lipoproteins (NMR):

LDL particle number 2310 nmol/L
Small LDL: 1893 nmol/L
(1893/2310 = 81.9% of total, a severe small LDL pattern)


Stan is 50 years old, also, 5 ft 10 inches tall, and weighs 148 lbs. BMI = 21.3. Starting lipoproteins:

LDL particle number 1424 nmol/L
Small LDL 1288 nmol/L
(1288/1424 = 90.4% of total, also severe)


Both Ollie and Stan go on the New Track Your Plaque diet and eliminate wheat, cornstarch, and sugars, while increasing oils, meats and fish, unlimited raw nuts, and vegetables. They add fish oil and vitamin D and achieve perfect levels of both. Six months later, Ollie has lost 55 lbs, Stan has lost 4 lbs. A second round of lipoproteins:

Ollie:

LDL particle number 1810 nmol/L
Small LDL: 193 nmol/L
(193/1810 = 10.6% of total)


Stan:

LDL particle number 1113 nmol/L
Small LDL 729 nmool/L
(729/1113 = 65.4% of total)


Ollie has reduced, nearly eliminated, small LDL through elimination of wheat, cornstarch, and sugars, along with weight loss, fish oil, and vitamin D.

Stan, beginning at a much more favorable weight, reduced both total and small LDL with the same efforts, but retains a substantial proportion (65.4%) of small LDL.

Stan's pattern is what I call "genetic small LDL." Of course, this is a presumptive designation, since we've not identified the specific gene(s) that allow this (e.g., gene for variants of cholesteryl ester transfer protein, hepatic lipase, lipoprotein lipase, and others). But it is such a sharp distinction that I am convinced that people like Stan have this persistent pattern as a genetically-determined trait.

Carbohydrate sins of the past

Fifty years ago, diabetes was a relatively uncommon disease. Today, the latest estimates are that 50% of Americans are now diabetic or pre-diabetic.

There are some obvious explanations: excess weight, inactivity, the proliferation of fructose in our diets. It is also my firm belief that the diets advocated by official agencies, like the USDA, the American Heart Association, the American Dietetic Association, and the American Diabetes Association, have also contributed with their advice to eat more “healthy whole grains.”

When I was a kid, I ate Lucky Charms® or Cocoa Puffs® for breakfast, carried Hoho’s® and Scooter Pies® in my lunchbox, along with a peanut butter sandwich on white bread. We ate TV dinners, biscuits, instant mashed potatoes for dinner. Back then, it was a matter of novelty, convenience, and, yes, taste.

What did we do to our pancreases eating such insulin-stimulating foods through childhood, teenage years, and into early adulthood? Did our eating habits as children and young adults create diabetes many years later? Could sugary breakfast cereals, snacks, and candy in virtually unlimited quantities have impaired our pancreas’ ability to produce insulin, leading to pre-diabetes and diabetes many years later?

A phenomenon called glucose toxicity underlies the development of diabetes and pre-diabetes. Glucose toxicity refers to the damaging effect that high blood sugars (glucose) have on the delicate beta cells of the pancreas, the cells that produce insulin. This damage isirreversible: once it occurs, it cannot be undone, and the beta cells stop producing insulin and die. The destructive effect of high glucose levels on pancreatic beta cells likely occurs through oxidative damage, with injury from toxic oxidative compounds like superoxide anion and peroxide. The pancreas is uniquely ill-equipped to resist oxidative injury, lacking little more than rudimentary anti-oxidative protection mechanisms.

Glucose toxicity that occurs over many years eventually leaves you with a pancreas that retains only 50% or less of its original insulin producing capacity. That’s when diabetes develops, when impaired pancreatic insulin production can no longer keep up with the demands put on it.

(Interesting but unanswered question: If oxidative injury leads to beta cell dysfunction and destruction, can antioxidants prevent such injury? Studies in cell preparations and animals suggest that anti-oxidative agents, such as astaxanthin and acetylcysteine, may block beta cell oxidative injury. However, no human studies have yet been performed. This may prove to be a fascinating area for future.)

