All posts by william-davis

Carbohydrate intolerance comes in many shades and colors, shapes and sizes.

I call all of its varieties the Carbohydrate Intolerance Syndrome, or CIS. (Not to be confused with CSI, or Crime Scene Investigation . . . though, come to think of it, perhaps there are some interesting parallels!)

At its extreme, it is called type II diabetes, in which any carbohydrate generates an extravant increase in blood sugar, followed by the domino effect of increased triglycerides, reduction in HDL, creation of small LDL, heightened inflammation, etc. and eventually to kidney disease, coronary atherosclerosis, neuropathies, etc.

An intermediate form of carbohydrate intolerance is called metabolic syndrome, or pre-diabetes. These people, for the most part, look and act like diabetics, though their reaction to carbohydrate intake is not as bad. Blood sugar, for instance, might be 125 mg/dl fasting, 160 mg/dl after eating. The semi-arbitrary definition of metabolic syndrome includes at least three of the following: HDL <40 mg/dl in men, <50 mg/dl in women; triglycerides 150 mg/dl or greater; BP 135/80 or greater; waist circumference >40 inches in men, >35 inches in women; fasting glucose >100 mg/dl.

This is where the conventional definitions stop: Either you are diabetic or have metabolic syndrome, or you have nothing at all.

Unfortunately, this means that the millions of people with patterns not severe enough to match the standard definition of metabolic syndrome are often neglected.

How about Kevin?

Kevin, a 56 year old financial planner, is 5 ft 7 inches, 180 lbs (BMI 28.2). His basic measures:

HDL 36 mg/dl
Triglycerides 333 mg/dl
BP 132/78
Waist circumference 34 inches
Blood sugar 98 mg/dl

Kevin meets the criteria for metabolic syndrome on only two of the five criteria and therefore does not "qualify" for the diagnosis.

Kevin's basic lipids showed LDL 170 mg/dl, HDL 36 mg/dl, triglycerides 333 mg/dl.

But take a look at his underlying lipoprotein patterns (NMR):

LDL particle number 2231 nmol/L (equivalent to a "true" LDL of 223 mg/dl)
Small LDL 1811 nmol/l
Large HDL 0.0 mg/dl

In other words, small LDL constitutes 81% of all LDL particles (1811/2231), a severe pattern. Large HDL is the healthy, protective fraction and Kevin has none. These are high-risk patterns for heart disease. These, too, are patterns of carbohydrate intolerance.

Foods that trigger small LDL and reduction in healthy, large HDL include sugars, wheat, and cornstarch. Kevin is carbohydrate-intolerant, although he lacks the (fasting) blood sugar aspect of carbohydrate intolerance. But he shows all the underlying lipoprotein and other metabolic phenomena associated with carbohydrate intolerance.

We could also cast all three conditions under the umbrella of "insulin resistance." But I prefer Carbohydrate Intolerance Syndrome, or CIS, since it immediately suggests the basic underlying cause: eating carbohydrates, especially those that trigger rapid and substantial surges in blood sugar.

CIS is the Disease of the Century, judging by the figures (both numbers and humans) we are seeing. It will dominate healthcare in its various forms for many years to come.

The first treatment for the Carbohydrate Intolerance Syndrome? Some would say the TZD class of drugs like Avandia. Others would say a DASH or TLC (American Heart Association) diet. How about liposuction, twice-daily Byetta injections, or even the emerging class of drugs to manipulate leptin and adiponectin? How do "heart healthy" foods like Cheerios and Cocoa Puffs fit into this? (Don't believe me? The American Heart Association says they're heart healthy!)

The first treatment for the Carbohydrate Intolerance Syndrome is elimination of carbohydrates, except those that come from raw nuts and seeds, vegetables, occasional real fruit (not those green fake grapes), wine, and dark chocolates.

Maggie had been doing well on her program, enjoying favorable lipids near our 60-60-60 targets (HDL 60 mg/dl or greater, LDL 60 mg/dl or less, triglycerides 60 mg/dl or less). Last fall, her last set of values were:

Total cholesterol: 149 mg/dl
LDL cholesterol: 67 mg/dl
HDL cholesterol: 73 mg/dl
Triglycerides: 43 mg/dl

The holidays, as with most people, involved a frenzy of indulgent eating: Christmas cookies, cakes, pies, stuffing, potatoes, candies, etc.

Maggie returned to the office 6 pounds heavier with these values:

Total cholesterol: 210 mg/dl
LDL cholesterol: 124 mg/dl
HDL cholesterol: 57 mg/dl
Triglycerides: 144 mg/dl

In other words, holiday indulgences caused an increase in LDL cholesterol, a reduction in HDL, an increase in triglycerides, an increase in total cholesterol.

What happened?

At first glance, many of my colleagues would interpret this as fat indulgence and/or a "need" for statin drug therapy.

Having done thousands of lipoprotein panels, I can tell you that, beneath the surface, the following has occurred:

--Overindulgence in carbohydrates from the goodies triggered triglyceride (actually VLDL) formation in the liver, released into the blood.
--Increased triglycerides and VLDL triggered a boom in conversion of large LDL to small LDL (since triglycerides are required to form small LDL particles) via cholesteryl-ester transfer protein (CETP) activity.
--Increased triglycerides and VLDL interacted with HDL particles, causing "remodeling" of HDL particles to the less desirable, less protective small particles, which do not persist as long in the blood, resulting in a reduction of HDL.

The critical factor is carbohydrate intake. This triggered a domino effect that is often misintepreted as excessive fat intake or a genetic predisposition. It is nothing of the kind.

I discussed this phenomenon with Maggie. She now knows to not overindulge in the holiday snacks in future and will revert promptly back to her 60-60-60 values.

I borrowed this from the enormously clever Dr. BG at The Animal Pharm Blog.

