Wheat-free pumpkin bread

Try this recipe for a wheat-free, gluten-free yet healthy "bread." Unlike many gluten-free foods that send blood sugar skyward, this will not.

Ingredients:
2 cups ground almond meal (Buy it from Trader Joe's--70% cheaper than other grocery stores.)
1/2 cup ground flaxseed
1/2 cup sour cream (full-fat, of course)
15 oz canned pumpkin (Trader Joe's is bisphenol A-free)
2 medium to large eggs
1/2 cup chopped walnuts or pecans
4 tablespoons butter, melted
2 teaspoons baking powder
2 teaspoons cinnamon
1 teaspoon nutmeg or allspice
Dash of salt
Choice of non-nutritive sweetener (I used 3 teaspoons Trader Joe's stevia extract powder, the one mixed with lactose. Two tablespoons of Truvia, 1/2 teaspoon of the more concentrated stevia extract, or 1/2 cup Splenda are other choices. You can taste the mixed batter to gauge sweetness if in doubt.)

Preheat oven to 350 degrees F. Grease baking pan (e.g., 10 x 6 inch). The pan should be big enough so that the mix will not be more than 2 inches deep, else it will require much longer to bake. (If you have only smaller pans, you will need to cook longer while the pan is covered with aluminum foil.)

Mix all ingredients thoroughly in large bowl. Pour mix into greased baking pan.

Cover with aluminum foil and bake for 30 minutes. Remove foil and bake for additional 30 minutes or until inserted toothpick or knife comes out dry.

Serve with cream cheese or as is.

(I'd have some pictures, but the kids and I ate it up before I thought to take any photographs.)

Vitamin D: Deficiency vs optimum level

Dr. James Dowd of the Vitamin D Cure posted his insightful comments regarding the Institute of Medicine's inane evaluation of vitamin D.

Dr. Dowd hits a bullseye with this remark:

The IOM is focusing on deficiency when it should be focusing on optimal health values for vitamin D. The scientific community continues to argue about the lower limit of normal when we now have definitive pathologic data showing that an optimal vitamin D level is at or above 30 ng/mL. Moreover, if no credible toxicity has been reported for vitamin D levels below 200 ng/mL, why are we obsessing over whether our vitamin D level should be 20 ng/mL or 30 ng/mL?

Yes, indeed. Have no doubts: Vitamin D deficiency is among the greatest public health problems of our age; correction of vitamin D (using the human form of vitamin D, i.e., D3 or cholecalciferol, not the invertebrate or plant form, D2 or ergocalciferol) is among the most powerful health solutions.

I have seen everything from relief from winter "blues," to reversal of arthritis, to stopping the progression of aortic valve disease, to partial reversal of dementia by achieving 25-hydroxy vitamin D levels of 50 ng/ml or greater. (I aim for 60-70 ng/ml.)

The IOM's definition of vitamin D adequacy rests on what level of 25-hydroxy vitamin D reverses hyperparathyroidism (high PTH levels) and rickets. Surely there is more to health than that.

Dr. Dowd and vocal vitamin D advocate, Dr. John Cannell, continue to champion the vitamin D cause that, like many health issues, conradicts the "wisdom" of official organizations like the IOM.

Large LDL counts, too

Chad is a 43-year old father of five kids.

Earlier this year, he developed chest pain that got worse and worse. He ended up with a total of five stents in all three coronary arteries. After a devastating experience with Lipitor that resulted from a ruptured tendon, he came to me for an option.

Chad's lipoproteins:

Slow Burn works

I have been impressed with the results I've been obtaining with Fred Hahn's Slow Burn strength training technique.

Because I have limited time to hang around the gym, any technique that provides outsized results in a limited amount of time, I have to admit, appeals to me. In past, I'd be lucky to squeeze in one or two strength training sessions per week, devoting the rest of the time to biking outdoors, biking on a sedentary bike (while playing XBox), jogging, or doing strenuous yard work like digging trenches and planting shrubs.

Over the years, I've gradually lost muscle, since the strength training effort suffered with my time limitations.

So Fred's time-efficient Slow Burn idea struck a chord. Having now done it with some regularity, usually 1-2 times per week since mid-September, I have gradually added back visible muscle. My Slow Burn workouts, involving 8-10 different movements, seem to have restored the muscle I've lost, with a very modest time effort.

