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.
All posts by william-davis

Does high cholesterol cause heart disease?

How often does someone develop coronary heart disease from high cholesterol alone?

Believe drug industry propaganda and you'd think that everyone does. Physicians have bought into this concept also, driving the $27 billion annual sales in statin cholesterol drugs.

In my experience, I can count the number of people who develop coronary disease from high cholesterol alone on one hand. It happens--but rarely.

That's not to say that cholesterol is not an issue. That rant populates many of the kook websites and conversations on the internet that argue that high cholesterol is a surrogate for some other health issue, or that it is part of a medical conspiracy.

The problem with conventional measurement of cholesterol is that it ignores the particle size issue: whether particles are large or small. Small LDL are flagrant causes of coronary atherosclerotic plaque. Large LDL is a rather meager cause. Simple cholesterol measurement also ignores the presence of other factors that lead to heart disease, like lipoprotein(a) and vitamin D deficiency.

Conventional total and LDL cholesterol do not distinguish between large and small particles, nor reveal the presence of other hidden patterns. An LDL cholesterol of 150 mg/dl, for instance, may contain 100% large LDL--a relatively good situation that by itself is unlikely to cause heart disease, or it might contain 100% small LDL--a very bad situation that is likely to cause heart disease. Just knowing that LDL is 150 mg/dl tells you almost nothing. In 2008, most people have some mixture of the two, particularly with the proliferation of "healthy whole grains" in the American diet, foods that trigger formation of small LDL.

The imprecision and uncertainty of conventional total and LDL cholesterol has provided ammunition for some to discount the entire cholesterol concept. And they are right to a degree: cholesterol by itself is indeed a lousy predictor of heart disease. But small LDL is a very reliable predictor of potential for heart disease. Dismissing the entire concept because the standard measurement stinks is not right, either.

It is therefore an unfortunate oversimplification to say that high cholesterol causes heart disease or that it doesn't. It can--but not always, depending on size and other factors. In my view, it is therefore irreponsible to treat total or LDL cholesterol without knowledge of particle size. I've seen this play out many times: Someone with an LDL cholesterol of 150 mg/dl but all large still gets prescribed a statin drug by his/her doctor. Or someone with an LDL of 100 mg/dl--generally "favorable" by most standards--is not treated but it is all small and the person is truly at high risk. (Also, knowledge that all LDL particles are small does not mean that statins are the preferred agent. In my view, they are not.)

Are humans meant to be omnivores?

Are humans meant to be omnivores?

Does the ideal human diet include animal products like meat, fish, cheese, eggs, and dairy products?

Or should the ideal diet be devoid of all animal products?a vegetarian diet?

Though the argument is distorted by modern food processing methods (e.g., factory farming, long-term administration of antibiotics), convenience foods, and pseudo-foods crafted by food manufacturers, there are, obviously, proponents of both extremes.

The Atkins’ diet, for instance, advocates unrestricted intake of animal products, regardless of production methods or curing (sausage and bacon). At the opposite extreme are diets like Ornish (Dr. Dean Ornish’s Program for Reversal of Heart Disease) and the experiences of Dr. Colin Campbell, articulated in his studies and book, The China Study, in which he lambasts animal products, including dairy, as triggers for cancer and heart disease.

So which end of the spectrum is correct? Or ideal?

For the sake of argument, let's put aside philosophical questions (like not wanting eat animal products because of aversion to killing any living being) or ethical concerns (inhumane treatment of farm animals, cruel slaughtering practices, etc.). Does the inclusion of animal products provide advantage? Disadvantage?

The traditional argument against animal products has been saturated fat. If we accept that we’ve demoted the saturated fat question to a place far down the list of importance (though this is yet another argument to discuss another time), several questions emerge:

• If humans were meant to be vegetarian, why do omega-3 fatty acids (mostly from wild game and fish) yield such substantial health benefits, including dramatic reduction in sudden death from heart disease?

• Why would vitamin K2 (from meats and milk, as well as fermented foods like natto and cheese), obtainable in only the tiniest amounts on a vegetarian diet, provide such significant benefits on bone and cardiovascular health?

• Why would vitamin B12 (from meats) be necessary to maintain a normal blood count, prevent anemia, keep homocysteine at bay, and lead to profound neurologic dysfunction when deficient?


Omega-3 fatty acids and vitamins K2 and B12 cannot be obtained in satisfactory quantities from a pure vegetarian diet. The consequences of deficiency are not measured in decades, but in a few years. The conclusion is unavoidable: Evolutionarily, humans are meant to consume at least some foods from animal sources.

That's not to say that we should gorge ourselves on animal products. Gout (excessive uric acid) and kidney stones are among the unhealthy consequences of excessive quantities of meats in our diets.

It pains me to say this, since I’ve always favored a vegetarian lifestyle, mostly because of philosophical concerns, as well as worries about the safety of our factory farm-raised livestock and rampant inhumane practices.

But, stepping back and objectively examining what nutritional approach appears to stack the odds in favor of optimal health, I believe that only one conclusion is possible: Humans are meant to be omnivorous, meant to consume some quantity of animal products in addition to vegetables, fruits, nuts, and other non-animal products.

The question is how much?

Are you wheat-free?

According to the recent Heart Scan Blog poll, Are you wheat-free?, the 173 respondents said:

Yes, I am free of wheat products.
87 (50%)

No, I include wheat products in my diet.
73 (42%)

I'm not sure.
1 (0%)

I think you're nuts.
12 (6%)


That's kind of what I expected.

There are people who have eliminated wheat and experienced nothing except a feeling of deprivation. These people are in the minority. Though the poll was not set up to reflect this (i.e., asked who tried it and experienced no perceptible benefit), in my experience, this applies to about 20% of people. Little happens with elimination of wheat beyond modest weight loss. Those are the people who generally think I'm nuts.

Or, these people may have been brainwashed by "official" agencies like the USDA, the American Diabetes Association, and American Heart Association and the constant marketing of (high markup) grain products like Cheerios and Shredded Wheat . Some people are really uncomfortable going against the "grain" of popular public opinion.

Then there are the people who try to eliminate wheat and fail. They can't deal with the overwhelming fatigue, mental fog, and moodiness that comes with withdrawal from wheat, the phenomenon of converting from a sugar-burning metabolism to a fat-burning metabolism. Although wheat withdrawal usually runs its course in 2-5 days, some people find it intolerable. (That would be another fun poll to run: Have you experienced wheat-withdrawal?) Occasionally, the withdrawal is replaced by endless cravings, a phenomenon that applies to only about 10% of people. These are the true "wheat addicts." These are the people who eliminate wheat, lose 40 lbs, then regain it when they have one cracker and the floodgates of impulse control crumble.

Then there are the majority, 50% in the poll, though more like 70% in my face-to-face experience. Why is my experience skewed? Well, the people I deal with every day come because of coronary disease in some form (abnormal heart scan score, for instance) or because of lipid or lipoprotein abnormalities. So my experienced is skewed towards people who are likely to have something abnormal, such as high triglycerides or small LDL particles, both of which are created by including wheat in the diet.

This last group also shows unexpected effects of wheat elimination: substantial weight loss, dramatic reductions in blood sugar and triglycerides, increase in HDL, reductions in small LDL, reduction in c-reactive protein and other inflammatory measures. Appetite shrinks considerably. Not uncommonly, improved well-being, reduction in bowel complaints like cramping or "irritable bowel syndrome" is experienced, some rashes clear, occasionally arthritis will improve. See below for some of the testimonials to this experience.