Now that 50% of American have diabetes or pre-diabetes, how much should we blame on eating habits when we were younger? I would wager that eating habits of youth play a large part in determining potential for diabetes or pre-diabetes as an adult.

The lesson: Don’t allow children to repeat our mistakes. Letting them indulge in a lifestyle of soft drinks, candy, pretzels, and other processed junk carbohydrates has the potential to cause diabetes 20 or 30 years later, shortening their life by 10 years. Kids are not impervious to the effects of high sugar, including the cumulative damaging effects of glucose toxicity.

Saturated fat and large LDL

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles


For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Is glycemic index irrelevant?



University of Toronto nutrition scientist, Dr. David Jenkins, was the first to quantify the phenomenon of "glycemic index," describing how much blood sugar increased over 90 minutes compared to glucose. The graph is from their 1981 study, The glycemic index of foods: a physiologic basis for carbohydrate exchange. The research originated with an effort to characterize carbohydrates for diabetics to gain better control over blood sugar.

Since Dr. Jenkins’ original work, thousands of clinical studies have been performed by others exploring this concept. The food industry has also devoted plenty of effort exploiting it (e.g., low-glycemic index noodles, low-glycemic index cereals, etc.).

Most Americans are now familiar with the concept of glycemic index. You likely know that table sugar has a high glycemic index (60), increasing blood sugar to a similar degree as white bread (glycemic index 71). Oatmeal (slow-cooked) has a lower glycemic index (48), since it increases blood sugar less than white bread.

A number of studies have shown that when low glycemic index foods replace high glycemic index foods (e.g., whole wheat bread in place of cupcakes), people are healthier: less diabetes, less heart attack, less high blood pressure. Books have been written about glycemic index, touting its benefits for health and weight control. Health-conscious people will try to substitute low-glycemic index foods for high-glycemic index foods.

So what’s not to like here?

There are several fundamental flaws with the notion that low-glycemic index foods are good for you:

1) Check your blood sugar after a low-glycemic index food like oatmeal. Most non-diabetic adults will show blood sugars in the 140 to 200 mg/dl range. The more central (visceral) fat you have, the higher the value will be. In other words, an apparently “healthy” whole grain food like oatmeal can generate extravagantly high blood sugars. Repeated high blood sugars of 125 mg/dl or greater after eating increase heart disease risk by 50%.

2) Foods like whole wheat pasta have a low glycemic index because the blood sugar effect over the usual 90 minutes is increased to a lesser degree. The problem is that it remains increased for an extended period of up to several hours. In other words, the blood sugar-increasing effect of pasta, even whole grain, is long and sustained.

3) Low-glycemic index foods trigger other abnormalities, such as small LDL particles, triglycerides, and c-reactive protein (a measure of inflammation). While they are not as bad as high-glycemic index foods, they are still quite potent triggers.

Low-glycemic index foods trigger the very same responses as high-glycemic index foods—they’re just less bad. But less bad does not equate to good. Low-glycemic index foods cause weight gain, trigger appetite, increase blood pressure, and lead to the patterns that cause heart disease.

High-glycemic index foods are bad for you. This includes foods made with white flour (bagels, white bread, pretzels). Low-glycemic foods (whole grain bread, whole wheat crackers, whole wheat pasta) are less bad for you—but they are not necessarily good.

Don’t be falsely reassured by foods because they are billed as “low-glycemic index.” View low-glycemic index foods as indulgences, something you might have once in a while, since a slice of whole grain bread is really not that different from a icing-covered cupcake.

What Mr. Clinton did NOT do

You've likely already heard that former President Bill Clinton underwent a heart catheterization today during which one of the bypass grafts to his coronary arteries was found to be occluded. The original coronary artery was therefore stented.

Dr. Alan Schwartz, Mr. Clinton's cardiologist, announced to the gathered press that Mr. Clinton had followed a good diet, had adopted a regular exercise program, but that his condition is a "chronic disease" like hypertension that is not cured by these efforts.