It took a little getting used to. After Fred showed me how to do the movements--slow motion movement in both the "positive" and "negative" directions, with smooth, non-jerking transitions, one set per muscle group, each taken to muscle exhaustion--it left me unusually tired and sore the next day. This surprised me, given the limited time involved. Breathing is also very important; the usual exhale-during-the-positive, inhale-during-the-negative pattern is replaced by breathing freely during the entire set. I didn't get this at first and ended up with headaches that got worse with each set. Breathing freely relieved me from the effect.

I have strength trained since I was around 15 years old. Back in the early 1970s, I had about 2000 lbs of barbells and dumbbells in my garage in New Jersey, while also driving back and forth to the Morristown, NJ, YMCA to train with friends. The Slow Burn movements forced me to break habits established over nearly 40 years of conventional strength training.

I've also played around with mixing conventional movements with Slow Burn movements to keep it fresh. This also seems to work.

If you're interested in giving it a try, here's an animation that demonstrates what Slow Burn movements look like. Fred has also produced an excellent 3-DVD set of videos that more fully describe the practice.

Do your part to save on healthcare costs

While many of the factors that drive the relentless increase in health care costs are beyond individual control, you are still able to exert personal influence over costs. Just as in political elections, your one vote alone may not count; it's the collective effort of many people who share similar opinions that results in real change.

I just got the new monthly premium for my high-deductible health insurance: Up $300 per month, putting my family's total premium over $2000 per month---for four healthy people. (My son fractured his wrist playing high school hockey earlier this year; that may explain at least some of the increase.)

I'm going to shop around for a better deal. However, shopping is likely to only stall the process. It will not address the systemic problems with healthcare that continue to drive premiums up and up and up.

So what can you do to help keep costs down? Here are a few thoughts:

Never accept a prescription for fish oil, i.e., Lovaza. Just buy far less costly over-the-counter fish oil. I treat complex hyperlipidemias, including familial hypertriglyceridemia, ever day. I NEVER use prescription fish oil. A typical 4 capsule per day Lovaza prescription adds around $280 to $520 per month to overall health costs (though your direct out-of-pocket costs may be less, since you shove the costs onto others in your plan).

Never accept a prescription for vitamin D. Prescription vitamin D is the mushroom or invertebrate form anyway. Just buy the human (cholecalciferol, D3) form from your health food store or "big box" store. They yield consistent increases in 25-hydroxy vitamin D levels, superior to the prescription form. And they're wonderfully inexpensive.

Eliminate wheat from your diet. If there is a dietary strategy that yields unexpected and outsized benefits across a wide spectrum of health, it's elimination of this thing we're sold called "wheat," you know, the genetically-transformed, high-yield dwarf mutant that now represents 99% of all wheat sold. Blood sugar drops, pre-diabetics become non-prediabetics, diabetics reduce need for medication or become non-diabetic, cholesterol values plummet, arthritis improves, acid reflux and irritable bowel symptoms improve or disappear, just to mention a few. Wheat elimination alone, I believe, would result in incalculable savings in both healthcare costs and lives saved.

Be sure to obtain iodine. In the fuss to cut salt use, everyone forgot about iodine. Lack of iodine leads to thyroid disease, usually hypothyroidism, that, in turn, causes cholesterol values to increase, weight to increase, and heart disease risk to double, triple, or quadruple. Iodine supplementation is easy and wonderfully inexpensive.

Over time, I hope that all of us can help develop the effort to self-direct more and more of our own health. Our Track Your Plaque program has shown me that, not only can people take the initiative to direct aspects of their own health, they can do it better than 99% of doctors.  

I'm sure there are many, many other ways to help reduce costs. Any suggestions?

Fish oil: What's the difference?

Ultra-purified, pharmaceutical grade, molecularly distilled. Over-the-counter vs. prescription. Gelcap, liquid, emulsion.

There's a mind-boggling variety of choices in fish oil today. A visit to any health food store, or any "big box" store for that matter, will yield at least several, if not dozens, of choices, all with varying and often extravagant claims of purity and potency.

So what's the real story?