How to Give Yourself Hashimoto's Thyroiditis: 101

--lack of sunlight/vitamin D/indoor habitation
--mental stress
--more mental stress
--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)
--excessive 'social' calendar
--inherent family history of autoimmune disorders (who doesn't??)
--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)
--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc
--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)
--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)

If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things.

We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected.

Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.

I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)?

I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.

Heart health without a 12" incision

Heart health for less than $44,483 (Cost of a coronary stent according to the American Heart Association 2008 Update)

Track Your Plaque: A drug-free zone

The Food and Nutrition Board (FNB) of the Institute of Medicine is charged with setting the values for the Recommended Daily Allowances of various essential nutrients. However, when it comes to vitamin D, the FNB decided that "evidence is insufficient to develop an RDA and [an Adequate Intake, AI] is set at a level assumed to ensure nutritional adequacy."

The National Institutes of Health Office of Dietary Supplements lists the AI's for various groups of people:

14-18 years
Male 200 IU
Female 200 IU

19-50 years
Male 200 IU
Female 200 IU

51-70 years
Male 400 IU
Female 400 IU

71+ years
Male 600 IU
Female 600 IU

A reconsideration is apparently being planned in near-future that will (hopefully) incorporate the newest clinical data on vitamin D.

My question: Who cares what the FNB decides? Let me explain.

I monitor blood levels of 25-hydroxy vitamin D to assess the 1) starting level of vitamin D without supplementation, and 2) levels while on supplementation, preferably every 6 months (during sunny weather, during cold weather). I have done for the past 3 years in over 1000 people.

The requirement for vitamin D dose in adults, in my experience, ranges from as low as 1000 units per day to as high as 20,000 units per day, rarely more. The vast majority of women require 5000 units per day, males 6000 units per day to maintain a blood level in the desirable range. (I aim for 60-70 ng/ml.) A graph of the distribution of vitamin D needs in my area (Milwaukee, Wisconsin) is a bell curve, a curve more heavily weighted towards the upper vitamin D dose range.

Need for vitamin D to achieve the same blood level is influenced by age, sex, body size, race, presence or absence of a gallbladder, as well as other factors. But needs vary, even among similar people. For instance, a 50-year old woman weighing 140 lbs might need 4000 units per day to achieve a blood level of 25-hydroxy vitamin D of 65 ng/ml. Another 50-year old woman weighing 140 lbs might need 8000 units to achieve the same level, and 4000 units might increase her level to only 38 ng/ml. Two similar women, very different vitamin D needs. The differences can be striking.

Being a hormone--not a vitamin, as it was incorrectly labeled--vitamin D needs to be tightly regulated. We should have neither too little nor too much. I would liken it to thyroid hormones, which need to be tightly regulated for ideal health.

Now the FNB, in light of new data, wants to set new AI's, or even RDA's, for vitamin D for the U.S. This is an impossible--impossible--task. There is no way a broad policy can be crafted that serves everyone. It is impossible to state that all men or women, categorized by age, require X units vitamin D. This is pure folly and it is misleading.

The only rational answer for the FNB to provide is to declare that:

It is not possible to establish the precise need for vitamin D in a specific individual because of the multiplicity of factors, only some of which are known, that determine vitamin D needs. Individual need can only be determined by assessing the blood level of 25-hydroxy vitamin D prior to initiation of replacement and periodically following replacement to assess the adequacy of replacement dose. Continuing reassessment is recommended (e.g., every 6-12 months), as needs change with weight, lifestyle, and age.

Sure, it adds around $100-150 per year per person for lab testing to assess vitamin D levels. But the health gains made--reduced fractures, reduced incidence of diabetes, reduced colon, breast, and prostate cancer, less depression, reduced heart attack and heart procedures--will more than compensate.

We use Armour thyroid almost exclusively. I take it myself.

I am thoroughly convinced that, for at least 70% of people requiring thyroid replacement, the added T3 component makes a world of difference compared to isolated T4: More energy, greater alertness, better mental clarity, better weight loss, larger effects on lipoprotein(a).

However, there are substantial price disparities in different pharmacies.

For instance, in Milwaukee, a one month supply of 1 grain (60 mg) tablets costs:

Walgreen's: $36.00

Walmart: $9.54

That's a considerable price difference of nearly 400%. It therefore always pays to do a little bit of shopping.

If you want information on how prescription drugs fit into your life, then go to WebMD.

But, if you are looking for information that cuts through the bullcrap, is untainted by the heavy-handed tactics of the drug industry, or doesn't support the "a heart catheterization for everyone" mentality, then don't go there.

A Heart Scan Blog reader turned up this gem on the WebMD site:

Should I have a coronary calcium scan to check for heart disease?

In their report, they list some reasons why a heart scan should not be obtained:

Most of the time, a physical exam and other tests can give your doctor enough information about your risk for heart disease.

You've got to be kidding me. What tests are they talking about?

EKG? An EKG is a crude test that tells us virtually nothing about the coronary arteries or risk for heart attack. It is helpful for heart rhythm disorders and other abnormalities, but virtually useless for coronary disease unless a heart attack is underway or has already occurred.

Cholesterol? What level of cholesterol tells you whether you have heart disease? Tim Russert, for instance, had the same cholesterol values 5 years before his death as on the day of his death. How would cholesterol have told his doctor that heart disease was present? Does an LDL cholesterol of 180 mg/dl tell you that someone has heart disease, while a value of 130 mg/dl does not?

Stress test? You mean like the normal stress test Bill Clinton had 3 months before his near-fatal collapse? Stress tests are a gauge of coronary flow, not of coronary atherosclerosis. Huge amounts of coronary plaque can be present while a stress test--flow--remains normal.

No, a physical exam does not uncover hidden heart disease. The annual physical is, in fact, a miserable failure for detection of hidden heart disease.

You already know that your risk for heart disease is low or high. The test works best in people who are at medium risk but have no symptoms.