Needing a stent just 6 years after four bypass grafts are inserted is awfully soon. I would propose that it has less to do with having a "chronic disease" and more to do with all the things that Mr. Clinton likely is NOT doing. (In addition to all the other things that Mr. Clinton did not do.) In other words, in the Track Your Plaque world, procedures are a rarity, heart attacks virtually unheard of. I would wager that Mr. Clinton has been doing none of the following:

--Taking fish oil. Or, if his doctor was "advanced" enough to have advised him to take fish oil, not taking enough.
--Vitamin D--Followers of the Heart Scan Blog already know that vitamin D is the most incredible health find of the last 50 years, including its effects on reducing heart disease risk. Unless Mr. Clinton runs naked in a tropical sun, he is vitamin D deficient. A typical dose for a man his size is 8000 units per day (gelcap only!).
--Eating a true heart healthy diet. I'll bet Mr. Clinton's doctor, trying to do the "right" thing, follows the prudent course of advising a "balanced diet" that is low in fat--you know, the diet that causes heart disease. Judging by Mr. Clinton's body shape (central body fat), it is a virtual certainty that he conceals a severe small LDL pattern, the sort that is worsened by grains, improved with their elimination.
--Making sure that hidden causes are addressed--In addition to the "hidden" small LDL, lipoprotein(a) is another biggie. Lp(a) tends to be the province of people with greater than average intelligence. I believe Mr. Clinton qualifies in this regard. I would not be at all surprised if Mr. Clinton conceals a substantial lipoprotein(a) pattern, worsened in the presence of small LDL.
--Controlling after-meal blood sugars--Postprandial (after-eating) blood sugars are a major trigger for atherosclerotic plaque growth. There are easy-to-follow methods to blunt the after-meal rise of blood sugar. (This will be the subject of an in-depth upcoming Track Your Plaque Special Report.)
--Thyroid normalization--It might be as simple as taking iodine; it might involve a little more effort, such as supplemental T3. Regardless, thyroid normalization is an easy means to substantially reduce coronary risk and slow or stop coronary plaque growth.


It's not that tough to take a few steps to avoid bypass surgery in the first place. Or, if you've already had a procedure, a few additional steps (of the sort your doctor will likely not tell you about) and you can make your first bypass your only bypass.

Magnesium and arrhythmia

Because magnesium is removed during municipal water treatment and is absent from most bottled water, deficiency of this crucial mineral is a growing problem.

Magnesium deficiency can manifest itself in a wide variety of ways, from muscle cramps (usually calves, toes, and fingers), erratic blood sugars, higher blood pressure, to heart rhythm problems. The abnormal heart rhythms that can arise due to magnesium deficiency include premature atrial contractions, premature ventricular contractions, multifocal atrial tachycardia, atrial fibrillation, and even ventricular tachycardia, fibrillation, and Torsade de Pointes (all potentially fatal). Magnesium is important!

Magnesium supplementation is therefore necessary for just about everybody to maintain normal tissue levels. (The exception is people with kidney disorders, who should not take magnesium without supervision, since they retain magnesium.)

Here is a Heart Scan Blog reader's dramatic rhythm-correcting response to magnesium supplementation:



Dr. Davis,

A few months ago, I contacted you inquiring if you had written any articles on arrhythmia. You were generous enough to answer and guide me to an LEF article you'd written in which you stressed fish oil and magnesium. I had been suffering with bad PVCs [premature ventricular contractions] for over 20 years, and they had gotten so bad recently that I was told my next options were ablation or pacemaker!

I was already on fish oil and had not seen any difference, and so I researched the magnesium you suggested more thoroughly and found a huge body of studies supportng its effect on arrhythmia. I also read many posts on heart forums with people having success with it. After getting advice from various bloggers, I tried magnesium taurate in the morning and Natural Calm (an ionized form of mag citrate) in the afternoon and evening. Within three days the PVCs were quite diminished and by 2 weeks totally gone! As long as I keep taking it, they never return---not even one irregular blip---even when I drink strong coffee! The magnesium also cleared up my restless leg syndrome, my eye twitching, and insomnia. (Apparently, I was the poster-girl for magnesium deficiency.)

I am so angry that after all these years of suffering, trying various medications, and seeing at least 4 different cardiologists that NOT ONE ever even mentioned trying magnesium. The generosity of the few minutes you took to answer my email and steer me in a helpful direction brought me total relief.