Given the analyses conducted over the years, along with my experience with dozens of different preparations, I believe that several conclusions can be reached about fish oil:

Fish oil is free of contamination with mercury, dioxin, PCBs, or furans. To my knowledge, only one fish oil preparation has been found to have a slight excess of PCBs. (This is different from cod liver oil that has been found by one source to have a slight excess of PCBs.)

Oxidative breakdown products differ among the various brands. Consumer Lab (http://www.consumerlab.org/), for instance, has found that several widely available brands of fish oil contained excessive oxidative breakdown products (TOTOX). You can perform you own simple test of oxidative breakdown products: Sniff it. Your fish oil should pass the "sniff test." High quality fish oil should smell non-fishy to lightly fishy. Rancid fish oil with excessive quantities of oxidative breakdown products will smell nasty fishy.

FDA approval does not necessarily mean greater potency, purity, or effectiveness. It just means that somebody assembled the hundreds of millions of dollars to obtain FDA approval, followed by lots of marketing savvy to squash the competition.

This means that there are a number of excellent fish oil products available. My favorites are the liquid fish oils from Pharmax, Nordic Naturals, and Barleans. Capsules from Carlson, PharmaNutrients, and Fisol have also performed consistently. The "big box" capsules from Sam's Club and Costco have also performed well and are wonderfully affordable.

Wheat-free pie crust

I've been working on wheat-free yet healthy recipes these past two months.

You can buy wheat-free, gluten-free foods at the store, of course. But the majority of these products are unhealthy because cornstarch, rice starch, potato starch, or tapioca starch are commonly used in place of wheat. Recall that these are among the few foods that increase blood glucose higher than even wheat.

Here's a simple recipe for wheat-free pie crust that works best for cheesecake, pumpkin pie, and cream pies, but not for berry or other fruit pies like apple.

You will need:
?
1½ cups ground pecans
6 tablespoons melted butter?or melted coconut oil
1 teaspoon vanilla extract?
2 teaspoons cinnamon
1 medium egg
2 tablespoons Truvia™ or ½ teaspoon stevia extract or ½ cup Splenda®

Mix all ingredients thoroughly in bowl. Pour mixture into pie pan and press onto bottom and sides.

Fill pie crust with desired filling. You can fill it with your favorite cheesecake recipe (e.g., Neufchatel or cream cheese, sour cream, eggs, vanilla, and stevia; add pumpkin for pumpkin cheesecake) and bake, usually at 350 degrees F for one hour. 

Yes, the butter provokes insulin and artificial sweeteners can trigger appetite. But, for the holidays, a slice or two of pie made with this crust will not increase blood sugar nor trigger the uncontrolled impulse eating that wheat crust will trigger.

Have a cookie

Here's a great insight dating all the way back to 1966 from one of the early explorations in lipoproteins from the National Institutes of Health lab of Levy, Lees, and Fredrickson:

The nature of pre-beta (very low density) lipoproteins

The subject is a 19 year old female (among the total of 11 in the this small, diet-controlled study) who was first fed a low-carbohydrate (50 grams per day), low-cholesterol diet; followed by a high-carbohydrate (500 grams per day), low-fat (5 grams per day) diet.






To B or not to B

Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)
All posts by william-davis

Fat and fiber composition of nuts



From Mukuddem-Petersen J, Oosthuizen1 W, Jerling JC. J Nutr 2005.



If you haven't yet done so, adding raw nuts to your health program yields a broad panel of health benefits.

Contrary to conventional advice, nuts can be eaten in unlimited quantities. Provided they are raw--unroasted, unsalted (since salting only accompanies roasted nuts), not roasted in unhealthy oils like hydrogenated cottonseed or soybean (very common)--they do not make you fat, regardless of the quantity consumed. Beer nuts, honey-roasted nuts, mixed nuts roasted in unhealthy oils with salt added are either fattening or exert other unhealthy effects (e.g., hypertension, rise in Lp(a), and cancer from the hydrogenated fats).

Some notable observations from the chart:

--Hazelnuts and macadamians are the richest in monounsaturates
--Walnuts are the richest in the omega-6 linoleic acid, while also richest in the "omega-3" linolenic acid.
--From a fat composition standpoint, raw cashews and dry roasted peanuts aren't so bad.
--Pistachios figure pretty favorably in this analysis, rich in monounsaturates.
--Coconuts are unusually rich in saturated fat, though about half is lauric acid--an issue for future conversation.