This bit of fiction comes from a compromise statement in the American College of Cardiology and American Heart Association "consensus" document detailing the role of heart scans in heart disease detection. Because conventional thinkers don't like the idea of very early detection in seemingly "low risk" people, nor do they like the idea of diabetics and smokers getting a heart scan because it's "obvious" that they are already at high risk, the middle ground was taken: Scan only people at "intermediate risk."

What the heck is "intermediate risk"? Are you intermediate risk?

In real life, using standard criteria (e.g., Framingham scoring) to decide who is low-, intermediate-, or high-risk fails to identify over 1/3 of people with heart disease, while subjecting many without heart disease (plaque) to needless treatment (meaning statins, since that's the only real preventive treatment on most doc's armamentarium).

Another fact: Heart scans are quantitative, not just normal or abnormal. Your heart scan score could be 5, it could be 150, it could be 500, or 5000---it makes a world of difference. The risk of someone with a score of 5000 is at very different risk than someone with a score of 5. It also provides much greater precision in determining a specific individual's risk.

The test could give a high score even if your arteries aren't blocked. This might lead to extra tests that you don't need.

This is true--if you doctor has no idea what he's doing.

This is like saying that you should never take your car to the repair shop because all mechanics are crooks. If you have an unscrupulous cardiologist who tells you that your heart scan score of 25 means you are a "walking time bomb" and heart catheterization is necessary to determine whether you "need" a stent . . . well, this is no different than the shady mechanic who advises you that your car's engine needs to be rebuilt for $3000, when all you really needed was a few new spark plugs.

Coronary plaque is coronary plaque, and all coronary plaque has potential for rupture (heart attack)--even if it doesn't block flow. This is true at a score of 10, or 100, or 1000--all plaque is potentially rupture-prone, though the more plaque you have, the greater the likelihood.

Not all blocked arteries have calcium. So you could get a low calcium score and still be at risk.

They're missing the point: ANY calcium score carries risk, so a low score should not be interpreted as having no risk. But, just because a procedure like stenting or bypass surgery is not necessary to restore flow, it does not mean that risk for plaque rupture is not present--it is.

Any heart scan score should be taken seriously, meaning sufficient reason to engage in a program of heart disease prevention.

Although not perfect, coronary calcium scoring remains the easiest, most accessible, and least expensive means for identifying and quantifying coronary atherosclerosis--whether or not WebMD and drug industry money endorse them.

The media outlets are gushing with the "research"/marketing spinoff of the JUPITER trial, an analysis conducted by Dr. Erica Spatz of Yale University, that suggests that statin use should be expanded to many millions more Americans.

USA Today: Study: 11M more should get statins

MedPage: JUPITER Findings Could Boost Statin Use by 20%

Health Day: Millions More Americans Might Be Placed on Statins

WebMD: More May Benefit From Cholesterol Drugs: Study Shows More Would Qualify for Statin Treatment if Levels of C-Reactive Protein Are Considered

You may recall that the JUPITER trial (discussed previously in a Heart Scan Blog post) studied the cardiovascular event risk in people with "normal" LDL cholesterols (calculated, of course, not measured) of 130 mg/dl or less, along with increased c-reactive protein, a crude inflammatory measure, of 2.0 mg/dl or greater. A 54% (relative) reduction in cardiovascular events occured in the group taking Crestor 20 mg per day.

What I see is a confluence of events that have brought us to the "statin drugs are necessary for everybody" mentality:

--The low-fat diet advice of the last 40 years has increased non-fat or low-fat foods that increase LDL, since removing fat from the diet provokes small LDL particle production and increases the inflammatory measure, c-reactive protein (CRP).

--The proliferation of "healthy whole grains" in the diet have also caused an enormous boom in small LDL particles, which is interpreted to the uninformed as "high cholesterol." It has also provoked CRP substantially.

--The advice to reduce salt intake has brought a broad re-emergence of iodine deficiency. When thyroid hormone production flags due to lack of iodine, LDL cholesterol (both large and small) increase.

--Our lives, which are increasingly conducted indoors, have worsened the already substantial vitamin D deficiency. While deficiency of vitamin D primarily reduces HDL cholesterol and increases triglycerides, it can also cause an increase in small LDL and a large increase in CRP.

In other words, a collection of events have converged to provide the appearance of high LDL cholesterol and high CRP. This creates the appearance of a "need" for statin drugs. The JUPITER trial now exploits both the LDL-reducing and CRP-decreasing effects of statins.

I view the foisting of Crestor via the JUPITER argument on the public as taking full advantage of the helpless situation many Americans find themselves in: Reduce fat intake, eat more healthy whole grains and . . . cholesterol and CRP skyrocket! "You need Crestor! See, I told you it was genetic," says the doctor after attending the nice AstraZeneca-sponsored drug dinner.

The notion of using a drug like Crestor to suppress inflammatory patterns is absurd. There are far better, easier, cheaper ways to achieve this goal, along with dramatic reduction in cardiovascular risk. But, to the ignorant, the helpless, or non-compliant with real change in diet and lifestyle, then Crestor does serve a purpose.

I can only hope that the excessive pushing of statin drugs on the public will sooner or later trigger a revolt.

Please be aware of the ignorant propagating information they have no business talking about.

This is one such example, a newsletter from pop exercise guru, Denise Austin.

Although I'm sure she means well, I have a problem with people who have little to no experience acting as experts, often simply repeating something they heard or read somewhere else. This has become particular problem with the internet, in which bad information can get repeated thousands of times, gaining a veil of "truth" through its repetition. I don't mean to pick specifically on Ms. Austin, since she joins a growing rank of pseudo-experts on vitamin D and other topics, but she provides a good example of how far wrong mainstream information can be.

Simple Steps
Do Your D!

Calcium often gets all the glory when it comes to bone health. But calcium wouldn't benefit your bones much without its partner, vitamin D!