When I first set out to advise people to eliminate wheat, I did it because I reasoned that it would be a quick and simple way to get people to reduce blood sugars and help correct the ubiquitous metabolic syndrome that afflicts nearly 50 million Americans now. And it did indeed accomplish that simple goal. But I did not expect all the other benefits to develop, the dramatic weight loss, improved well-being, reduction in hunger, etc.

I view wheat elimination as an easy-to-remember, digestible way to obtain enormous health benefits in a coronary plaque-control program, one that works for most--but not all--people. And I relate this experience not to sell you something, but to simply relate what I see as the truth, a way that is contrary to conventional advice yet works enormously well.



Unsolicited testimonials of people who have successfully been wheat-free:

Barbara W said:

It's true! We've done it. My husband and I stopped eating all grains and sugar in February. At this point, we really don't miss them any more. It was a huge change, but it's worth the effort. I've lost over 20 pounds (10 to go)and my husband has lost 45 pounds (20 to go). On top of it, our body shapes have changed drastically. It is really amazing. I've got my waist back (and a whole wardrobe of clothes) - I'm thrilled.

I'm also very happy to be eating foods that I always loved like eggs, avocados, and meats - without feeling guilty that they're not good for me.

With the extremely hot weather this week in our area, we thought we'd "treat" ourselves to small ice cream cones. To our surprise, it wasn't that much of a treat. Didn't even taste as good as we'd anticipated. I know I would have been much more satisfied with a snack of smoked salmon with fresh dill, capers, chopped onion and drizzled with lemon juice.

Aside from weight changes, we both feel so much better in general - feel much more alert and move around with much greater flexibility, sleep well, never have any indigestion. We're really enjoying this. It's like feeling younger.

It's not a diet for us. This will be the way we eat from now on. Actually, we think our food has become more interesting and varied since giving up all the "white stuff". I guess we felt compelled to get a little more creative.

Eating out (or at other peoples' places) has probably been the hardest part of this adjustment. But now we're getting pretty comfortable saying what we won't eat. I'm starting to enjoy the reactions it produces.


Weight loss, increased energy, less abdominal bloating, better sleep--I've seen it many times, as well.


Dotslady said:

I was a victim of the '80s lowfat diet craze - doc told me I was obese, gave me the Standard American Diet and said to watch my fat (I'm not a big meat eater, didn't like mayo ... couldn't figure out where my fat was coming from! maybe the fries - I will admit I liked fries). I looked to the USDA food pyramid and to increase my fiber for the constipation I was experiencing. Bread with 3 grams of fiber wasn't good enough; I turned to Kashi cereals for 11 years. My constipation turned to steattorrhea and a celiac disease diagnosis! *No gut pains!* My PCP sent me to the gastroenterologist for a colonscopy because my ferritin was a 5 (20 is low range). Good thing I googled around and asked him to do an endoscopy or I'd be a zombie by now.

My symptoms were depression & anxiety, eczema, GERD, hypothyroidism, mild dizziness, tripping, Alzheimer's-like memory problems, insomnia, heart palpitations, fibromyalgia, worsening eyesight, mild cardiomyopathy, to name a few.

After six months gluten-free, I asked my gastroenterologist about feeling full early ... he said he didn't know what I was talking about! *shrug*

But *I* knew -- it was the gluten/starches! My satiety level has totally changed, and for the first time in my life I feel NORMAL!



Feeling satisfied with less is a prominent effect in my experience, too. You need to eat less, you're driven to snack less, less likely to give in to those evil little bedtime or middle-of-the-night impulses that make you feel ashamed and guilty.



An anonymous (female) commenter said:

My life changed when I cut not only all wheat, but all grains from my diet.

For the first time in my life, I was no longer hungry -no hunger pangs between meals; no overwhelming desire to snack. Now I eat at mealtimes without even thinking about food in between.

I've dropped 70 pounds, effortlessly, come off high blood pressure meds and control my blood sugar without medication.

I don't know whether it was just the elimination of grain, especially wheat, or whether it was a combination of grain elimnation along with a number of other changes, but I do know that mere reduction of grain consumption still left me hungry. It wasn't until I elimnated it that the overwhelming redution in appetite kicked in.

As a former wheat-addicted vegetarian, who thought she was eating healthily according to all the expert advice out there at the time, I can only shake my head at how mistaken I was.




Stan said:

It's worth it and you won't look back!

Many things will improve, not just weight reduction: you will think clearer, your reflexes will improve, your breathing rate will go down, your blood pressure will normalize. You will never or rarely have a fever or viral infections like cold or flu. You will become more resistant to cold temperature and you will rarely feel tired, ever!



Ortcloud said:

Whenever I go out to breakfast I look around and I am in shock at what people eat for breakfast. Big stack of pancakes, fruit, fruit juice syrup, just like you said. This is not breakfast, this is dessert ! It has the same sugar and nutrition as a birthday cake, would anyone think cake is ok for breakfast ? No, but that is exactly the equivalent of what they are eating. Somehow we have been duped to think this is ok. For me, I typically eat an omelette when I go out, low carb and no sugar. I dont eat wheat but invariably it comes with the meal and I try to tell the waitress no thanks, they are stunned. They try to push some other type of wheat or sugar product on me instead, finally I have to tell them I dont eat wheat and they are doubly stunned. They cant comprehend it. We have a long way to go in terms of re-education.

Yes. Don't be surprised at the incomprehension, the rolled eyes, even the anger that can sometimes result. Imagine that told you that the food you've come to rely on and love is killing you!



Anne said:

I was overweight by only about 15lbs and I was having pitting edema in my legs and shortness of breath. My cardiologist and I were discussing the possible need of an angiogram. I was three years out from heart bypass surgery.

Before we could schedule the procedure, I tested positive for gluten sensitivity through www.enterolab.com. I eliminated not only wheat but also barley and rye and oats(very contaminated with wheat) from my diet. Within a few weeks my edema was gone, my energy was up and I was no longer short of breath. I lost about 10 lbs. The main reason I gave up gluten was to see if I could stop the progression of my peripheral neuropathy. Getting off wheat and other gluten grains has given me back my life. I have been gluten free for 4 years and feel younger than I have in many years.

There are many gluten free processed foods, but I have found I feel my best when I stick with whole foods.



Ann has a different reason (gluten enteropathy, or celiac disease) for wanting to be wheat-free. But I've seen similar improvements that go beyond just relief of the symptoms attributable to the inflammatory intestinal effects of gluten elimination.



Wccaguy said:

I have relatively successfully cut carbs and grains from my diet thus far.

Because I've got some weight to lose, I have tried to keep the carb count low and I've lost 15 pounds since then.

I have also been very surprised at the significant reduction in my appetite. I've read about the experience of others with regard to appetite reduction and couldn't really imagine that it could happen for me too. But it has.

A few weeks ago, I attended a party catered by one of my favorite italian restaurants and got myself offtrack for two days. Then it took me a couple of days to get back on track because my appetite returned.

Check out Jimmy Moore's website for lots of ideas about variations of foods to try. The latest thing I picked up from Jimmy is the good old-fashioned hard boiled egg. Two or three eggs with some spicy hot sauce for breakfast and a handful of almonds mid-morning plus a couple glasses of water and I'm good for the morning no problem.

I find myself thinking about lunch not because I'm really hungry but out of habit.

