Wheat elimination continues to yield explosive and unexpected health benefits.

I initially asked patients in the office to eliminate wheat because I wanted to help them reduce blood sugar and pre-diabetic tendencies.

A patient would come to the office, for example, with a blood sugar of 118 mg/dl (in the pre-diabetic range) and the other phenomena of pre-diabetes or metabolic syndrome (high blood pressure, high inflammation/c-reactive protein, low HDL, high triglycerides, small LDL), and the characteristic wheat belly. Eliminate wheat and, within three months, they lose 30 lbs, blood sugar drops to normal, blood pressure drops, triglycerides drop by several hundred milligrams, HDL goes up, small LDL plummets, c-reactive protein drops.

People also felt better, with flat tummies and more energy. But they also developed benefits I did not anticipate:

--Improved rheumatoid arthritis--I have seen this time and time again. Eliminate wheat and the painful thumbs, fingers, and other joints clear up dramatically. Many former rheumatoid sufferers people tell me that one cracker or pretzel will trigger a painful throbbing reminder that lasts a couple of hours.

--Improved ulcerative colitis--People incapacitated with pain, cramping, and diarrhea of ulcerative colitis (who are negative for the antibodies for celiac disease) can experience marked improvement. I've seen people be able to stop all their nasty colitis medications just by eliminating wheat.

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

--Better mood--Eliminating wheat makes you happier and experience more stable moods. Just as wheat is responsible for a subset of schizophrenia and bipolar illness (this is fact), and wheat elimination generates dramatic improvement, when you or I eliminate wheat, we also experience a "smoothing" of mood swings.

--Better libido--I'm not sure whether this is a consequence of losing a belly the size of a watermelon or improvement in sex hormones (esp. testosterone) or endothelial responses, but more interest in sex typically develops.

--Better complexion--I'm not entirely sure why, but various rashes will often dissipate, bags under the eyes are reduced, itching in funny places stops.

It's also peculiar how, after someone eliminates wheat for several months, re-exposure of an errant cracker or sandwich results in cramping and diarrhea in about 30% of people.

Obviously, people with celiac disease, who can even die of exposure to wheat, are even worse. What other common food do you know of that makes us sick so often, even occasionally with fatal outcome?

If you have lipoprotein(a), Lp(a)--the most aggressive known cause of heart disease that no one has heard of--then you need to tell your children.

Lp(a) is a "cleanly" inherited genetic pattern: If either parent has it, there's a 50% chance that you have it. If you have it, then there's a 50% likelihood that each of your children has it. (Note that each child experiences a likelihood of 50%, not 50% of your children. This is because each child is conceived as an independent statistical event. So much for romance!)

The atherogenicity (plaque-causing potential) of Lp(a) also tends to get transmitted. In other words, if your Dad had a heart attack at age 50 due to Lp(a) and you share Lp(a), then you likely share a similar magnitude of risk as your Dad. If your Mom had Lp(a), though passed quietly at age 89 without any overt evidence of heart disease, then you are likely to share the relatively benign form of Lp(a).

For most of us with Lp(a), however, it is best to assume that it has at least some potential for causing heart disease, being the most aggressive cause known. (That is, until we have the ability in everyday clinical practice to characterize Lp(a) by assessing such factors as the size of the apoprotein(a) molecule, the number of kringle "repeats" on the tail, etc. Until then, we need to rely on the crude, though helpful, observation of family history.)

At what age should you inform your children? There's no hard-and-fast rule. However, I generally suggest to patients that they talk about Lp(a) with their children when they reach their 20s or 30s, old enough to begin to understand the implications and begin to think about adopting healthier lifestyles. Is treatment required at, say, age 35? That depends on the pattern of Lp(a)-related heart disease in the family: With exceptionally aggressive forms, it might be reasonable to begin treatment at this relatively early age.

The sterol question continues to pop up.