Why? Vitamin D helps your body absorb calcium and keeps your bones strong; without enough vitamin D, the bones become weak and brittle, a condition called rickets in children, and osteomalacia in adults. Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

Unfortunately, not too many foods contain vitamin D naturally. (Tuna and sardines canned in oil are exceptions.) The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals. You can check the Nutrition Facts panel on packages and containers to see which products contain vitamin D. It should be listed after vitamins A and C, along with the percentage of the Daily Value that a serving of the food contains. The Daily Value (a standardized amount) for vitamin D is 400 IU, so if your milk has 25 percent of the Daily Value, it provides 100 IU per serving.

Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week to make enough. However, because of the increasing incidence of skin cancer in recent years, many experts are wary about recommending sun exposure.

So take a closer look at milk, yogurt, cereal, and margarine selections when you're doing your weekly shopping, and stock up on brands that are fortified with vitamin D. Challenge yourself to consume one source of vitamin D at least three days in the coming week! If you cannot eat or do not like any foods that contain vitamin D or are fortified with it, talk with your health care provider ASAP about taking a supplement. Your bones will thank you for it!

Let me list the mistakes in this piece:

Adults from 19 to 50 need 200 IU (international units) per day, while those from 51 to 70 need 400 IU daily. Those over 70 need 600 IU per day.

This is the same non-information that was the advice originally offered by the Food and Nutrition Board based on a best guesstimate due to lack of data. It is clear from newer data that doses required for full restoration of vitamin D are in the thousands of units. (My personal dose for full restoration of vitamin judged by serum levels of 25-hydroxy vitamin D is 8000 units per day.)

The information coming from the Food and Nutrition Board is about as good as the information coming from the USDA (you know, that "government" agency meant to represent the interests of ConAgra, Cargill, and Big Farming) and the American Heart Association (that represents consensus opinion from data 20 years out of date and now arm-in-arm with Big Food like General Mills, Kraft, and Nabisco). These agencies and the advice they offer has, over the past few years, become increasingly irrelevant and outdated. It is the Information Age, in which ulterior motives are becoming more readily exposed, yet they still operate by the rules of the Industrial Age and deliver a message that serves their own purposes.

Ms. Austin fell for it.

The good news is that many foods are now regularly fortified with vitamin D, including milk, some yogurts, margarines, and cereals.

First of all, what is a "diet expert" doing advocating industrial foods? Cereals, in particular, are among the worst foods on the supermarket shelves, whether or not they are fortified. Candy bars can be fortified, too; that doesn't make them any better for you.

The vitamin D added to these foods is, more often than not, the ergocalcferol, or D2, form that is woefully ineffective. And the dose added is trivial, usually in the 100-200 unit range per serving. The same goes for the milk, an inadequate source that we don't even factor into total intakes because of the low quantity.

Your skin can also make vitamin D using sunlight — you need about a half hour of exposure to the midday sun twice a week.

Nope. This might be true for a young person below age 30 in a southern environment. It is NOT true for the majority of people in northern climates and anyone over age 30 or 40, since we lose most of the capacity to activate vitamin D in the skin as we age. A deep, dark Florida tan does not necessarily mean that vitamin D has been activated. See A tan does not equal vitamin D. Here in Wisconsin, where, despite this darn cold winter, does enjoy wonderfully warm and beautiful summers, the average vitamin D dose need ranges from 4000-8000 units per day in summer, slightly more in winter.

By the way, it is not calcium that is instrumental to bone health. It is vitamin D. Calcium is the passive bricks and mortar of bones, while vitamin D is the bricklayer, the determinant of calcium's fate, the master control of bone health. Calcium supplementation becomes almost immaterial when vitamin D is restored.

I praise Ms. Austin for her hard work, trying to help fat Americans lose weight. But please ignore her advice on vitamin D, along with the numbing repetition of this mis-information that will likely propagate from other exercise gurus, dietitians, and pseudoexperts.

Kurt, a 50-year old businessman with a heart scan score of 323, had a :

--Conventional (calculated) LDL of 128 mg/dl
--Real measured LDL 241 mg/dl.

Laurie, a 53-year old woman who underwent a coronary bypass operation last year (before I met her), had a:

--Conventional LDL of 142 mg/dl
--Real measured LDL was 85 mg/dl.

(By "real, measured" LDL, I'm referring to LDL particle number in units of nmol/L obtained through NMR lipoprotein testing and dividing by 10, or just dropping the last digit to convert the value to mg/dl. This technique was arrived at by comparing the population distributions of these two parameters, LDL particle number and calculated LDL. This is the gold standard in my view. Similar numbers can be obtained by measuring apoprotein B, direct LDL, or calculated non-HDL, with diminishing reliability from first to last.)

In other words, Kurt's conventional LDL underestimated real LDL by 88%. Laurie's conventional LDL overestimated real LDL by 40%.

Interestingly, Laurie's doctor had insisted she take Lipitor for a high LDL cholesterol. Her real LDL was, in fact, low to begin with and benefits of a statin drug would be little to none. (Remember, in our Track Your Plaque approach, multiple other treatments are included, such as omega-3 fatty acids from fish oil, vitamin D normalization, and wheat elimination, strategies that yield benefits that others expect to obtain with statins.) Laurie's real cause of her heart disease proved to have nothing to do with LDL cholesterol, but involved lipoprotein(a) and thyroid issues.

Kurt proved to have a severe preponderance of small LDL particles--the worst kind of LDL, while Laurie had none--a benign pattern.

Then how can anyone make sense of the conventional, calculated LDL cholesterol that is generally (95% of the time) provided? If accuracy can stretch to plus or minus 80% . . . you can't. Conventional LDL is a miserably inaccurate number. The problem is that obtaining a superior number requires a step or two more testing and insight, something most busy primary care doc's simply don't have in the midst of a day filled with arthritis, bronchitis, diarrhea, belly aches, and seborrhea.

Yet conventional--I call it "fictitious"--LDL serves as the basis for this $27 billion (annual revenues) industry selling statin drugs.