Here's a listing of the fiber composition of nuts per 1 oz serving (about a handful):

Almonds (24 nuts) 3.5 g
Brazilnuts, dried (6-8 nuts) 2.1 g
Cashew nuts, dry roasted, with salt added (18 nuts) 0.9 g
Hazelnuts or filberts 2.7 g
Macadamia nuts, dry roasted, with salt added (10-12 nuts) 2.3 g
Mixed nuts, dry roasted, with peanuts, with salt added 2.6 g
Peanuts, all types, dry-roasted, without salt 2.3 g
Pecans (20 halves) 2.7 g
Pine nuts, dried 1.0 g
Pistachio nuts, dry roasted, with salt added (47 nuts) 2.9 g
Walnuts, English (14 halves) 1.9 g

Data courtesy USDA Nutrient Database


Note that almonds are the winners with 3.5 grams fiber per ounce, pistachios a close second. Pine nuts and cashews place last on the fiber content chart.

Not addressed by the charts is protein content of nuts, as well as the low sugar content, all additional beneficial aspects of nuts. Nuts are also a moderate source of magnesium (though seeds like pumpkin and sunflower shine in the magnesium content area).

Rather than micromanage the specific fat and fiber content of your diet, why not get a little of the good of everything on the list and just mix and match the nuts? (Mixed and matched on your own, of course, not a hydrogenated cottonseed oil nut mixture).

Flush-free niacin kills

Here, I re-post a conversation I've posted before, that of the scam product, "no-flush" niacin, also known as "flush-free" niacin.

I find this issue particularly bothersome, since I have a patient or two each and every week who forgets the explicit advice I gave them to avoid these scam products altogether. Despite costing more than conventional niacin, they exert no effect, beneficial or otherwise. Niacin--the real thing--exerts real and substantial beneficial effects. No-flush or flush-free does nothing except drain your wallet. I continue to marvel at the fact that supplement manufacturers persist in selling this product. Ironically, it commands a significant premium over other niacin forms.

They are outright scams that should be avoided altogether.


My former post, No-flush niacin kills:

Gwen was miserable and defeated.

No wonder. After a bypass operation failed just 12 months earlier with closure of 3 out of 4 bypass grafts, she has since undergone 9 heart catheterization procedures and received umpteen stents. She presented to me for an opinion on why she had such aggressive coronary disease (despite Lipitor).

No surprise, several new causes of heart disease were identified, including a very severe small LDL pattern: 100% of LDL particles were small.

Given her stormy procedural history, I urged Gwen to immediately drop all processed carbohydrates from her diet, including any food made from wheat or corn starch. (She and her husband were shocked by this, by the way, since she'd been urged repeatedly to increase her whole grains by the hospital dietitians.) I also urged her to begin to lose the 30 lbs of weight that she'd gained following the hospital dietitians' advice. She also added fish oil at a higher-than-usual dose.

I asked her to add niacin, among our most effective agents for reduction of small LDL particles, not to mention reduction of the likelihood of future cardiovascular events.

Although I instructed Gwen on where and how to obtain niacin, she went to a health food store and bought "no-flush niacin," or inositol hexaniacinate. She was curious why she experienced none of the hot flush I told her about.

When she came back to the office some weeks later to review her treatment program, she told me that chest pains had returned. On questioning her about what she had changed specifically, the problem became clear: She'd been taking no-flush niacin, rather than the Slo-Niacin I had recommended.

What is no-flush niacin? It is inositol hexaniacinate, a molecule that indeed carries six niacin molecules attached to an inositol backbone. Unfortunately, it exerts virtually no effect in humans. It is a scam. Though I love nutritional supplements in general, it pains me to know that supplement distributors and health food stores persist in selling this outright scam product that not only fails to exert any of the benefits of real niacin, it also puts people like Gwen in real danger because of its failure to provide the effects she needed.

So, if niacin saves lives, no-flush niacin in effect could kill you. Avoid this scam like the plague.

No-flush niacin does not work. Period.


Disclosure: I have no financial or other relationship with Upsher Smith, the manufacturer of Slo-Niacin.


Copyright 2008 William Davis, MD

CT coronary angiography is NOT a screening procedure

I've recently had several hospital employees tell me that their hospitals offered CT coronary angiograms without charge to their employees.