Sterols are an ingredient widely added by food manufacturers that allows a "heart healthy" claim, since sterols have been shown to reduce LDL cholesterol (at least transiently). HOWEVER, sterols have also been implicated in possibly increasing risk for heart disease. After all, people with the genetic condition called sitosterolemia absorb sterols into the blood and develop coronary heart disease in their teens and twenties. Those of us without sitosterolemia who increase sterol intake with sterol-enriched foods increase blood levels of sterols several-fold. Is this healthy, or does it contribute to coronary plaque as it does in people with sitosterolemia?

Below, I've reprinted a previous Heart Scan Blog post on sterols.

Sterols should be outlawed

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

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

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

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

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

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

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

Though the data are mixed:

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

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

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

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

Each Nature Valley Healthy Heart Bar contains 400 mg sterols.

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

Promise SuperShots contains 400 mg sterols per container.

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

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

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

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

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

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

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

Why do obese people claim it is impossible to fast?

Most overweight people are terrified at the prospect of facing any period of time without ready access to food. Persuading them to begin a program of intermittent fasting is a hopeless cause. They just refuse.

Contrary to popular opinion, this is not just glutonny at work. It is the effect of what I call "the cycle of hunger," the 2-hour up and down cycle of rising sugar and insulin, followed by their inevitable fall. The precipitous fall of sugar and insulin triggers mental fogginess, fatigue, and insatiable hunger. (By the way, this is the same phenomenon underlying the silly notion of "grazing.")

According to an LA Times article, fasting may be difficult to impossible for some people:

"Ruth Frechman, a registered dietitian in Burbank and spokeswoman for the American Dietetic Assn., says she frequently sees such extreme strategies backfire. 'You're hungry, fatigued, irritable. Fasting is not very comfortable. People try to cut back one day and the next day they're starving and they overeat.'"
(Not surprising, coming from the American Diatetic Assn. They, along with such agencies as the American Diabetes Association, are vocal proponents of low-fat, high-carbohydrate, "healthy whole grain" diets--you know, the diets that make us fat and diabetic.)

Ms. Frechman is correct: Having someone engage in a period of fasting, no matter how brief, when the diet leading up to the fast is filled with "healthy whole grains" and other carbohydrates will result in painful hunger that eventually overcomes any effort. A period of overeating typically follows the aborted attempt.

Fasting cannot work as long as the 2-hour cycle of hunger continues. The first step: Eliminate the 2-hour cycle of hunger by dramatically reducing or eliminating carbohydrates. Our preferred method is to eliminate wheat, cornstarch, and sugars. (Just be aware of wheat withdrawal, the fatigue that develops in the first 5 days after wheat elimination that affects up to 30% of people.)

Once wheat, cornstarch, and sugars are eliminated, hunger reverts to that of physiologic need--appetite will be smaller and less intense, since it is driven by your body's needs, not by abnormal stimulation from wheat, cornstarch, and sugar. The fear of not having food dissolves, the 2-hour cycle of mental fogginess, fatigue, and hunger will be gone.

Intermittent fasting is a wonderful strategy for reducing weight; gaining control over lipids, lipoproteins, and coronary plaque; regaining appreciation for food; reducing appetite. But it's not even worth trying unless you've already eliminated the unnatural appetite triggers that will booby-trap any fasting effort.

134 people responded to the latest Heart Scan Blog poll:

When I ask my doctor to test my thyroid, he/she:

Accommodates me without question 45 (33%)

Questions why, but orders the tests 49 (36%)

Refuses because you seem "healthy" 20 (14%)

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)

That's better than I anticipated: 69% of physicians complied with this small request. After all, you're not asking for major surgery. You're just asking for a very basic test, as basic as a blood count or electrolytes. 36% of respondents said that their doctor asked why, but still complied; this is simply practicing good medicine--If there is a problem, your doctor would like to know about it.

However, the remainder--31%--were refused in one way or another. Incredibly, 11% were ridiculed.

Although this was not asked in the poll, I believe that it is a safe assumption that you asked with good reason: you're abnormally fatigued, you have been gaining weight for no apparent reason or can't lose weight despite substantial effort, or you feel cold at inappropriate times.

Let's say you're tired. Ever since last summer, you've suffered a gradual decline in energy.

So you ask your doctor to assess your thyroid. He refuses. "You're just fine! There's nothing wrong with you."