The cool thing too now is that the more I do this, the more I'm just not tempted much to do anything but this diet.

No more canned foods

If you haven't already caught the news, it's time to eliminate canned foods and exposure to plastics that contain the chemical, bisphenol A (BPA). A worrisome and unexpected association with heart disease and diabetes has been found.

This issue has been debated for some years ever since scientists at the NIH detected BPA in the blood samples of 93-95% of Americans, with consumer protection advocates calling for more research or even the outright banning of BPA , while industry representatives have argued that the data fail to conclusively prove adverse health effects.

Well, the argument has been tilted heavily in favor of increased consumer protection with the publication of a study in the Journal of the American Medical Association by Dr. Iain Lang and associates at the University of Exeter, UK, and the University of Iowa. Their study, released Sept. 17, 2008, Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults, persuasively demonstrated a 40% increased incidence of coronary heart disease, heart attack, and diabetes with increasing exposure to BPA (as judged by urine levels) among the nearly 1500 adults aged 18-74 years. People with coronary heart disease had double the blood level of BPA compared to those without.

In addition, higher urine levels of BPA were associated with abnormalities of two liver tests, GGT and alkaline phosphatase.

Interestingly, although much of the debate over adverse health effects of BPA have centered around concern over cancer and reproductive risks, an association with cancer did not hold. (No analysis for reproductive issues was conducted in these adults, since most of the concern is for children exposed through polycarbonate baby bottle use. Some BPA critics have raised questions like low birth weight developing from exposure.) No relationship to thyroid disease was identified, also.

The editorial accompanying the study added some sharp commentary:

"Subsequent to an unexpected observation in 1997, numerous laboratory animal studies have identified low-dose drug-like effects of BPA at levels less than the dose used by the US Food and Drug Administration and the Environmental Protection Agency to estimate the current human acceptable daily intake dose (ADI) deemed safe for humans. These studies have shown adverse effects of BPA on the brain, reproductive system, and--most relevant to the findings of Lang et al--metabolic processes, including alterations in insulin homeostasis and liver enzymes. . . For example, when adults rats were fed a 0.2 microgram/kg per day dose of BPA for 1 month (a dose 250 times lower than the current ADI), BPA significantly decreased the activities of antioxidant enzymes and increased lipid peroxidation, thereby increasing oxidative stress. When adult mice were administered a 10 microgram/kg dose of BPA once a day for 2 days ( a dose 5 times lower than the ADI), BPA stimulated pancreatic beta cells to release insulin."

This study, piled on top of the worrisome literature that precede it, are enough for me: No more tin cans (which are lined with BPA), no more hard plastics labeled with recycling code #7 or #3, no more polycarbonate water bottles (the hard ones, often brightly colored). Microwaveable-safe may also mean human-unsafe, as highlighted by this damning assurance from the Tupperware people that BPA is not a health hazard.

The National Toxicology Program also issued these advice in response to the Lang study to reduce BPA exposure (reported by the Washington Post) :

· Don't microwave polycarbonate plastic food containers. Polycarbonate may break down from overuse at high temperatures and release BPA. (Manufacturers are not required to disclose whether an item contains BPA, but polycarbonate containers that do usually have a No. 7 on the bottom.)

· Reduce use of canned foods, especially acidic foods such as tomatoes that can accelerate leaching of BPA from plastic can linings. Opt for soups, vegetables and other items packaged in cardboard "brick" cartons, made of safer layers of aluminum and polyethylene plastic (labeled No. 2).

· Switch to glass, porcelain or stainless-steel containers, particularly for hot food or liquids.

· Use baby bottles that are BPA-free; in the past year, most major manufacturers have developed bottles made without BPA.

Add Boston Globe to the list of heart scan blunders

Yet another piece of mass media misinformation hit the airwaves today. This time it's not from the New York Times or the LA Times, both of which have previously mangled the issues surrounding heart scans. This time it's from the Boston Globe.

In an article titled What is a calcium scan for heart disease, and who should undergo the test?, the report states:

". . . calcium scans may not be a good idea, or prove terribly useful, for most people. For one thing, the scans expose a patient to significant radiation - equivalent to roughly 50 chest X-rays" said Dr. Warren Manning, chief of noninvasive cardiac imaging at Beth Israel Deaconess Medical Center."

As many before him, Dr. Manning is confusing two tests: CT coronary angiography and CT heart scanning. Perhaps we can't blame him: This technology has had its weakest following in the northeast, for reasons not entirely clear to me. (In fact, Track Your Plaque followers have had the greatest struggle obtaining heart scans in that part of the country.) Nonetheless, you'd think he'd have his simple facts straight before talking to the press. Unfortunately, hospital public relations departments will usually just grab whoever they can willing to talk to the press--regardless of their expertise or lack of.


The story goes on to say:

. . ." it's not clear what to do with the results from a calcium scan. If you have diabetes, high cholesterol, high blood pressure, or a family history of heart disease, you already know - or should know - that you are at increased risk of heart problems and should lower these risk factors. So, a calcium scan provides little additional information," Manning said.

"Moreover, even a high score doesn't necessarily mean that the calcified plaque in your arteries is obstructing blood flow, said Dr. Adolph Hutter, a cardiologist at Massachusetts General Hospital."

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death," said Manning.

And if you get a low calcium score, a sign of little or no calcification of plaques, that's not very useful, either, because it could be wrong, or it could be right but lull you into believing you do not have to exercise and watch your diet, cholesterol, and blood pressure levels. "You can still be at risk even if your calcium test is negative," Hutter said.



It is truly shocking how little many (not all, thank goodness) of my colleagues really know about 1) heart scans, 2) coronary disease prevention, and 3) prevention in general. These same "experts" likely advocate high-dose statin drugs and low-fat diets for people at risk. They likely refer patients to the American Heart Association for diet advice and themselves obtain a lot of information from the pharmaceutical industry. The notion of identification, tracking, and purposeful reversal of coronary plaque is entirely foreign to this bunch.

"The vast majority of people with high calcium tests don't have obstructions and they do fine long-term. So you'd have to test lots and lots of people to prevent one heart attack or sudden death." Well, take a look at a graph from a database of 25,000 people undergoing heart scans then observed for several years afterwards:




You can see quite clearly from the curves that heart scan scores very clearly predict your future (if no preventive action is taken). The higher the score, the greater the likelihood of heart attack and death. How much clearer can it get?

The most recent addition to this literature is the PREDICT study which concluded:

Hazard ratios relative to CACS [coronary artery calcium scores] in the range 0-10 Agatston units (AU) were: CACS 11-100 AU, 5.4 (P = 0.02); 101-400 AU 10.5 (P = 0.001); 401-1000 AU, 11.9 (P = 0.001), and >1000 AU, 19.8 (P < 0.001).

In other words, a heart scan score of >1000 is associated with a 20-fold increased risk of cardiovascular events (without preventive efforts). That kind of predictive power and quantitative confidence simply cannot be squeezed out of blood pressure and cholesterol values.

How about the 2008 University of California-Irvine study from the New England Journal of Medicine (do the northeast docs even pay attention to something that is published in their own neighborhood?) that reported:

There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%.

How about the Prospective Army Coronary Calcium (PACC) project (men average age 43 years):

"In these men, coronary calcium was associated with an 11.8-fold increased risk for incident coronary heart disease (CHD) (p = 0.002) in a Cox model controlling for the Framingham risk score. Among those with coronary artery calcification, the risk of coronary events increased incrementally across tertiles of coronary calcium severity (hazard ratio 4.3 per tertile)."