This is meant to be neither an argument in favor of nor against statin drugs. However, it is plain as day that any study designed to reduce LDL cholesterol will be hopelessly clouded by calculated LDL imprecision. A calculated LDL of, say, 143 mg/dl might really be 187 mg/dl, or it might be 74 mg/dl--you can't tell by looking just at LDL. Yet billions of dollars of research and billions of dollars of healthcare costs are based on the treatment of this number.

This reminds me of the mark-to-market accounting magic that helped topple Wall Street.

I don't think that the statin world is poised for such a huge downfall. But I do see this as a source of enormous dilution of the effects of statin drugs. People who barely stand to benefit get the drugs, while others who might truly benefit are treated inadequately. It provides fuel to the growing idea that reducing LDL cholesterol fails to truly provide benefit.

I am no lover of statin drugs nor drugs in general. But I am a fan of knowing the truth. Despite my bashing of the drug industry (and make no mistake: the drug industry is a cutthroat, profit-seeking, do-anything-to-increase-sales industry), I do believe that there is a role for statin drugs (though far smaller than $27 billion per year). But the usual method of selecting people for treatment is pure fiction. The ATP-III cholesterol treatment guidelines? An anemic attempt to apply structure to meaningless values.

You and I do not need to subscribe to this sort of non-quantitative nonsense.

You can always count on Dr. John Cannell for unique perspectives on vitamin D. I reprint here his unfailingly entertaining and informative Vitamin D Newsletter on whether vitamin D replacement enhances physical performance.

The whole vitamin D "discovery" sometimes worries me. Vitamin D has proven to be an unbelievable, remarkable, dramatic boon to health, including facilitation in dropping CT heart scan scores. Yet the answer was always right in front of us. It worries me that you and I might have the answer to important questions right within our grasp all along--but don't know it. What if the same were true, say, for cancer? That is, a profound answer is right there, but our eyes just pass right over it.

Anyway, we should all keep our eyes open and perhaps you and I will continue to identify the most powerful tools available that return control over heart disease to us and take it away from the perverse, procedural hospital formula that still reigns.

If you haven't done so already, be sure to visit Dr. Cannell's website, www.vitamindcouncil.com.

The Vitamin D Newsletter
March, 2007

Peak Athletic Performance and Vitamin D

"No way doc." I had just finished telling my patient about the benefits of vitamin D, telling him he should take 4,000 IU per day, using all the techniques I had learned in 30 years of medical practice to convince someone proper treatment is important. But, he knew the U.S. government said he only needed 200 IU per day, not 4,000. He also knew the official Upper Limit was 2,000 IU a day. "What are you trying to do doc, kill me?" I told him his 25(OH)-vitamin D blood test was low, only 13 ng/ml. He had read about that too, in a medical textbook, where it said normal levels are between 10 and 40 ng/ml. "I'm fine doc;" adding "Are you in the vitamin business?" I explained I was not; that the government used outdated values; that recent studies indicate ideal 25(OH)D levels are about 50 ng/ml; and that they indicated that he needed about 4,000 IU per day to get his level up to 50. "No thanks doc, I'm fine."

So I tried a different tact. I brought him copies of recent press articles. "Look," I said, "look at these." Science News called vitamin D the Antibiotic Vitamin. The Independent in England says vitamin D explains why people die from influenza in the winter, and not the summer. U.S. News and World Report says almost everyone needs more. Newsweek says it prevents cancer and helps fight infection. In four different recent reports, United Press International says that: it reduces falls in the elderly, many pregnant women are deficient , it reduces stress fractures, and that it helps heals wounds.

He glanced at the articles, showing a little interest in stress fractures. Then he told me what he was really thinking. "Look doc, all this stuff may be important to old guys like you. I'm 22. All I care about are girls and sports. When I get older, maybe I'll think about it. I'm too young to worry about it. I'm in great condition." I couldn't argue. He was in good health and a very good basketball player, playing several hours every day, always on indoor courts.

What could I do to open his eyes? As an African American, his risk of early death was very high, although the risk for blacks doesn't start to dramatically increase until their 40's and 50's. Like all young people, he saw himself as forever young. The U.S. government was no help, relying on a ten-year-old report from the Institute of Medicine that is full of misinformation.

I tired to tell him that the 200 IU per day the U.S. government recommends for 20-year-olds is to prevent bone disease, not to treat low vitamin D levels like his. I pointed out the U.S. government's official current Upper Limit of 2,000 IU/day is the same for a 300 pound adult as it is for a 25 pound toddler. That is, the government says it's safe for a one-year-old, 25-pound, child to take 2,000 IU per day but it's not safe for a 30-year old, 300-pound, adult to take 2,000 and one IU a day. I mean, whoever thought up these Upper Limits must have left their thinking caps at home. Nevertheless, nothing worked. My vitamin D deficient patient was not interested in taking any vitamin D.

What are young men interested in? I remembered that he had told me: "Sex and sports." Two years ago I had researched the medical literature looking for any evidence vitamin D enhanced sexual performance. Absolutely nothing. That would have been nice. Can you imagine the interest?

Then I remembered that several readers had written to ask me if vitamin D could possibly improve their athletic performance? They told me that after taking 2,000 to 5,000 IU per day for several months, they seemed just a little faster, a little stronger, maybe had a little better balance and timing. A pianist had written to tell me she even played a better piano, her fingers moved over the keys more effortlessly! Was vitamin D responsible for these subtle changes or was it a placebo effect? That is, did readers just think their athletic performance improved because they knew vitamin D was a steroid hormone precursor (hormone, from the Greek, meaning "to set in motion")?

The active form of vitamin D is a steroid (actually a seco-steroid) in the same way that testosterone is a steroid and vitamin D is a hormone in the same way that growth hormone is a hormone. Steroid hormones are substances made from cholesterol, which circulate in the body, and work at distant sites by "setting in motion" genetic protein transcription. That is, both vitamin D and testosterone regulate your genome, the stuff of life. While testosterone is a sex steroid hormone, vitamin D is a pleomorphic (multiple function) steroid hormone.