You disagree. In fact, you are quite convinced that there is something physically wrong. What do you do?

You could:

--Drink more coffee
--Exercise more in the hopes that it will snap you out of your lethargy
--Sleep more
--Take stimulants of various sorts

Or, you could get your thyroid assessed and settle the issue. But how can you get this done when your doctor won't accommodate you, even though you have perfectly fine health insurance and are simply interested in feeling better and preserving your health?

You could test your thyroid yourself. This is why we're making self-testing kits available. Test kits are available here.

This is yet another facet of the powerful revolution that is emerging: Self-directed health.

A Heart Scan Blog reader posted the following question:

It is not clear to me why getting a cardiac scan is the necessary first step, if in fact the next step would be to bring down small LDL particles which is revealed on a NMR lipoprofile or VAP test. Why isn't the NMR or VAP test the first thing?

Good question. Think of it this way:

Lipoproteins, as measured via VAP (Vertical Auto Profile) or NMR (Nuclear Magnetic Resonance), provide a snapshot of risk from a metabolic viewpoint at that moment. Lipoproteins shift with the tides of age, menopause, weight changes, even what you ate last evening for dinner (especially small LDL). There are also other factors that cause coronary plaque, as well, not revealed through lipoprotein testing, such as vitamin D deficiency, smoking, high blood pressure, phosopholipase A2, lipoprotein(a), inflammatory factors, thyroid dysfunction, omega-3 fatty acid deficiency, etc.

A heart scan, providing a coronary calcium score, provides an indirect measure of coronary plaque that is the sum total of lipoprotein and other plaque-causing factors that have accumulated up to the time of your scan--regardless of the cause.

It means that two females, each 60 years old, with 70% small LDL, HDL 42 mg/dl, triglycerides 150 mg/dl, and mild hypertension, have identical markers for potential coronary risk, but can have widely different heart scan scores. One might have a score of zero, while the other might have a score of 300.

Why would the same panel of causes measured at one moment yield wildly different quantities of plaque? Several reasons:

1) The lifestyles, eating habits, and weight of each woman differed during their earlier years, not currently reflected in this moment's lipid or lipoprotein patterns. Perhpaps one experienced several years of extraordinary stress from a failed marriage, or suffered through two years of depression that caused her to smoke and overeat.

2) There are hidden factors that affect coronary plaque growth that we are presently not able to detect, e.g., vitamin D receptor genotype, cholesteryl-ester transfer protein variants, variation in inflammatory factors. If we can't measure it, we won't know whether it might influence coronary plaque risk.

With all the changes that occur over a person's life, with the uncertainties of yet-to-be-identified causes for coronary plaque, how can you possible know what your risk for heart disease truly is? Yup--a heart scan. Do it and you will know.

Helena posted this instructive comment in response to the Heart Scan Blog post, Weight loss and vitamin D. It illustrates the confusion common among physicians and pharmacists on the differences between D2 and D3.

(Edited slightly for clarity.)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from wool. In other words, D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not.)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware that he had gotten his Vitamin D by prescription, I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong.”

Eric called his pharmacy right away and got the answer I was expecting: ergocalciferol. On confronting the person Eric was talking to, the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric. “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still believing that stamp the doctor had given Eric earlier, he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on. The thing that jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that were called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferred Vitamin D3. The brand name, Drisdol, had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I know that people are most likely to be prescribed a D2 pill than to be told to buy over-the-counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol, as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!

Incredible.

Why prescribe plant form D2 when you can get perfectly reliable, safe, effective D3--the human form, at the health food store for about $6?

Once again, it's the peculiar false bias of physicians and pharmacists: If it's prescription, it must be good; if it comes from a health food store, it must be bogus.

Humans need human vitamin D. Plain and simple.

For more on the D2 vs. D3 issue, see the Heart Scan Post, The case against vitamin D2.

Heart Scan Blog reader, Kris, related this enlightening story of weight loss (slightly edited for clarity).

Kris learned that excess weight is gained through multiple causes. The solutions are therefore multiple, not just one change in diet or two.