Among these hospital employees were several women in their 30s and 40s.

Why would young, asymptomatic, pre-menopausal women be subjected to the equivalent of 100 chest x-rays or 25 mammograms? Is there an imminent, life-threatening, symptomatic problem here?

All of these women were without symptoms, some were serious exercisers.

There is NO rational justification for performing CT coronary angiography, free or not.

What they really want is some low-risk, yet confident means of identifying risk for heart disease. Cholesterol, of course, is a miserable failure in this arena. Framingham risk scoring? Don't make me laugh.

Step in CT coronary angiography. But does CT coronary angiography provide the answers they are looking for?

Well, it provides some of the answers. It does serve to tell each woman whether she "needs" a heart procedure like heart catheterization, stent, or bypass surgery, since the intent of CT angiography is to identify "severe" blockages, sufficient to justify heart procedures.

Pitfalls: Because of the radiation exposure, CT angiography is not a procedure that can be repeated periodically to reassess the status of any abnormal findings. A CT angiogram every year? After just four years, the equivalent of 400 chest x-rays will have been performed, or 100 mammograms. Cancer becomes a very real risk at this point.

CT angiography is also not quantitative. Sure, it can provide a crude estimation of the percent blockage--the value your cardiologist seeks to "justify" a stent. But it does NOT provide a longitudinal (lengthwise) quantification of plaque volume, a measure of total plaque volume that can be tracked over time.

What's a woman to do? Simple: Get the test that, at least in 2008, provides the only means of gauging total lengthwise coronary plaque volume: a simple CT heart scan, a test performed with an equivalent of 4 - 10 chest x-rays, or 1 - 2.5 mammograms.

Perhaps, in future, software and engineering improvements will be made with CT coronary angiography that reduce radiation to tolerable levels and allows the lengthwise volume measurement of plaque. But that's not how it's done today.

The Wheat Deficiency Syndrome

Beware the dreaded Wheat Deficiency Syndrome.

Like any other syndrome, you can recognize this condition by its many tell-tale signs:

--Flat abdomen
--Rapid weight loss
--High energy
--Less mood swings
--Better sleep
--Diminished appetite
--Reduced blood sugar
--Reduced blood pressure
--Reduced small LDL and total LDL
--Increased HDL
--Reduced triglycerides
--Reduced C-reactive protein and other inflammatory measures


Of course, you could choose to cure yourself of this syndrome simply by taking the antidote: foods made with wheat flour, like bread, breakfast cereals, pastas, pretzels, crackers, and muffins.

All the signs of the syndrome will then disappear and you can have back your protuberant abdomen, irrational mood swings, exagerrated appetite, higher blood sugar, etc.

The Framingham Crap Shoot

The Framingham risk score is a risk-assessment tool that has become the basis for heart disease prediction used by practicing physicians.

The Framingham system determines that:

· 35% of the adult population in the U.S., or 70 million, is deemed “low-risk.” Low-risk is defined as the absence of standard risk factors for heart disease; low-risk persons have no more than a 1-in-20 chance (5%) of dying from heart disease in the next 10 years. Physicians are advised by the American Heart Association (AHA) and its experts that no specific effort at risk reduction is necessary.

· 25%, or approximately 50 million, U.S. adults are deemed “high-risk,” based on the presence of 2 or more risk factors. High-risk persons experience a 20%-30% likelihood of heart attack in the next 10 years. People at high-risk are candidates for preventive efforts according to the guidelines set by the Adult Treatment Panel-III (Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults; ATP-III) for cholesterol-reducing statin drug treatment and for “lifestyle-modifying” advice.

· The remaining 40% of the adult population, or 80 million people, are judged “intermediate-risk,” with the likelihood of heart attack between 5-20% over the next 10 years. This group should receive preventive advice and might be considered for statin drug treatment.


Let’s do some arithmetic. By the above scheme, the low-risk population will experience 3,500,000 heart attacks over the next decade, or 350,000 heart attacks per year.

The intermediate-risk population (without preventive treatment) will experience 8,000,000 heart attacks over the 10-year time period, or 800,000 per year.