Calcium score provided additional information even after factoring in the Framingham risk score.

That's just a sample of the studies. There are a number more.

Add to these conversations the fact that, unlike reducing blood pressure or LDL cholesterol, the heart scan score is a quantification of the disease itself. It can also be tracked over time to gauge the success or failure of prevention efforts. To believe that blood pressure reduction or LDL cholesterol reduction is sufficient to eliminate risk is something only a fool would believe.



Contary to the above statements, the data are clear:

--The higher the heart scan score, the greater the risk. This has been demonstrated beyond any shadow of a doubt in at least a dozen published studies. In fact, heart scan scores outshine lipid/cholesterol values several-fold.

--A person with a zero score has a nearly zero risk for cardiovascular events over a 5-year timeline.

--Heart scans are the only quantitative test available of coronary atherosclerotic plaque. This means that they can be repeated to gauge progression or regression. Cholesterol does not do that. Stress tests do not do that.

--Heart scans are not the same as CT coronary angiography.

--The lack of "need" for a procedure does not equate to the absence of disease.

The power of heart scans is that they can uncover evidence for coronary atherosclerotic plaque 10 years before a cardiac disaster strikes. Witness Tim Russert's heart scan score of 210 in 1998 at age 48. 10 years later, you know what happened.

Beware the camipaign of misinformation and ignorance that continues that is hell-bent on maintaining the procedural status quo or locking us into a "drugs for all" mentality.

What's worse than sugar?

There are a number of ways to view the blood sugar-raising or insulin-provoking effect of foods.

One way is glycemic index (GI), simply a measure of how high blood sugar is raised by a standard quantity of a food compared to table sugar. Another is glycemic load (GL), a combination (multiplied) of glycemic index and carbohydrate content per serving.

Table sugar has a GI of 65, a GL of 65.

Obviously, table sugar is not good for you. The content of white table sugar in the American diet has exploded over the last 100 years, totaling over 150 lb per year for the average person. (Humans are not meant to consume any.)

What is the GI of Rice Krispies cereal, organic or not? GI = 82-- higher than table sugar. GL is 72, also higher than table sugar.

How about Corn Flakes? GI 81, GL 70--also both higher than sugar.

How about those rice cakes that many dieters will use to quell hunger? GI 78, GL 64.

How about Shredded Wheat cereal? GI 75, GL 62.

All of the above foods with GI's and GL's that match or exceed that of table sugar are made of wheat and cornstarch. Some, like Shredded Wheat cereal and rice cakes, don't even have any added sugar.

Stay clear of these foods if you have low HDL, high triglycerides, high blood sugar, or small LDL. Or, for that matter, if you are human.

Keep the eloquent words of New York University nutritionist, Marion Nestle, author of the book, Food Politics, in mind:

“Food companies—just like companies that sell cigarettes, pharmaceuticals, or any other commodity—routinely place the needs of stock holders over considerations of public health. Food companies will make and market any product that sells, regardless of its nutritional value or its effect on health. In this regard, food companies hardly differ from cigarette companies. They lobby Congress to eliminate regulations perceived as unfavorable; they press federal regulatory agencies not to enforce such regulations; and when they don’t like regulatory decisions, they file lawsuits. Like cigarette companies, food companies co-opt food and nutrition experts by supporting professional organizations and research, and they expand sales by marketing directly to children, members of minority groups, and people in develop countries—whether or not the products are likely to improve people’s diets.” ??

Are sterols the new trans fat?

By now, I'm sure you're well-acquainted with the hydrogenated, trans fat issue.

Hydrogenation of polyunsaturated oils was a popular practice (and still is) since the 1960s, as food manufacturers sought a substitute for saturated fat. Bubbling high-pressure hydrogen through oils like cottonseed, soybean, and corn generates trans fatty acids. These man-made fatty acids, while safe in initial safety testing, proved to be among the biggest nutritional mistakes of the 20th century.

Trans fatty acids have been associated with increased LDL cholesterol, reduction in HDL, oxidative reactions, abnormal rigidity when incorporated into cell membranes, and cancer. Trans fats still dominate many processed foods like chips, cookies, non-dairy creamers, food mixes, and thousands of others. They're also found prominently in fast foods.

Fast forward to today, and most Americans have become aware of the dangers of trans fats and many try to avoid them.

But I worry there is yet another substance that has worked its way into the American processed food cornucopia that has some potential for repeating the trans fat debacle: sterol esters.


Sterols are naturally-occurring oils found in vegetables, nuts, and numerous other foods in small quantities. Most of us take in 200-400 milligrams per day just by eating plant-sourced foods.

Curiously, the chemical structure of sterols are very similar to human cholesterol (differing at one carbon atom). Sterols, by not fully understood means, block the intestinal absorption of cholesterol. Thus, sterol esters, as well as the similar stanol esters, have been used to reduce blood levels of total and LDL cholesterol.

So far, so good.

The initial commercial products, released in the late 1990s, were Take Control (sterol) and Benecol (stanol), both of which were marketed to reduce cholesterol when 2-3 tbsp are used daily, providing 3400 – 5100 mg of sterol or stanol esters, about 10- to 20-fold more than we normally obtain from foods. Several clinical trials have conclusively confirmed that these products reduce cholesterol levels.

They do indeed perform as advertised. Add either product to your daily diet and LDL cholesterol is reduced by about 10-15%. In fact, in the original Track Your Plaque book, these products were advocated as a supplemental means of reducing LDL when other methods fell short.

In 2008, there are now hundreds of products that have additional quantities of sterol esters in them, such as orange juice, mayonnaise, yogurt, breakfast cereals, even nutritional supplements. Most of these products proudly bear claims like "heart healthy." Stanol esters have not enjoyed the same widespread application. (I believe there may be patent issues or other considerations. However, it's the sterols that are the principal topic here, not stanols.)

Now, here's where it gets a bit tricky. There is a rare (1 per million) disease called sitosterolemia, a genetic disorder that permits the afflicted to absorb more than the usual quantity of sterols from the intestine. While you and I obtain some amount of sterols from plant-based foods, absorption is poor, and we absorb <10% of sterols ingested. However, people with sitosterolemia absorb sterols far more efficiently, resulting in high blood levels of sterols that result in coronary disease and aortic valve disease, with heart attacks occurring as young as late teens or 20s. Treatment to block sterol absorption are used to treat these people.

There are also a larger number, though still uncommon (1/500) of people who have only one of the two genes that young people with sitosterolemia have. These people may have an intermediate capacity for sterol absorption.

Okay, so what does this have to do with you? Well, if you and I now take in 10-20 times greater amounts of sterol esters, do our blood levels of sterols increase?

Several studies now suggest that, yes, sterol blood levels increase with sterol ingestion. One study from Finland, the STRIP Study, showed that children who had double usual sterol intake increased blood levels by around 50%.

Similarly, a Johns Hopkins study in adults with only one of the genes ("heterozygotes") for sitosterolemia increased sterol blood levels by between 54-116% by ingesting 2200 mg of sterols added per day, despite reduction of LDL cholesterol levels.

Even people with neither gene for sitosterol hyperabsorption can increase their blood levels of sterols. But the crucial question: Do the blood levels of sterols that occur in unaffected people or in heterozygotes increase the risk of coronary heart disease? The answer is not known.