I started studying about my thyroid issue much earlier and did lose some weight. But ever since I started following Dr. Davis’s blog, it has given me confidence that I was on the right track. I did have my thyroid and iodine figured out from other sources, but Dr. Davis helped me to understand the issues with not only the thyroid but vitamin D3, fructose, fish oil, niacin, wheat etc. I have lost 43lb in last 14 months.

It seems to me that there are certain percentages of weight connected with different issues. For example, after I gave up alcohol and sugar, I lost about 14lbs from total weight of 243lbs, weight came down to about 229lb. Then it stopped at 229lb, even though I was in the gym almost 5 to 6 days a week with full workouts.

After I changed my thyroid medication to natural thyroid hormones (took synthetic T4 for over 10 years), the weight dropped down further 13lbs or so in matter of few days, shape of the face changed from moon shape/double chin to ordinary long face. Then it kind of stopped at around 213-216 lbs.

After giving up wheat, reducing carbs, increasing protein intake (whey protein, chicken etc. no soya, no fructose) the weight came down another 14lbs. Now it is around 200-202lbs and I am over 6.2 tall with heavy set of bones.

I feel better than I have ever in my life. More stamina, more clarity/no fog, more confidence and 99% of the time relaxed and being able to see the situation from multiple angles.

I use to be able to drink a liter or more jack denial without a problem in one evening but now can’t stand half a can of beer (I miss JD). Drinking alcohol makes me sick. I sleep well and if I wake up in the middle of the night, I have no problem going back to sleep. No more out of breath stair climbing at all.

One other thing: I used to be the most attractive meal to the mosquitoes, but not anymore. This year I haven’t been bitten once. I take my dog to the park everyday and I do not use any mosquito repellent, what a relief. I don’t know if it is because of thyroid, iodine, wheat or something else. Skin texture has changed dramatically. I do not use full soap or shampoo, 20% borax, 10 percent of my soap or shampoo for scent and rest water, mixed in a 500ml bottle. No more dandruff, dry skin, pimples for me.

Dr. Davis I am thankful to people like you who have the ability to see beyond what you have been taught and have the guts to say the way it is. Most of us work to make living on daily basis but some make their living while spreading their knowledge to save lives. Dr Davis you are one of those few people. Please keep it going.

I'd like to invite anyone who has followed the Track Your Plaque Break the Weight Barrier program to consider posting their stories and photos on the Heart Scan Blog.

Because our focus is prevention and reversal of coronary heart disease, we have not made an effort to catalog the weight loss experience that people have while on the program. For many, weight loss has been substantial. (Several people this week alone have reported weight loss of 9 to 46 lbs in the past 6 months.)

It would be helpful to hear and see these results.

For those of you who don't mind having a story and photo on this Blog, please come back in future to post your results. You will find this post by entering "weight loss" into the site-specific search bar at the top of the page.

At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.

She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.

But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.

Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.

Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Some references on this effect:

Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.

Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables

Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.

African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.

Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.

What will we do if or when CT heart scans become outdated and something better comes along?

Heart scans are, after all, our principal tool for detection and precise quantification of coronary atherosclerotic plaque. They provide the basis for the Track Your Plaque program: serial heart scans to track progression or regression of coronary plaque.

So what the heck will we do if heart scans become obsolete, if some other technology proves superior for precise lengthwise quantification of coronary plaque?

Simple: Then we will convert to that measure.

Say, for instance, that in 5 years, MRI advances to the point where it is quick and precise, despite the rapid motion of the heart that has, in past, caused this technology to stumble for plaque quantification. Instead of obtaining a heart scan score of, say, 350, instead an MRI might yield information like:

Calcium volume: 350 cubic mm
Soft plaque elements: 200 cubic mm
Fibrous tissue: 700 cubic mm

In other words, while a CT heart scan provides a calcium score that serves as a surrogate measure of total plaque volume, perhaps the next wave of technology will directly measure total plaque volume.

Don't CT coronary angiograms already measure total plaque volume?