All of a sudden, it didn't seem so silly. Certainly steroids can improve athletic performance although they can be quite dangerous. In addition, few people are deficient in growth hormone or testosterone, so when athletes take sex steroids or growth hormone they are cheating, or doping. The case with vitamin D is quite different because natural vitamin D levels are about 50 ng/ml and, since almost no one has such levels, extra vitamin D is not doping, it's just good treatment. I decided to exhaustively research the medical literature on vitamin D and athletic performance. It took me over a year.

To my surprise, I discovered that there are five totally independent bodies of research that all converge on an inescapable conclusion: vitamin D will improve athletic performance in vitamin D deficient people (and that includes most people). Even more interesting is who published this literature, and when. Are you old enough to remember when the Germans and Russians won every Olympics in the 60's and 70's? Well, it turns out that the most convincing evidence that vitamin D improves athletic performance was published in old German and Russian medical literature.

With the help of my wife and mother-in-law, both of whom are Russian, and with the help of Marc Sorenson, whose book Solar Power is a must read, I finally was able to look at translations of much of the old Russian and German literature. When one combines that old literature with the modern English language literature on neuromuscular performance, the conclusion is inescapable. The readers who wrote me are right.

If you are vitamin D deficient, the medical literature indicates that the right amount of vitamin D will make you faster, stronger, improve your balance and timing, etc. How much it will improve your athletic ability depends on how deficient you are to begin with. How good an athlete you will be depends on your innate ability, training, and dedication. However, peak athletic performance also depends upon the neuromuscular cells in your body and brain having unfettered access to the steroid hormone, activated vitamin D. In addition, how much activated vitamin D is available to your brain, muscle, and nerves depends on having ideal levels of vitamin D in your blood - about 50 ng/ml, to be precise.

Why would I write about such a frivolous topic like peak athletic performance when cancer patients all across this land are dying vitamin D deficient? Like many vitamin D advocates, I have been disappointed that the medical profession and the public don't seem to care about vitamin D. Maybe people, like my young basketball player, will care if it makes better athletes. So, Hey! You jocks! Listen up! I'm talking speed, balance, choice reaction time, muscle mass, muscle strength, squats, reps, etc. Important stuff. Here's the Vitamin D Council's first ever sports quiz.

1. Vitamin D-producing UVB radiation improves athletic performance and may have been widely practiced by German and Russian Olympic athletes in the 1960's and 70's.

True. I found tantalizing evidence the Russians and especially the Germans were on to this during the 60's and 70's when those two nations took turns placing number one and number two in the Olympics every year?

For example, in 1938, Russian researchers reported that a course of ultraviolet irradiations improved speed in the 100-meter dash in college students compared to matched controls, both groups undergoing daily training. Average 100-meter dash times decreased from 13.51 seconds to 13.28 seconds in the non-irradiated controls, but from 13.63 seconds to 12.62 seconds in the irradiated students. Here we see training improved times but training and irradiation improved times much more. Obviously, irradiation or vitamin D would not render the same magnitude of improvements in world-class sprinters, but they would be happy with a few milliseconds.

Gorkin Z, Gorkin MJ, Teslenko NE. [The effect of ultraviolet irradiation upon training for 100m sprint.] The Journal of Physiology of the USSR [Fiziol, z. (RSSR)] 1938; 25: 695-701. (In Russian)

If you want to know what early German thinking was on this, read this summation of the German literature:

"It is a well-known fact that physical performance can be increased through ultra-violet irradiation. In 1927, a heated argument arose after the decision by the German Swimmers' Association to use the sunlamp as an artificial aid, constituting an athletic unfairness, doping, so to speak. In 1926, Rancken had already reported the improving effect of sunlamp irradiation on muscle work with the hand-dynamo-graph. Heib observed an improvement in swimming times after repeated irradiations. In thorough experiments, Backmund showed that a substantial increase in muscle activity happens after radiation of larger portions of the body with an artificial sunlamp; that this performance increase is not caused through local - direct or indirect - effects on the musculature, but through a general effect. This general effect, triggered by ultra-violet irradiation, is caused by a systemic effect on the nervous system." (p. 17)

Parade GW, Otto H. Die beeinflussung der leistungsfahigkeit durch Hohensonnenbestrahlung. Zeitschrift fur Klinische Medizin (Z Klin Med),1940;137:17-21 [In German]

In 1945, two Americans measured the cardiovascular fitness and muscular endurance of 11 male Illinois subjects undergoing training in an indoor physical education class, comparing them to 10 matched controls. Both groups underwent similar physical training. Treatment consisted of ultraviolet irradiation, given in the nude, up to two minutes per session, three times per week, for ten weeks in the late fall and winter. After ten weeks, the treatment group had a 19% standard score gain in cardiovascular fitness compare to a 2% improvement in the control students. To regular readers of this newsletter, it should come as no surprise that the un-irradiated control group reported twice as many viral respiratory infections as the treatment group.

Allen R, Cureton T. Effects of Ultraviolet Radiation on Physical Fitness. Arch Phys Med 1945: 10: 641-44.