Despite the several clinical trials performed with sterol esters, all of them have examined LDL and total cholesterol reduction as endpoints, not cardiovascular events. It is conceivable that, while sterol esters reduce cholesterol, risk for heart disease is increased due to higher blood levels of sterols.

The question is not settled. For now, it is just a suspicion. But that's enough for me to steer clear of processed foods supplemented with these uncertain sterol esters. My previous recommendations for sterol ester products will be removed with the next edition of Track Your Plaque. Until we have solid evidence that there are no adverse cardiovascular effects of sterol esters, in my view they should not be part of anyone's heart-disease prevention program.

(The same argument does not seem to apply to stanol esters, such as that contained in butter-substitute Benecol, since stanol esters are not absorbed at all and remain confined to the intestine.)

The Diabetes Gold Rush

Lou came into the office. Clearly, his program had gone sour.

Lou had initially obtained wonderful control over his heart scan score of 1114, having reversed modestly in his first three years of effort through correction of his multiple causes (including low HDL, severe small LDL, Lp(a), and a diabetic tendency).

But Lou now came into the office red-faced and sporting a big bulging abdomen. Blood sugar? Now in the overtly diabetic range. Lou said that his primary care doctor had suggested that he start on three new medications (glucophage, injectable Byetta, and Actos) to control his blood sugar. His doctor also told him to increase his intake of fibers by eating more "healthy" breakfast cereals like Cheerios.

Lou had apparently done just that (added "healthy" fiber-rich foods) even before his doctor had suggested it. (Lou failed to remember the several conversations we'd had about healthy eating.) Unfortunately, Lou also failed to connect his increased intake of "healthy fiber-rich foods" and his growing abdominal girth (his "wheat belly").

Here's the dirty little secret: Much of the world wants you to be diabetic. It is the health gold rush of this century. "Go West, young man!"




To find out what I mean, you need only ask: Who profits when people become diabetic? That's easy:

The pharmaceutical industry--Diabetes is a booming growth industry, a source of tens of billions of dollars of revenue, poised for enormous growth as the population ages and gets fatter. It is common for a newly-diagnosed diabetic to be given new prescriptions for two or three drugs with a monthly cost of $300. Of course, the chronic nature of the disease make this far more profitable than, say, a two week course of antibiotics. Presently, 70 new drugs are under development.

Diabetes drug maker Novo Nordisk reported a 25% increase in revenues in 2007 from diabetic agents in the North American market, along with near $2 billion increase in profit for the year. Merck's recently-released DPP-4 inhibitor, Januvia, has already sold $668 million in 2007 and is growing rapidly.

The medical device and supply industry. Take a look at the Medtronic quarterly earnings report, detailing the breakdown of their record-setting quarterly revenue of $3.7 billion:

Diabetes revenue of $269 million grew 12 percent driven by sales
of consumables, the accessories required by insulin pump users, and
continuous glucose monitoring products. Revenue from international
sales grew 31 percent over the same quarter last year.


That's what I call a growth industry.

The processed food industry. The food industry is as big or bigger than the drug industry. ADM, Kraft, General Mills all have annual revenues in the $12-50 billion range. There are plenty of others.

When we're told, for instance, that Cheerios reduces cholesterol, we're not told that it skyrockets blood sugar or triggers small LDL. When we're sold whole wheat crackers, Cocoa Puffs (which the American Heart Asscociation says is heart-healthy), or granola bars, hunger is stimulated, impulse to eat more grows, blood sugar escalates, we get fat, we get diabetic. It's a simple formula.

So be aware that there is little incentive among corporate giants in the food, medical device, or drug industries to encourage behaviors that decrease the incidence of diabetes. In fact, there is enormous financial incentive to make sure that diabetes continues to grow at the startling rate it has over the last decade.

To be sure, the drug and medical device industry will also develop better tools to deal with diabetes and its complications. But the very best way to deal with diabetes is to not develop it in the first place.

What else is there?

This question comes up frequently:

Aren't there any alternatives to heart scans performed on a CT or EBT device?

Yes, there are.

First of all, heart scans are performed best on an electron-beam CT device (EBT) or a 64-slice multi-detector CT (MDCT) device. (While they are also obtainable through less-than-64 slice CT devices (e.g., 16 slices and less), I would advise against it because of the excessive radiation exposure and poor accuracy.) CT heart scans are not to be confused with now more popular CT coronary angiograms, which are performed on the same devices but require intravenous x-ray dye and many times more radiation.(See CT scans and radiation exposure and Heart scan frustration.) Heart scans currently form the basis for the Track Your Plaque program, a program of tracking plaque in the hopes of stopping or reversing the otherwise inevitable 30% per year increase.

Let's confine our discussion to people without symptoms, meaning people like you and me sitting at home, not in an emergency room having chest pain or other similar acute symptomatic presentation.

Among the other ways to uncover hidden coronary plaque:

--Heart catheterization--to yield a coronary angiogram. Yes, this does tell us whether coronary plaque is present. However, it is invasive, expensive, and crude. (I've performed 5000 over my career; they are crude, though useful, tools in acute settings like unstable symptoms or heart attack, a different situation.) Coronary angiography is also non-quantitative. While they provide a value like "40% blockage mid-way in right coronary" or "90% blockage in left anterior descending" they do not provide a trackable lengthwise index of total plaque volume. Identifying severe blockages in people with symptoms leads to stents, bypass surgery and the like, but it is not practical nor of long-term usefulness in apparently, healthy people without symptoms.

--Carotid ultrasound--Here's is where a lot of confusion comes from. Standard carotid ultrasound (U/S) performed in virtually every hospital and many clinics will yield crude qualitative results, e.g., "16-49% stenosis (blockage) in right internal carotid artery". The crude value range is because much of carotid U/S is based on flow velocities, not just direct visualization of the plaque itself ("2-D imaging). However, if carotid stenosis of any degree is identified, the likelihood of silent coronary plaque is much greater.

Limitations: The qualitative, non-quantitative nature of carotid U/S make it difficult to follow long-term in a precise way. Also, this is carotid plaque, not coronary plaque. It makes it very difficult to follow carotid plaque as an indirect means of tracking coronary plaque. The two arterial territories, carotid and coronary, do not track together: there are divergences in many people, with carotid plaque absent in some people with advanced coronary plaque, carotid plaque more susceptible to different risk factors than coronary. So carotid U/S is helpful for its own purposes, but not terribly helpful for coronary tracking.

How about carotid intimal-medial thickness (CIMT) obtained also with carotid U/S? CIMT is a useful index of bodywide atherosclerosis. CIMT is simply a measure not of plaque (and is measured in regions of the carotid artery away from plaque), but of the thickness of the lining of the carotid arteries. Everybody has a measurable CIMT, but it thickens as atherosclerosis grows. CIMT is a radiation-free test that takes several minutes.

Limitations: Hardly anybody does it outside of research protocols. I know of no hospital or clinic in my area that performs CIMT, though it is slowly being adopted in some centers. It is also difficult to rely on repeated tests, because there is substantial variation when one technologist or another performs it. CIMT is also a flawed index of coronary plaque. When CIMT is compared to heart scan scores, CT coronary angiography, or conventional coronary angiography, CIMT correlates about 60-70% with the degree of coronary atherosclerosis.

CIMT is therefore a useful test for research, but a distant 2nd choice--if you can obtain it.