Thank you SO MUCH!

Warmly,
Catherine C.

Video teleconference with Dr. Davis


Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil



Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Thinner by Thursday

You want to lose a few pounds . . . Okay, maybe 50 or 75.

Should you exercise? Lengthen you workout? Push the plate away, deny yourself seconds, use a smaller plate?

Of all the weight loss strategies I've tried in patients, there's only one that stands out as a means of obtaining immediate--meaning within 3 days--weight reduction.

Wheat elimination.

Omega-3 Index: 10% or greater?

We've previously considered the question:

What is an ideal level of omega-3 fatty acids in the blood?

Recall that omega-3 levels in red blood cells (RBCs), a measure called the "omega-3 index," have been associated with risk for sudden cardiac death:





In a recent analysis, 265 people experiencing sudden death during a heart attack (ventricular fibrillation, successfully resuscitated) showed an omega-3 index of 4.88%, while 185 people not experiencing sudden death during a heart attack showed an omega-3 index of 6.08%.

We have more ambitious goals than just avoiding sudden death, of course! How about the omega-3 index associated with reduced risk for heart attack? A recent analysis of females from the Harvard School of Public Health suggested that RBC omega-3 levels as high as 8.99% were still associated with non-fatal heart attack (myocardial infarction), compared to 9.36% in those without heart attacks, suggesting that even higher levels are necessary to prevent non-fatal events.

Most recently, another study comparing 50 people after heart attack with 50 controls showed that people with heart attack had an omega-3 index of 9.57% vs 11.81% in controls--even higher. (This study was in a Korean population with higher fish consumption. There was also a powerful contribution to risk from trans fat RBC levels.) The investigators concluded: "The area under the receiver operating characteristic curve of fatty acid profiles was larger than that for traditional risk factors, suggesting that fatty acid profiles make a higher contribution to the discrimination of MI cases from controls compared with modified Framingham risk factors."

The data suggest that, while an omega-3 index of 7.3% is associated with reduced risk for sudden cardiac death, a higher level of 10% or greater is associated with less risk for heart attack. Surprisingly, fish consumption and fish oil intake account for only 47% of the variation in omega-3 index.

I believe the emerging data are becoming increasingly clear: If you desire maximal control over heart health, know your omega-3 index and keep it 10% or higher.

Let's soak 'em with fish oil

If you don't think that charging drug prices for fish oil is wrong, take a look at a letter from an angry Heart Scan Blog reader:


Hello Dr. Davis,

My 44 year old brother had an MI [myocardial infarction, or heart attack] in June. He got pushed around due to "bad government insurance," a state-run program for the "uninsured": government pays 1/3, job pays 1/3, and individual pays 1/3.

What they didn't tell him is that there is no major medical coverage and little to no prescription coverage. We fought for 4 months to get him open heart surgery that the insurance was not going to pay for.

Now, with no assistance, terrible insurance, and no disability he has little to no income. He is a heavy equipment mechanic and is trying to be the "good American"-- take care of his bills, not file bankruptcy, etc.

Anyway, the doctors never seem to pay attention to what they prescribe. Lipitor was not working for him, due to side effects. Now they want to give him Zetia and Lovaza....Zetia at $114, and Lovoza is $169.85! Wow! For dead fish???? I think this is a little fishy! I looked up Lovaza, gee how nice, they will give you a $20 coupon....

Forget it, he can't afford this stuff. So I am All posts by william-davis

Statin stupid

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

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

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

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

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

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

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

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

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

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

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

I just got back from Jimmy Moore's low-carb cruise to the Bahamas.

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

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

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






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

Oatmeal: Good or bad?


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

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

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

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

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

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

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

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

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

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

Mustard: Super health food?

Could mustard--yes, the yellow condiment you smear on hot dogs--be a super heart healthy food in disguise?

Consider that mustard contains:

Vinegar

Turmeric

No appreciable sugar


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

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

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

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

Exercise and blood sugar

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

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

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

Think about it. Reduced blood sugar:

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

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

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

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

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