No, they definitely do not. At present, the best they can do is visualize the non-calcific elements and suggest the diameter reduction created by plaque at a specific point. Thus, results like "50% blockage in the mid-left anterior descending." What they do not provide is a lengthwise total volume of plaque and all its elements. Perhaps some software manipulation in future will yield such information (and I think it will, though I personally have been unable to accomplish it).

So neither the Track Your Plaque program nor the Heart Scan Blog are necessarily bound to heart scans. But heart scans, in 2008, remain the number one best tool for plaque quantification that is easy, precise, available, and inexpensive. For those reasons, CT heart scans continue to serve as the basis for these programs, and not CT angiograms, MRI, or other non-quantitative technology.

Does the media engage in scare tactics?

Read the headlines in local newspapers, and you'd believe that your friends and neighbors are dropping like flies, all victims of heart attacks.

I occasionally peruse the headlines run in newspapers and magazines around the U.S. by subscribing to a feed service through Google. For the phrase, "heart attack," you can get a sample of what is being said around the country about people having heart attacks.

What continues to impress me is just how far off a truly constructive and helpful message the media provides every day. Not only are they guilty of delivering a flawed message, they also favor headlines and stories that scare the heck out of people. "This could happen to you!"

Is it just the quest for headlines that grab readers' attentions? Is there some complicity with the medical systems that pay significant advertising revenues for their heart disease programs and hospitals?

I doubt such complicity exists to any substantial degree. But the fact remains: Every day across the U.S., the media does an effective job of scaring the heck out of the public--enough for you to run to your doctor or hospital to find out if you, too, could fall victim to heart disease. A stress test, perhaps heart catheterization, three stents or bypass often results.

In effect, these headlines make great hospital PR, an inducement that flushes out the patient highly motivated to pursue further costly heart testing--whether or not it's needed.

A sampling:

Stress test could help prevent sudden heart attack

DAWN ZERA Times Leader Correspondent

Bob Schultz, 67, was feeling a persistent pain in his back, which he was pretty sure was caused by working on a deck for his son’s home.

But after the deck was finished, the pain was still there.

“It was nagging, but not enough to hurt,” Schultz said.

He visited his primary care physician, thinking maybe some muscle relaxants would be prescribed. The doctor sent him to a clinic in Tunkhannock to do a complete body CAT scan, and then had Schultz do a stress test. The on-site cardiac stress testing at a Geisinger Medical Group office in Tunkhannock showed that things did not look good: Schultz had a blockage. He was scheduled for a cardiac catheterization.

It was a surprise; a heart problem had not even crossed Schultz’s mind as a possible cause of his back pain.

“I had good cholesterol, have been the same weight for years, and had excellent blood pressure,” Schultz said.

He went for the catheterization at Geisinger Wyoming Valley, and there doctors discovered Schultz’s condition was even more serious. He had three blockages – 99 percent, 95 percent and between 80 and 90 percent.

“It shocked the living daylights out of everyone. It was surreal,” Schultz said.

The catheterization turned into open heart surgery that very same day.

The surgery was on a Tuesday, and he was home by Sunday. He never even had time to fully think about having the operation. And he had never experienced the typical warning signs of a heart problem, such as chest pain or shortness of breath.

“The doctors said I had the worst alarm system they’d ever seen,” Schultz said. “They probably saved my life, with me not knowing I had a problem.”

It also made him think about his brother, who had had been in good health but suddenly died in his 40s of a suspected heart attack.

“We never had any heart problems in our family, so we never believed it. But now I think, geez, it probably was true,” Schultz said.

His experience has served as a cautionary tale for friends and family. Just this past month, a friend specifically requested a stress test for himself.

“It sets off alarms in your circle. People think ‘if it can happen to him, it could happen to me,’ ” Schultz said. “It triggered people to think about what could happen to them.”

Firefighter Saves Heart-Attack Victim on D.C. Court

ABC News

A 30-year-old man suffered a heart attack while playing basketball on a D.C. court.

That's when a Brian Long's firefighter training kicked into action. The 25-year-old D.C. firefighter's team had just finished their pick-up league game Friday evening at Lafayette Elementary School's basketball court when the man stumble to the ground.