In 1952, the German sports medicine researcher, Spellerberg, reported on the effects of wholesale irradiation of athletes studying and training at the Sports College of Cologne - including many elite athletes - with a "central sun lamp." He irradiated the athletes in their bathing suits, on both sides of their bodies, for up to ten minutes, twice a week, for 6 weeks. He reported a "convincing effect" on athletic performance and a 50% reduction in sports injuries. Results were particularly impressive for swimmers, soccer, handball, hockey, and tennis players, as well as for boxers and most track and field athletes. He reported that irradiation leading to burns, further irradiation of athletes having achieved peak performance, and irradiation within 24 hours of competition, all impaired athletic performance. Their results were so convincing, the Sports College of Cologne officially notified the "national German and International Olympic committee." (p. 570)

Spellerberg AE. [Increase of athletic effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 567-70. [In German]

In 1952, Ronge exposed 120 German schoolchildren to UV lights installed in classrooms and compared them to 120 un-irradiated control children. Over a two-year period - excluding summer vacations - he tested both groups with a series of six cardiovascular fitness tests using a bike ergometer. Un-irradiated children showed a distinct seasonality in fitness, with the highest values right after summer break and the lowest values in the spring. Treated children showed no seasonal differences in physical performance. Differences in work performance between the irradiated and un-irradiated children were most conspicuous in the spring with 56% difference between the two groups. In a final experiment, he gave 30 children in the control classrooms 6.25 mg (250,000 IU) of vitamin D as a single dose in February and found their performance had "increased considerably," one month later but did not report the actual numbers. He concluded that vitamin D, either as a supplement or induced via UV irradiation, improved physical performance.

Ronge HE. [Increase of physical effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 563-6. [In German]

In 1954, another researcher, at the Max-Planck Institute for Industrial Physiology in Dortmund, Germany, administered three different wavelengths of UV light over 8 weeks to university students. He found that ultraviolet light in the vitamin D-producing UVB range was consistently effective in reducing resting pulse, lowering the basal metabolic rate, and increasing athletic performance. UVA had no effect; interestingly, artificial UVC irradiation (the atmosphere normally completely filters out UVC radiation and thus it's not naturally present on earth) also gave some positive results.

Lehmann G. [Significance of certain wave lengths for increased efficacy of ultraviolet irradiation.] Strahlentherapie. 1954 Nov;95(3):447-53. [In German]

In 1956, Hettinger and Seidel irradiated seven subjects in two different experiments: athletic performance on bike-ergometers and forearm muscle strength. They found that UV radiation induced a significant improvement in both muscle strength and athletic performance.

Hettinger T, Seidl E. [Ultraviolet irradiation and trainability of musculature.] Internationale Zeitschrift für angewandte Physiologie, einschliesslich Arbeitsphysiologie 1956; 16: 177-83. [In German]

Another German researcher, at the Institute for Medical Physics and Biophysics at the University of Gottiingen, studied reaction times (the time needed to recognize a light and switch it off) during October and November in a series of controlled experiments on 16 children and an unspecified number of adults. He first controlled for practice effects (getting better by practicing) and then administered nine full-body UV radiation treatments over three weeks to the two treatment groups, using placebo radiation in the two control groups. UV radiation improved choice reaction time by 25% in children and 20% in adults while reaction time worsened in controls. The improvements in the irradiated groups peaked at the end of the three weeks of UV treatments and reverted to baseline levels three weeks later. In the two control groups, he found distinctly improved reaction times in the sunnier months.

Sigmund R. [Effect of ultraviolet rays on reaction time in man.] Strahlentherapie. 1956; 101: 623-9. [In German]

The next study threw me because it was very well conducted, meticulously designed, and completely negative. In 1963, Berven reported on the effects of ultraviolet irradiation and vitamin D supplementation in a group of 30 Stockholm schoolchildren, aged 10 -11, comparing them to appropriate controls. He found no seasonality of fitness in the control group and no effect from either irradiation or two different vitamin D supplementation protocols (1500 IU of cholecalciferol daily for two months and a single dose of 400,000 IU of ergocalciferol) on performance on a bike ergometer.

Berven H. The physical working capacity of healthy children; seasonal variations and effect of ultraviolet irradiation and vitamin-D supply. Acta paediatrica. Supplementum 1963; 148: 1-22.

However, two things were not right and got me thinking. One, Berven found no seasonality of physical fitness and was the only author who found no such seasonal variations in athletic performance. Second, he found no effect from irradiation, again, the only author. Then I realized he was working with Swedish children in the late 1950's. Supplementation of children with high doses of vitamin D - often as cod liver oil - was routine in Scandinavia in the past, particularly in children. For example, in neighboring Finland, the official recommended daily dose of vitamin D for children - including infants - was 4,000 IU per day until 1964, when authorities reduced it to 2,000 IU/day. (That's right, you read that correctly, 4,000 IU per day for infants, which is too much by the way.)

In 1975, Finnish authorities reduced it to 1,000 IU per day, and, in 1992, to 400 IU per day. I emailed Professor Elina Hypponen who confirmed that the Swedish recommendations were similar to the Finnish ones. Therefore, it seems highly unlikely that many of Berven's Swedish children, studied in 1958 and 1959, all from "families with a good standard of living," were vitamin D deficient. Therefore, this study showed that vitamin D will not improve athletic ability in vitamin D replete people. That's very important because it indicates more is not necessarily better. More is only better if you are not taking enough.

Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001 Nov 3;358(9292):1500-3.

In the 1960's, three American researchers conducted experiments with university students. Rosentswieg studied the effects of a single six-minute dose of UV light on each side of the trunk in 23 college women, recording changes in various tests of muscle strength at one and five hours. He found a trend towards significance after five hours in white but not African American students. In 1968, Cheatum found that a six-minute administration of UV light, on each side of the trunk, increased the speed of 15 college women in the 30-yard dash. In 1969, Rosentswieg found a six-minute dose of UV light, on each side of the trunk, finding improved performance on a bicycle ergometer in college women. However, unlike the Germans and Russians, I could find no evidence that any of these American findings interested any American professionals involved in the care or training of athletes.

Rosentsweig J. The effect of a single suberythemic biodose of ultraviolet radiation upon the strength of college women. J Assoc Phys Ment Rehabil. 1967 Jul-Aug;21(4):131-3.

Cheatum BA. Effects of a single biodose of ultraviolet radiation upon the speed of college women. Res Q. 1968 Oct;39(3):482-5.