--Ankle-brachial index (ABI)--ABI is a crude measure, simply a comparison of the blood pressure (obtained with a blood pressure cuff) in the legs divided by blood pressure in the arms. The ratio is called ABI. Any ABI <1.0, meaning less pressure in the legs compared to the arms, is indirectly indicative of advanced coronary disease. ABI is, in fact, a very powerful predictor of cardiovascular events. If ABI is <1.0, your future risk for heart attack is very high, even in the absence of symptoms.

Limitations: The vast majority of people with heart disease, even those having undergone stents or bypass surgery, have normal ABI's. Virtually all people with high heart scan scores have normal ABI's. In other words, ABI is a measure of very advanced atherosclerosis only.

--Stress tests--I lump all stress tests together in their various forms, e.g., stress thallium, stress Cardiolite, stress Myoview, persantine/adenosine Cardiolite, dobutamine echocardiography, etc. Stress tests are tests of coronary blood flow, not of plaque. Stress tests are useful in people with symptoms, like chest pain or breathlessness, since stress tests are provocative tests that can help determine whether reduced coronary blood flow is the cause behind a symptom, or whether hiatal hernia, esophagitis, gallstones, pleurisy, musculoskeletal causes, or some other process is behind symptoms.

Limitations: Stress test are virtually useless in people without symptoms. This is why people like Tim Russert and Bill Clinton, both without symptoms, underwent several (Russert 3, Clinton 5) nuclear stress tests---all normal. You know what happened to them. Stress tests do not reliably uncover hidden coronary plaque in people without symptoms. Stress tests are, like coronary angiograms, non-quantitative. They are normal or abnormal.


Outside of experimental settings, that's it.

You can probably see why I advocate CT heart scans for tracking plaque. I do not advocate heart scans because I sell them (I don't), because scan centers pay me to say these things (they don't, and in fact my relationship with my usual heart scan centers has become deeply contentious, though I still endorse the technology). I say that heart scans are superior because they are, in 2008, the only way to 1) identify and 2) track coronary plaque that is easy, safe, low-radiation, and reasonably priced (<$200 in Milwaukee at 5 centers).

The need for a technology that allows tracking of plaque, not just initial identification, is also an important distinction. People who've had some measure of atherosclerosis all catch on to this eventually. "Can I reverse it?" is an inevitable question once the disease is identified in some way. So a tool for tracking over time to gauge the success or failure of a program of prevention can be assessed.

Perhaps in 10 years, another technology will emerge as the preferred means to do the same, but better. If that proves true, we will convert to that technology. But today heart scans performed on CT heart scans are the only rational way to both detect, then track, coronary atherosclerotic plaque.

Let's gamble with your health

Let's play a game.

I'm going to list some lipid patterns and you tell me whether or not the person with these values has heart disease.

Patient 1

Total cholesterol 150 mg/dl
LDL cholesterol 75 mg/dl
HDL 50 mg/dl
Triglycerides 125 mg/dl


Patient 2

Total cholesterol 300 mg/dl
LDL cholesterol 200 mg/dl
HDL cholesterol 35 mg/dl
Triglycerides 325


Patient 3

Total cholesterol 300 mg/dl
LDL cholesterol 100 mg/dl
HDL cholesterol 25 mg/dl
Triglycerides 875 mg/dl



Let's say that any one of these profiles is yours. Should you be getting your affairs in order, preparing for your cardiac catastrophe? Should you demand a stress test from your doctor, hoping that it will shed some light on your dilemma? Should you go ahead and go to the all-you-can-eat rib restaurant, content that you will be attending your granddaughger's wedding in 2020 in full health?

If you can tell, you're a lot better at this than I am.

I provide consultation to other physicians and patients on complex hyperlipidemias in my area. In other words, if someone has a difficulty to manage lipid disorder, the doctor sends the patient to me.

Managing these wildly variable values is the easy part. Deciding whether or not heart disease is concealed within the patient . . . well, that's the hard part.

Let's take it a step further: Suppose all three profiles also have 50% of all LDL particles as the abnormal small particles. And they all have a lipoprotein(a) level of 50 mg/dl, an abnormally high level.

How about now: Can you tell whether any or all of these people have hidden heart disease?

What if they are 20 years old? Does that make a difference?

What if they are all females over 65 years--how about now?

If the only tool you have to divine the presence of hidden heart disease is a lipid panel, or even a lipoprotein panel, then the best you can manage is to hazard a guess based on statistical probability. You also assume that this "snapshot" represents the sorts of values someone has had for their entire lives. You cannot factor in the fact that the first person gained 60 lbs in the last three years since completing menopause. You can't factor in that patient 2 smoked two packs of cigarettes a day for 25 years, but quit 10 years ago.

It's also foolhardy to believe that every known cause of heart disease is currently identifiable and revealed by modern-day blood testing.

A heart scan is simply a means to quantify the sum-total of risk factors--causes--that have exerted an effect up until the moment of your scan. It will reveal the quantity of coronary atherosclerotic plaque present, regardless of whether you stopped smoking 20 years ago or lost 30 lbs last year.

For these reasons, nothing can replace the value of quantifying plaque: not cholesterol, not the Framingham risk calculation, not measures of small LDL or lipoprotein(a), not the presence or absence of symptoms. In 2008, the method of choice for measuring plaque remains a CT heart scan. Perhaps in 10 years it will be some other method.

As always, let me remind Heart Scan Blog viewers that I make this point NOT to sell heart scans, which I have no reason whatsoever to do. I say this because we require a tool to track this potentially fatal disease. We require a yardstick for tracking progression or regression. The only tool that suits these purposes in 2008 is a CT heart scan.

Is there something fishy about fish oil?

To be sure, there's plenty of misinformation out there about fish oil. Take a look at the swill that passes for health information on Woman's Day: On Call with Dr. Sandy: Fish Oil and Mercury:



Reader Question: My doctor recommended that I take a fish oil supplement, but I'm concerned about mercury. Is there any way to tell which brands are lowest in mercury content?



On Call Response: When it comes to OTC supplements, the answer is no. Though most fish oil supplements sold by major brands are probably safe, there's really no way to tell what's in the bottle or how much mercury it might contain.




Perhaps Dr. Sandy should read the many independent analyses performed on nutritional supplement fish oil, including those at Consumer Lab and Consumer Report before she offers her blind criticisms.

Lovaza vs fish oil supplements?

Lovaza is the FDA-approved form of fish oil that is available only by prescription. It contains 842 mg of the omega-3 fatty acids, EPA and DHA, per capsule.

The FDA application for Lovaza is viewable here on the FDA website. Interestingly, while there is plenty of the usual regulatory gobbledy-gook about toxicology, dose escalation, and efficacy in the extensive documentation, there is little said about the issue of contamination.

In other words, critics of nutritional supplement fish oil harp on the possibility of contamination with mercury and pesticide residues, like dioxin and PCBs (polychlorinated biphenyls). Yet there is virtually nothing about these same issues in the FDA application for Lovaza.

Let's take a look at a sample over-the-counter fish oil product. Our friends at PharmaNutrients (a new Track Your Plaque partner for nutritional supplements) have a fish oil product called PharmaNutrients" Cardio. Here's an independent analysis of the Cardio product (per 1000 mg fish oil capsule):

EPA content: 566.1 mg
DHA content: 216.6 mg
(Total EPA + DHA 782.7 mg)

Cardio passed all tests for peroxides, PCBs, dioxin, furans, dioxin-like PCBs, and heavy metals (arsenic, cadmium, lead, mercury) using criteria at least 60% more stringent than European Commission (EC) standards (EC standard <2 picograms/gm for dioxins and furans, PharmaNutrients <1 picograms/gm; EC standard <10 picograms/gm for dioxin-like PCBs, PharmaNutrients <3 picograms/gm). PCBs levels in particular are less than 0.009 ppm, 90% below the industry-wide purity standard of 0.09 ppm. Likewise, mercury is >90% lower than European Commission standards.