"He ran a few feet and collapsed again so I turned him over and I looked at him his eyes rolled back and he just stopped breathing," Long said.

Long began performing chest compressions and soon he was joined by Anthony Gadson, a pharmaceutical sales representative, who learned CPR years ago and starting assisting with mouth to mouth resuscitation.

"If that were me, somebody would've done the same thing for me, so I feel like I did what I was supposed to do," Gadson explained.

While Long and Gadson worked to keep the victim's heart going, all the players and spectators, including teammate and league commissioner Bob Johnson, gathered around the lifesaving effort.

"We gathered in a circle and one of the wives of one of the players just led us in this huge prayer," said Johnson.

"It makes me feel great," Long told ABC 7/NewsChannel 8. "I am just glad that I am a D.C. Firefighter."

Free Drugs After Heart Attack Would Save Money, Lengthen Lives
More patients would take recommended medications, study says

By Ed Edelson

MONDAY, Feb. 18 (HealthDay News) -- Eliminating the cost of medications for people who have heart attacks would lead to longer lives and lower overall medical costs, new research suggests.

"These are highly effective medications that are relatively inexpensive, and the events they are designed to prevent are extremely expensive," said study author Dr. Niteesh K. Choudhry, a researcher in the division of pharmacoepidemiology and pharmacoeconomics at Brigham and Women's Hospital in Boston and an assistant professor at Harvard Medical School. His report is published in the Feb. 19 issue of Circulation.

The study covered four drugs commonly prescribed after heart attacks -- aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers (ARBs), and statins. Use of those drugs is relatively low under the current system, in which people share the cost with Medicare or other health insurance plans, Choudhry said. For example, only 46 percent of people take beta blockers after heart attacks, and only 50 percent take cholesterol-lowering statins. Less than 20 percent of heart patients used all four of the medications, according to the study.

The model set up by Choudhry and his colleagues doesn't assume a major increase in compliance with prescriptions, because "cost is just one reason why patients do not take medications," he said, adding that relying on previous studies of drug cost and use, the model assumes an increase of about 14 percent, with perhaps 64 percent of people taking the medicines if they were free.

The result would be an increase in average survival after a heart attack, from the present 8.21 quality-adjusted life years to 8.56 years. "That is small in an absolute sense, but in an aggregate sense, it is very large," Choudhry said.

And medical costs over a lifetime would go down, from the current $114,000 to $111,600, the study added.

"This study adds to a growing body of research showing how important it is to reduce or eliminate patient co-payment for drugs," said Robert M. Hayes, president of the Medicare Rights Center in New York. "Medicare should take the lead in forging the creation of drug coverage that allows patients to get the medications their doctors consider vital."

"It certainly makes sense from the medical point of view," said Dr. Richard A. Stein, a professor of medicine at New York University. "Studies have shown that giving even middle-income people free drugs improves outcome. The greatest benefit will go to people in the lower socioeconomic and immigrant population."

But the study is theoretical, Stein noted. "One would like to see some real-world trial to determine whether this works in fact, whether providing free drugs without co-payment would make a difference, he said.

Such a study has begun at Harvard, Choudhry noted. His group is working with a major health insurer, not Medicare, in a trial that assigns some people to get medications without cost, while others will get the standard co-payment.

"It will take several years for us to get answers," Choudhry said. But similar investigations are being started by other medical insurers and corporations, he added.

The idea is potentially applicable to some other chronic conditions, such as congestive heart failure and diabetes, Choudhry noted. And, if the use of recommended medications after a heart attack goes up more than predicted by the model, "the cost savings would be phenomenal," he said.

More information

To learn about how to stay on your statins, consult the National Heart, Lung, and Blood Institute.

Heart Attack Threatens Young, Old

BAKERSFIELD, Calif. -- Nearly 1.2 million men and women suffer a heart attack every year in the United States, according to the American Heart Association. However, not all of the victims are old.

Brian Connell considers himself a lucky guy. At the age of 39, he's physically active, he has a high-level job, and he is also a heart attack survivor. "I know I was overweight and obviously had some other risk factors against me," said Connell. "I wish I did more to prevent it, certainly."