The high-risk population, the group most likely to receive standard advice on diet, exercise, and be prescribed statin cholesterol drugs, will have their risk reduced by 35% by preventive efforts over the 10-year period. This means that heart attacks over 10 years will be reduced from 12,500,000 to 8,125,000 by standard prevention efforts, or reduced to 812,500 heart attacks per year.

These numbers are no secret. They are well known facts that have simply come to be accepted by the medical community. In other words, the standard approach to heart attack prediction makes the fact that two million people will succumb to cardiovascular events in the next year no mystery. This exercise in prediction is coldly accurate when applied to a large population.

The problem is that this approach cannot reliably distinguish which individuals will have a heart attack from those who will not.

From 100 people chosen at random, for instance, the numbers game played above will not confidently identify who among those 100 will have a heart attack, who will not, who will develop anginal chest pains and end up with stents or bypass surgery, or who will die. We just know that some of them will. Some people at high risk will have a heart attack, some people at intermediate risk will have a heart attack, some people at low risk will have a heart attack.

For any specific individual (like you or me), it’s a crap shoot.

That's why precise individual measurement of cardiovascular risk is required for real risk assessment, not applying broad statistical observations and forcing them to conform to the unique life of a specific individual, particularly risk calculators with as few risk parameters as the Framingham risk score.

At what score should a heart catheterization be performed?

That's easy: NONE.

(Although I've addressed this previously, the question has come up again many times and I thought it'd be worth repeating.)

In other words, no heart scan score--100, 500, 1000, 5000--should lead automatically to procedures in someone who underwent a heart scan but has no symptoms.

This question is a common point of confusion.

In other words, is there a specific cut-off that automatically triggers a need for catheterization?

In my view, there is no such score. We can't say, for instance, that everybody with a score above 1000 should have a catheterization. It is true that the higher your score, the greater the likelihood of a plaque blocking flow. A score of 1000 carries an approximately 25-30% likelihood of reduced blood flow sufficient to consider a stent or bypass. This can nearly always be settled with a stress test. Recall that, despite their pitfalls for uncovering hidden heart disease in the first place, stress tests are useful as gauges of coronary blood flow.

But even a score of 1000 carries a 70-75% likelihood that a procedure will not be necessary. This is too high to justify doing heart catheterizations willy-nilly.

Unfortunately, some of my colleagues will say that any heart scan score justifies a heart cath. I believe this is absolutely, unquestionably, and inexcusably wrong. More often than not, this attitude is borne out of ignorance, laziness, or a desire for profit.

Does every lump or bump justify surgery, radiation, and chemotherapy on the chance it could represent cancer? Of course not. There is indeed a time and place for these things, but judgment is involved.

In my view, no heart scan score should automatically prompt a major heart procedure like heart catheterization in a person without symptoms. If a stress test is normal, signifying normal coronary flow (and there are no other abnormal phenomena, such as abnormal left ventricular function), then there is no defensible rationale for heart procedures. Heart procedures like stents and bypass cannot prevent heart attacks in future; they can only restore flow when flow is poor, or stop the heart attack that is about to occur.

However, EVERY heart scan score above zero is a reason to engage in a program of prevention.

"It's genetic"

At 53, Sam had been through the wringer with heart disease. After his first heart attack at age 50, he'd undergone four heart catheterizations, 5 stents, and, most recently, a bypass operation. He came to us to see if there was a better solution.

After hearing Sam's story, I asked,"Did your doctors suggest to you why you had heart disease?"

"Well, they said it was genetic, since my father went through the same thing in his early 50s, though he died after his second heart attack at age 54. They said it was bad luck and nothing could be done about it."

Though Sam's case is more dramatic than most, I hear this argument every day: Risk for heart disease is genetic.

It's true: There are indeed multiple reasons for inheriting causes for coronary heart disease, genes that heighten inflammatory responses, oxidative responses, modify lipoprotein particles, increase blood pressure, etc. There has even been some excitement over developing chromosomal markers for heightened risk.

That's all well and fine, but what can we do about it today?

In practical life, many inherited genetic patterns can be expressed in ways that you and I can identify--and correct. They are not chromosomal markers, but end products of genetic patterns. (Although there are indeed identifiable chromosomal markers, they have not yet led to meaningful treatments to my knowledge.)

These readily identifiable patterns include:

--Lipoprotein(a)--Clearly genetically transmitted, passed from mother or father to each child with a 50% likelihood, then you onto your children if you have it.