In other words, this over-the-counter "pharmaceutical grade" fish oil has virtually nothing but omega-3 fatty acids.

Interestingly, the PharmaNutrients fish oil capsule also contains the third omega-3 fatty acid, docosapentaenoic acid (DPA), a neglected form that some authorities have proposed has superior cardiovascular protective properties over eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). If DPA is included in the analysis, PharmaNutrient's Cardio contains a total of 900 mg omega-3 fatty acids per capsule.

At some point, I'd like to see a head-to-head comparison not just on purity grounds, since I am convinced that high-quality products like Cardio can match or exceed the purity of prescription fish oil, but on efficacy in raising omega-3 blood levels, the omega-3 index. (The omega-3 index is a predictor of heart attack and sudden cardiac death--the higher, the better.) My prediction: High-quality fish oil supplements will match or exceed prescription fish oil.

More on blood sugar

Take any of the following foods:

One chicken breast
Quarter-pound ground beef
6 oz salmon steak
½ cup raw almonds
3 eggs scrambled in olive oil

How much is blood sugar increased by any item in the above list?

If you said virtually zero, you’re correct. Eat any of these foods, regardless of portion size, and blood sugar won’t change substantially. If you started with a blood sugar of, say, 90 mg/dl, 1-2 hours later it would be 90 mg/dl. It might go up or even down a few milligrams, but for all practical purposes it remains substantially unchanged.

How much is blood sugar increased by the foods in this list:

2 slices multigrain bread
1 whole wheat bagel
4 oz high-fiber breakfast cereal
2 whole grain pancakes, 2 oz maple syrup

The foods in this list are a different story from the first. Depending on your body weight, exercise habits, and other factors, a typical blood sugar response in an otherwise healthy non-diabetic person would be 120 mg/dl to 160 mg/dl. In someone with diabetes, it could easily exceed 200 mg/dl.

That isn’t good. Large blood sugar excursions to 140 mg/dl have been clearly associated with greater risk for heart attack, progression to diabetes, inflammatory responses, and other adverse health effects. In fact, blood sugars as low as 100 mg/dl after eating have been associated with increased cardiovascular risk.

Then why are the USDA, American Heart Association, the American Dietetic Association, and the American Diabetes Association telling us to eat more of the foods that shoot blood sugar up to such high levels? “Eat more healthy whole grains”?

To see how much the issue of exaggerated blood sugars after eating applies to you, a simple blood sugar check 1-2 hours after eating can show you. Either your doctor can have the test drawn or you can purchase your own inexpensive glucose meter (e.g., Walmart, Wagreens).

My prediction: You will be very surprised at blood sugar responses after common foods, including “healthy whole grains.” And, by the way, keeping blood sugar excursions to a minimum will facilitate weight loss.

Postprandial blood sugar: Almonds vs. whole wheat bread

Here's my postprandial (after-eating) blood glucose demonstration.



I tested raw almonds vs. 100% whole wheat bread, matched for calories. (Full nutritional composition below.)



Blood sugars:

Raw almonds

Start:

One-hour after eating:





2 slices 100% whole wheat bread

Start:

One-hour after eating:





100% whole wheat bread, 2 large slices

Water (g) 24.69

Energy (kcal) 158

Protein (g) 8.29

Fat, total (g) 2.14

Carbohydrate (g) 26.43

Sugars, total (g) 3.56

Fiber, total dietary (g) 4.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 0.478

Monounsaturated fatty acids, total (g) 1.022

Polyunsaturated fatty acids, total (g) 0.384





23 almonds, raw



Energy (kcal) 159

Protein (g) 5.86

Fat, total (g) 13.64

Carbohydrate (g) 5.98

Sugars, total (g) 1.07

Fiber, total dietary (g) 3.4

Cholesterol (mg) 0

Saturated fatty acids, total (g) 1.03

Monounsaturated fatty acids, total (g) 8.525

Polyunsaturated fatty acids, total (g) 3.331



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

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

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

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

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

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

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

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

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

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

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

Food sources of vitamin K2: Reprint

For some reason, my December, 2007, Heart Scan Blog post, Food sources of vitamin K2, has been receiving a lot of traffic.

I therefore reprint the vitamin K2 post below.





Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.















Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Family lessons

Lou was recovering from his 3rd bypass operation. This third go-round left him weaker, slower, less quick on the rebound. In fact, he was lucky to have survived.

At 71 years old, Lou went a good 15 years since his second bypass, another 10 years prior to his first bypass at age 46.

In the days immediately following Lou's bypass, I had a chance to talk to his son, who stayed at his Dad's bedside while Lou struggled through post-op recovery.

"Did your Dad tell you about why this has happened, what caused his heart disease?" I asked.

"Sort of. He just said I should get checked," Lou's son, Aaron, replied.

"Did he mention the lipoprotein(a) pattern he has?"

"No. He never mentioned anything like that. He just said to get checked."

That's how it gets played out more often than not: Mom or Dad has a heart attack, stents, or (3rd) bypass, the children are told to get checked. Getting "checked" assumes that the doctor knows what to check for.

In Lou's case, the reason why he was in the hospital getting his 3rd (and final) bypass was lipoprotein(a), along with genetically-determined small LDL particles, low HDL, a postprandial (after-eating) disorder, hypertension, and borderline diabetes, not to mention vitamin D deficiency, omega-3 fatty acid deficiency, and marginal thyroid function. (Lou, a retired city employee, had showed only marginal interest in correcting these patterns. While he accepted medications, he proved unwilling to engage in the diet and nutritional supplement strategies required to correct his patterns.)

So Lou's 3rd bypass operation provided a moment of reflection for Aaron to ask: "Could I share the fate of my Dad?" With Lou's combination of genetic patterns, there was at least a 75% likelihood that he did. Sadly, going to his doctor would likely yield little more than a cholesterol panel, a question about smoking, and a prescription for Lipitor.

Just getting "checked" would be, more than likely, a recipe for disaster for Aaron: heart disease in his 40s or 50s. That's why you need to take control over this sad state of affairs and ask--no, insist--that an effort be made to determine whether you might share your parents' fate.

Look like Jimmy Stewart


"This diet works great," Don declared. "But I think I've lost too much weight."

At 67 years old and 5 ft. 11 inches, Don began the program weighing 228 lbs (BMI 31.9). Because of high triglycerides, high blood sugar, high c-reactive protein, and excessive small LDL, I instructed Don to eliminate all wheat products from his diet, along with cornstarch and sweets. His intake of lean meats, eggs, vegetables, oils, raw nuts, etc. was unlimited.

Don now weighed 194 lbs, down 34 lbs over 6 months (BMI 27.1). Triglycerides, blood sugar, blood pressure, and well-being had improved dramatically; small LDL, however, had dropped only 30%--still room for improvement.

"My friends say I'm too skinny. They ask if I have cancer!"

I've heard this many times: Someone loses weight in a relatively short period of time and friends and family tell you you're too skinny. "It must be cancer. Nobody loses weight like that."