Connell is doing plenty of things now. He met with a nutritionist and changed his diet. He gets regular exercise and takes medication to control his cholesterol. He also gets regular checkups.
Click here to find out more!

Cardiologist Jeffrey Popma said it's not unusual to see younger heart attack patients. "We have dozens of patients in our system every year who have been under 40 years old who have suffered a major heart attack," said Dr. Popma.

Popma said getting medical help quickly is the key to survival. Connell said that is what made all the difference for him. And when people ask him if that was his first heart attack, Connell said he is quick to tell them it was his last heart attack.

Copyright 2008 by TurnTo23.com. The Associated Press contributed to this report. All rights reserved.

The messages I take from such stories:

1) Get yourself to a hospital ASAP for any symptoms even vaguely suspicious of heart disease, because they will know what to do. You'll be doomed if you don't.

2) Hospitals and doctors are expert at saving you from the brink of disaster. The process, once you enter, is rapid and smooth and you will be eternally grateful.

3) Medicines save lives. You're going to die if you don't take medication.

As I've often said, one of the toughest battles of all in health and heart disease is sorting out fact from fiction. Unfortunately, the media continues to propagate the scare tactics that support the status quo of procedural heart care. Wittingly or unwittingly, they serve a $400 billion dollar a year gargantuan industry that remains hungry for growth.

Lost in the headlines are the messages that could have been included, like:

Heart disease detectable decades before disaster

Or:

"Heart disease preventable, reversible, and--curable?"

Copyright 2008 William Davis, MD

The statin drugs can indeed play a role in a program of coronary plaque control and regression.

However, thanks to the overwhelming marketing (and lobbying and legislative) clout of the drug manufacturing industry, they play an undeserved, oversized role. I get reminded of this whenever I'm pressed to answer the question: "Which statin drug is best?"

In trying to answer this question, we encounter several difficulties:

1) The data nearly all use statins drugs by themselves, as so-called monotherapy. Other than the standard diet--you know, the American Heart Association diet, the one that causes heart disease--it is a statin drug alone that has been studied in the dozens of major trials "validating" statin drug use. The repeated failure of statin drugs to eliminate heart disease and associated events like heart attack keeps being answered by the "lower is better" argument, i.e., if 70% of heart attacks destined to occur still take place, then reduce LDL even further. This is an absurd argument that inevitably encounters a wall of limited effects.

2) The great bulk of clinical data examining both the incidence of cardiovascular events as well as plaque progression or regression have all been sponsored by the drug's manufacturer. It has been well-documnted that, when a drug manufacturer sponsors a trial, the outcome is highly likely to be in favor of that drug. Imagine Ford sponsors a $30 million study to prove that their cars are more reliable and safer. What is the likelihood that the outcome will be in favor of the competition? Very unlikely. Such is human nature.

If we were to accept the clinical trial data at face value and ignore the above issues, then I would come to the conclusion that we should be using Crestor at a dose of 40 mg per day, since that was the regimen used in the ASTEROID Trial that achieved modest reversal of coronary atherosclerotic plaque by intravascular ultrasound.

But I do not advocate such an ASTEROID-like approach for several reasons:

1) In my experience, nobody can tolerate 40 mg of Crestor for more than few weeks, a few months at most. Show me someone who can survive and tolerate Crestor 40 mg per day and I'll show you somebody who survived a 40 foot fall off his roof--sure, it happens, but it's a fluke.

2) The notion that only one drug is necessary to regress this disease is, in my view, absurd. It ignores issues like hypertension, metabolic syndrome, inflammatory phenomena, lipoprotein(a), post-prandial (after-eating) phenomena, LDL particle size, triglycerides, etc. You mean that Crestor 40 mg per day, or other high-intensity statin monotherapy should be enough to overcome all of these patterns and provide maximal potential for coronary plaque reversal? No way.

3) Plaque reversal can occur without a statin agent. While statin drugs may provide some advantage in the reduction of LDL, much of the benefit ends there. All of the other dozens of causes of coronary atherosclerotic plaque need to be addressed.