--Small LDL--Although small LDL is amplified by high-carbohydrate diets and obesity, it can also occur in slender people who do not indulge in carbohydrates --i.e., a genetic tendency. Or, it can be a combination of poor lifestyle magnifying the genetic tendency for small LDL.

--Low HDL--Particularly the extremes of low HDL below 30 mg/dl. (Although, interestingly, I am seeing more of these people, though not all, respond to vitamin D replacement. Perhaps an important subgroup of low HDL people are really Vitamin D Receptor (VDR) variants.)

--ApoE--Two variants are relevant: ApoE2 and ApoE4. In my experience, it's the E2 that carries far greater significance, though the data are somewhat scanty. ApoE4 people are more sensitive to the fats in their diet (greater rises in LDL with fats; thus, some people advocate a tighter saturated fat restriction with this pattern, though I am not convinced that is the best solution), while ApoE2 people are exceptionally sensitive to carbohydrates, develop extravagant increases in triglycerides, and are very diabetes-prone with even the most minimal weight gain. If two "doses" of the E2 gene are present (homozygotic), then the tendencies are very exagerrated. E4 people are also subject to greater likelihood of Alzheimer's, though it is not a certain risk in a specific individual.

--Postprandial disorders--We use the fasting intermediate-density lipoprotein (IDL) as an easy, obtainable index of the ability to clear after-eating byproducts of meals from the blood. Increased IDL has been related to increased coronary, carotid, and aortic aneurysmal disease.

--Hypertriglyceridemia-i.e., increases in triglycerides, While not all forms of high triglycerides confer risk for atherosclerosis, many do, particularly if associated with IDL, small LDL, increased LDL particle number and/or apoB.


There are more, but you get the point. There are clear-cut genetically-transmitted reasons for greater risk for cardiovascular disease. Some, like lipoprotein(a), yield very high risk. Others, like increased triglycerides, yield mixed levels of risk.

Importantly, all of these patterns--ALL--are identifiable and are treatable. Treatment may not always be the easiest thing, but they are treatable nonetheless. While lipoprotein(a), for instance, is the most difficult pattern to correct in the above list, I remind everyone that our current "record holder" for reversal of plaque and heart scan scores--63% reduction--has lipoprotein(a) that we corrected.

If you've been told that your risk for cardiovascular disease or coronary plaque is "genetic" and thereby uncorrectable and hopeless, run the other direction as fast as you can. Get another opinion from someone willing to take the modest effort to tell you precisely why.

Tim Russert Revisited

A Heart Scan Blog reader brought this piece by Dr. MacDougall to my attention.

Dr. MacDougall created a fictitious posthumous conversation between himself and the late Tim Russert. MacDougall paints a picture of a hardworking, hard-living man who adhered to an overindulgent lifestyle of excessive eating. He concludes that a vegetarian, low-fat diet would have saved his life.

Beyond being disrespectful, I would differ with Dr. MacDougall’s assessment. In fact, I’ve heard an interview with Mr. Russert’s primary care physician in which the doctor claimed that Mr. Russert had been counseled on the need for a low-fat diet and, in fact, adhered to it quite seriously. Far from being an overindulgent, overeating gourmand, he followed the dictates of conventional dietary wisdom according to the American Heart Association. The low-fat diet articulated by Dr. MacDougall is simply a little more strict than that followed by Mr. Russert.

What exactly could Mr. Russert have done to prolong his life? Several basic strategies:

--Added fish oil. This simple strategy alone would have reduced the likelihood of dying suddenly by almost half.

--Eliminated wheat and cornstarch—Mr. Russert developed diabetes in the last few years of his life. By definition, diabetes is an inability to handle sugars and sugar-equivalents. Wheat and cornstarch yield immediate and substantial surges in blood sugar greater than table sugar; elimination causes weight to plummet, blood sugar to drop, and diabetes (at least in its early phases) can be eliminated in many people, particularly those beginning with substantial excess weight.

Just those two strategies alone would more than likely have avoided the tragic death that brought Mr. Russert’s wonderful life and career to an abrupt end.

Of course, he could have even taken his heart health program even further, as we do in the Track Your Plaque program. While the conversation has focused on how to avoid tragic events like sudden cardiac death, why not take it a step farther and ask, "How can coronary plaque be measured, tracked, and reversed?"