Unfortunately, many Americans have forgotten what normal looks like. Normal is certainly not a 190-lb, 5 ft 4 in woman, nor is it a 228 lb, 5 ft 11 inch man. But Americans have put on so much weight that the prevailing view of what constitutes "normal" weight has been revised upward. Normal is closer to what we see in old movies from the 1940s and '50s with people like Jimmy Stewart and Donna Reed. That's what we are supposed to look like.

So Don actually remains mildly overweight but is judged as "too skinny," or even cancer-ridden, by friends and family.

Ignore such comments. As you lose pounds and approach a truly desirable weight, realize that you are returning to the normal state, not the vision of "normal" now held by most Americans.

Getting vitamin D right

Vitamin D is, without a doubt, the most incredible "vitamin"/prohormone/neurosteroid I have ever encountered. Frankly, I don't know how we got anything accomplished in health pre-D.

Unfortunately, people I meet rarely take their vitamin D in a way that accomplishes full restoration of vitamin D blood levels. It really isn't that tough.

Here's a list of common tripping points with vitamin D:

"I take vitamin D: 1000 units a day."
This is probably the most common mistake I see: Taking a dose that is unlikely to yield a desirable blood level. (We use 60-70 ng/ml of 25-hydroxy vitamin D as our target.) Most men and women require 6000 units per day to achieve this level. There is substantial individual variation, however, with an occasional person needing much more, a rare person requiring as little as 1000 units.


"I bought some vitamin D on sale. They were white tablets."
Time and again, patients in my office who initially have had successful vitamin D replacement, despite being reminded that only oil-based forms should be taken, switch to tablets. While they initially showed a 25-hydroxy vitamin D blood level, for instance, of 67 ng/ml on 8000 units per day with an oil-based capsule, they switch to a tablet form and the next blood level is 25 ng/ml. In other words, tablets are very poorly or erratically absorbed.

I have had people use tablets successfully, however, by taking their vitamin D tablets with a teaspoon of oil, e.g., olive oil. Oil is necessary for full absorption.


"I'm going to Florida. I'll stop my vitamin D because I'm going to lay in the sun."
Wrong. 90% of adults over 40 years old have lost the majority of their ability to activate vitamin D in the skin. A typical response might be an increase in blood level from 25 to 35 ng/ml--a 10 ng increase with a dark brown tan.

There is an occasional person who, with sun exposure, increases blood levels substantially. This can occur in both fair-skinned and dark-skinned people, though I've never seen it happen in an African-American person. The occasional person who maintains the ability to convert vitamin D with sun exposure, or young people, should seasonally adjust their vitamin D dose, e.g., 6000 units winter, 3000 units summer, or some other regimen that maintains desirable blood levels. You can see that monitoring blood levels (we check levels every 6 months for the first 2 years) is crucial: You cannot know what your vitamin D needs are unless you assess 25-hydroxy vitamin D levels.


"I drink plenty of milk. I don't think I need to take vitamin D."
Oh, boy. This is so wrong on so many levels.

First of all, no adult should be drinking plenty of cow's milk. (A discussion for another day.) Second of all, cow's milk averages 70 units of vitamin D, often the D2 form (ergocalciferol), per 8 oz. Even if the FDA-mandated 100 units per day were present, an average adult dose of 6000 units would require 60 glasses of milk per day. Can you say "diarrhea"?

Likewise, other food sources of vitamin D, such as fish (300-400 units per serving) and egg yolks (20 units per yolk), are inadequate. This makes sense: Humans are not meant to obtain vitamin D from food, but from sun exposure over a large body surface area. And this is a phenomenon that is meant to occur only in the youthful, ensuring that nature takes its course and us older folks get old and make way for the young (i.e., unless we intervene by taking vitamin D supplements).


"My doctor said that my vitamin D blood level was fine. It was 32 ng/ml."

Let's face it: By necessity, your overworked primary care physician, who manages gout, hip arthritis, migraine headaches, stomach aches, prostate enlargement, H1N1, depression, etc., is an amateur at nearly everything, expert in nothing. Nobody can do it all and get it right. Likewise vitamin D. The uncertain primary care physician will simply follow the dictates of the laboratory form that specifies "30-100 ng/ml" as the "normal" or "reference range." Unfortunately, the laboratory often quotes population distributions of a lab measure, not an ideal or desirable level.

To illustrate the folly of population distributions of a measure, imagine you and I want to know what women weigh. We go to a local mall and weigh several thousand women. We tally up the results and find that women weigh 172 lbs +/- 25 lbs (the mean +/- 2 standard deviations). (That's true, by the way.) Is that desirable? Of course it isn't. Population average or population distribution does not necessarily mean ideal or desirable.


"My husband's doctor said he should take 4000 units per day. So I just take the same dose."
That would be fine if all adults required the same dose. However, individual needs can vary enormously. A dose that is grossly insufficient for one person may be excessive for another. Once again, vitamin D dose needs can be individualized by assessing 25-hydroxy vitamin levels in the blood.


"I don't need to take vitamin D. I already take fish oil."
I suspect this mistaken belief occurs either because people confuse fish oil with cod liver oil, which does contain some vitamin D. (Cod liver oil is not the best source of vitamin D, mostly because of the vitamin A content; also a discussion for another time), or because they've heard that eating fish provides vitamin D. However, fish oil capsules do not contain vitamin D unless it is added, in which case it should be prominently and explicitly stated on the label.


"I don't have to take vitamin D. It's summer."

For most people I know, if it's a bright, sunny July day, where are they likely to be? In an office, store, or home--NOT lying in the sun with a large body surface area exposed. Also, most people expose no more than 5-10% of surface area in public. I doubt you cut the grass in a bathing suit. Because of modern indoor lifestyles and fashion, the majority of adults need vitamin D supplementation year-round.


I advise everyone that gelcap vitamin D is preferable. Some, though not all, liquid drop forms have also worked. Take a dose that yields desirable blood levels. And blood levels of 25-hydroxy vitamin D are ideally checked every 6 months: in summer and in winter to provide feedback on how much sun activation of D you obtain.

If your doctor is unwilling or unable to perform vitamin D testing, fingerstick vitamin D test kits can be obtained from Track Your Plaque.

Jimmy Moore's thyroid adventure

My friend, Jimmy Moore of Living La Vida Low Carb, describes his thyroid experience here.

As Jimmy points out, he was looking for a way to jump-start a 50-lb weight loss. In my experience, low thyroid hormone levels ("hypothyroidism") are an exceptionally common cause for weight gain. Correcting even marginal hypothyroidism can facilitate weight loss, often resulting in 10 or more pounds of weight loss within the first month.

Unfortunately, Jimmy's thyroid hormone panel proved normal: TSH 1.3, thyroid hormones free T3 and free T4 in the mid- to upper-half of the reference range.

I say "unfortunately" because it is really an easy, inexpensive, and benign solution for losing weight. (I don't, of course, wish that Jimmy or anyone else develops a thyroid condition. But it really can provide gratifying weight loss results when thyroid function is low.) Jimmy might consider taking his oral temperature first thing in the morning as another means of assessing the adequacy of thyroid function.

Perhaps you will be luckier than Jimmy and have thyroid dysfunction that can be corrected and jump-start your weight loss program. Fingerstick thyroid test kits like the one Jimmy used are available here from Track Your Plaque.
All posts by william-davis

High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Restaurant eating: A fructose landmine

There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.