So which statin is best? This question is evidence of the brainwashing that has seized the public and my colleagues. The question is not which statin is best. The question should be: What steps do I take to maximize my chances of reversing coronary atherosclerotic plaque?

The answer may or may not involve a statin drug, regardless of the subtle differences among them.

Copyright 2008 William Davis, MD

Lipoprotein(a), or just Lp(a) to its close friends and neighbors, is among the most underappreciated and neglected of causes of coronary plaque. It's the Rodney Dangerfield of lipoproteins.

Lp(a) rarely gets diagnosed before people come to my office. They've often been through the ringer: doctors have thrown their hands up in frustration because of poor response to "standard" treatment (AKA statin drugs); the patient doesn't understand why they might be thin and active yet have the high blood pressure of someone 70 lbs heavier; they have heart disease despite wonderful cholesterol values.

One blood test and the answer becomes clear: They have Lp(a). It explains all these phenomena.

They why don't more physicians order this simple test? Why don't we hear more about this prevalent (1 in 5 people with coronary plaque have it) genetic pattern that accelerates risk for heart disease?

There are a number of reasons. But I believe the most powerful reason is simply that there is no big revenue-generating drug to treat it. Statins reduce LDL cholesterol to the tune of $27 billion dollars a year (2007 revenue). There's no such blockbuster for Lp(a). Of course, Niaspan represents the relatively anemic attempt to commercialize a pharmaceutical treatment for Lp(a), but side-effects and the lack of FDA trials for the Lp(a)-reducing indication have stalled its commercial success. (Efforts to block the flush with various products, by the way, may re-invigorate niacin as a pharmaceutical agent. The drug companies smell money here.)

Another reason for Lp(a)'s unpopularity: Though there are mounds of data that document--without question--that Lp(a) is an important risk for coronary disease and other forms of atherosclerotic disease, we lack treatment trials. For instance, niacin vs. placebo for 5 years, then count the number of heart attacks and deaths. We have numerous, repetitive, overlapping, redundant trials with statins adhering to this design. We have none for niacin and the treatment of Lp(a).

Niacin is also a pain in the neck for your doctor. He/she rapidly tires of the calls about the crazy and disconcerting flushing with niacin. Most are unaware that proper hydration reduces or eliminates the flush for the majority of people. It takes too much time and energy to educate people. (By the way, prescription Niaspan makes no mention of purposeful hydration. They only suggest the nonsensical "Take with a low-fat snack," i.e., snacks that actually counter the therpaeutic effects of niacin. What they should be saying is "take with a high-fat snack" like raw almonds, foods that facilatate the benefits of niacin.)

Should someone concoct a successful pharmaceutical treatment for Lp(a), it will make the news, headlines in health magazines and health sections of the newspaper will blare about how important Lp(a) is. Yet it has been there all along, frustrating people and their physicians.

In the Track Your Plaque experience, Lp(a) clearly 1) correlates with heart scan scores, 2) correlates with progression of heart scan scores without treatment, and 3) poses special challenges for treatment. Interestingly, some of our biggest failures have been with Lp(a), as well as some of our biggest successes. (Our current record holder for the largest percentage reduction in heart scan score has Lp(a).)

If you have coronary plaque, or if there is family risk of heart disease, then Lp(a), in my view, is an absolutely essential factor to test for. Yes, treatment poses challenges. But once you know who your enemy is, then you can focus your efforts on it. Not knowing whether or not you have it leaves your efforts unfocused and generally flawed.

Track Your Plaque Members, be sure to read our in-depth Special Report, Unique Treatments for Lipoprotein(a) Reduction.

Copyright 2008 William Davvis, MD

Unexpected effects of a wheat-free diet

Is Lp(a) part of your legacy to your children?

Do "Heart Healthy" sterols cause heart disease?

Why obese people can't fast

Test your own thyroid

Trains, planes, and heart scans

D2 and D3 are two different things

Weight loss: Different causes, different solutions

Calling all losers!

Weight loss and vitamin D

Scare tactics

Which statin is best?

Lipoprotein(a)--neglected and unappreciated