In that vein, Mr. Rusert could have restored vitamin D to normal levels; identified all hidden sources of heart disease using lipoprotein testing (though he had small LDL without a doubt, given his generous waist size, HDL of 36 mg/dl and high triglycerides); considered niacin. Simple, yet literally lifesaving efforts, that make reversal much more likely.

Those simple steps, in fact, would have tipped the scales heavily in Mr. Russert’s favor, making a heart attack and/or sudden death from heart disease exceptionally unlikely.

Water: Bottled vs. tap

The Fanatic Cook has a great post discussing the findings of the Environmental Working Group (EWG) on the quality of bottled water.

The full text of the study from the EWG can be viewed here.

They report that "the bottled water industry promotes an image of purity, but comprehensive testing by the Environmental Working Group (EWG) reveals a surprising array of chemical contaminants in every bottled water brand analyzed" . . . After analyzing 10 brands, they conclude that "tests strongly indicate that the purity of bottled water cannot be trusted. Given the industry's refusal to make available data to support their claims of superiority, consumer confidence in the purity of bottled water is simply not justified."

"EWG's study has revealed that bottled water can contain complex mixtures of industrial chemicals never tested for safety, and may be no cleaner than tap water. Given some bottled water company's failure to adhere to the industry's own purity standards, Americans cannot take the quality of bottled water for granted. Indeed, test results like those presented in this study may give many Americans reason enough to reconsider their habit of purchasing bottled water and turn back to the tap."


For these reasons, as well as environmental reasons (plastic bottles filling up dumpsites), I think it is becoming clearer and clearer that bottled water is something we should only use in a pinch, not habitually.

Can CRP be reduced?

The JUPITER study has sparked a lot of discussion about c-reactive protein, or CRP.

If we follow the line of reasoning that prompted this study, reducing CRP may correlate with reduction of cardiovascular events. Thus, in the JUPITER study, Crestor 20 mg per day reduced cardiovascular events by nearly half.

From a CRP perspective, starting values were 4.2 mg/dl in the Crestor group of the trial, 4.3 mg/dl in the placebo group. After 24 months, CRP in the Crestor group was 2.2 mg/dl, 3.5 mg/dl in the placebo group, representing a 37% reduction.

Now, in our Track Your Plaque program--an experience that has yielded the virtual ELIMINATION of cardiovascular events--we aim for a CRP level of 1.0 mg/dl or less, ideally 0.5 mg/dl or less. The majority of people achieve these ambitious levels. In fact, it is a rare person who does not.

How do we achieve dramatic reductions in CRP? We use:

--Weight loss through elimination of wheat and cornstarch--This yields impressive reductions.

--Vitamin D--I have no doubt whatsoever of vitamin D's capacity to exert potent anti-inflammatory effects. I am not entirely sure why this happens (enhanced sensitivity to insulin, reduced expression of tissue inflammatory proteins like matrix metalloproteinase and others, etc.), but the effect is profound.

--Elimination of junk foods--like candies, cookies, pretzels, rice cakes, potato chips, etc.

--Exercise--Amplifies the benefits of diet on CRP reduction.

--Not allowing saturated fats to dominate--Yes, yes, I know. The demonization of saturated fat conversation has been largely replaced by the Taubesian saturated fat has not been confidently linked to heart disease conversation. But controlled feeding studies, in which a single component of diet is manipulated (e.g., saturated vs. monounsaturated vs. polyunsaturated fat) have clearly shown that saturated fats do activate several factors in the inflammatory response.

--Fish oil--Though I am a firm believer in the huge benefits of omega-3 fatty acid supplementation/restoration, the anti-inflammatory effect is modest from a CRP perspective. However, there are anti-inflammatory benefits beyond that of simple CRP (via normalization of eicosanoid metabolism and other pathways).

--Weight loss--A BIG effect. Weight loss drops CRP like a stone. The CRP-reducing effect is especially large if achieved via carbohydrate reduction.

Of course, this is much more complicated than taking a pill. But it is effective to achieve health benefits outside of cardiovascular risk, is enormously useful as part of a weight loss effort, and doesn't cost $1400 per year like Crestor.

In short, if CRP reduction is the goal, it certainly does not have to involve Crestor.