Rosentswieg J. The effect of a single suberythemic biodose of ultraviolet radiation upon the endurance of college women. J Sports Med Phys Fitness. 1969 Jun;9(2):104-6.

2. Athletic performance peaks in the summer when vitamin D levels peak, and is at its lowest in the winter when vitamin D levels are at their lowest.

A. True
B. False

True. The studies below - all I could find in the literature - show tests of physical performance peak in the summer, when vitamin D levels peak, start to decline in early autumn, as vitamin D levels decline, and athletic performance reaches its lowest point in late winter, when vitamin D levels bottom out. However, it is reasonable to assume that any associations between athletic performance and summer season may be due to "reverse causation." That is, improved athletic performance in the summer might be secondary to increased outdoor physical and recreational activity in the warmer weather with an indoor sedentary lifestyle during the colder months. Maybe people have better athletic ability in the summer because they exercise more. If that is true - and using the same logic - athletic performance should not begin to decline until late autumn, because at most temperate latitudes early fall weather is ideal for outdoor physical activities.

However, some of the studies below controlled for seasonal variations in time spent exercising. Furthermore, besides a consistent positive association of summer season with improved athletic performance, the below studies found an abrupt - and unexplained - reduction in athletic performance beginning in the early fall - when vitamin D levels decline - but when the weather is ideal for outdoor activities.

For example, in 1956, German researchers found a distinct seasonal variation in the trainability of musculature, studying wrist flexor strength in 21 German subjects undergoing daily training. They found highly significant seasonal differences with peak performance during the later part of the summer, nadirs in the winter, and an unexplained sharp autumn decline beginning in October.

Hettinger T, Muller EA. Seasonal course of trainability of musculature. Int Z Angew Physiol. 1956;16(2):90-4.

A study of Polish pilots and crew found physical fitness and tolerance to hypoxia were highest in the late summer with an unexplained sharp decline starting in September. The authors hypothesized that seasonal variations in an unidentified hormone best explained their results.

Kwarecki K, Golec L, Klossowski M, Zuzewicz K. Circannual rhythms of physical fitness and tolerance of hypoxic hypoxia. Acta Physiol Pol. 1981 Nov-Dec;32(6):629-36.

Cumulative work ability among 1,835 mainly sedentary Norwegian men during bicycle exercise tests showed an August peak, a sharp decline starting in the autumn, and a wintertime nadir. There were no seasonal changes in body weights, as might be expected if more caloric-demanding recreational activity during the sunnier months explained their results.

Erikssen J, Rodahl K. Seasonal variation in work performance and heart rate response to exercise. A study of 1,835 middle-aged men. Eur J Appl Physiol Occup Physiol. 1979 Oct;42(2):133-40.

Koch and Raschka reviewed the mostly German literature on the seasonality of physical performance, discussing studies indicating that muscle strength and stamina peak in the late summer. The authors then attempted to control for seasonal variations in the time spent exercising by instituting a controlled yearlong training regimen, beginning in December. The training regimen consisted of at least 20 push-ups per day and 2 or 3 long-distances races per week for the entire year. They found the both the number of push-ups and muscle strength peaked in late summer followed by a rapid decline in the fall, and a nadir in the winter, despite continued training. They concluded that seasonal variations in an unidentified hormone best explained their results. In addition, by now we all know that vitamin D is a seasonal hormone, and a steroid hormone precursor to boot.

Koch H, Raschka C. Circannual period of physical performance analysed by means of standard cosinor analysis: a case report. Rom J Physiol. 2000 Jan-Dec;37(1-4):51-8.

3. Vitamin D has direct muscle-building (anabolic) effects.

A. True
B. False

True, but only in vitamin D deficient subjects. Both animal and human studies have found that vitamin D directly affects muscle. That is, vitamin D increases muscle mass.

For example, Birge and Haddad found that vitamin D caused new protein synthesis in rat muscle.

Birge SJ, Haddad JG. 25-hydroxycholecalciferol stimulation of muscle metabolism. J Clin Invest. 1975 Nov;56(5):1100-7.

What about humans? In 1981, Young performed muscle biopsies on 12 severely vitamin D deficient patients before and after vitamin D treatment. They found type-II (fast-twitch) muscle fibers were small before treatment and significantly enlarged after treatment. Sorensen performed muscle biopsies on eleven older patients with osteoporosis before and after treatment with vitamin D. The percentage and area of fast twitch fibers increased significantly after treatment, despite the lack of any physical training.

Young A, Edwards R, Jones D, Brenton D. Quadriceps muscle strength and fibre size during treatment of osteomalacia. In: Stokes IAF (ed) Mechanical factors and the skeleton. 1981. pp 137-145.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Sato reported that two years of treatment with 1,000 IU of vitamin D per day significantly increased muscle strength, doubled the mean diameter, and tripled the percentage of fast-twitch muscle fibers, in the functional limbs of 48 severely vitamin D deficient elderly stroke patients. The placebo control group suffered declines in muscle strength, and in the size and percentage of fast-twitch muscle fibers.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

These studies clearly show that vitamin D when administered to vitamin D deficient people stimulates the growth and number of those muscle fibers critical to athletic ability, type-2, or "fast twitch," muscle fibers.

4. Many studies have found direct associations between physical performance and vitamin D levels. That is, the higher your vitamin D level, the better your athletic performance.

A. True
B. False

True. I found 13 positive studies of associations between vitamin D levels and various parameters of neuromuscular performance. However, they were all in old people. Of course, old people can be athletes too. Furthermore, age differences in physiology and pharmacology are quantitative, not qualitative. That is, what is true in old people will be true in young people, although the magnitude might be different. Higher vitamin D levels are associated with a wide variety of athletic performance but appear to have the strongest associations with balance, timing, and timed tests of physical performance.

The three largest studies had more than 7,000 elderly subjects. All found evidence of a vitamin D threshold of between 30 - 50 ng/ml, above which further improvements in athletic performance were not seen. Wicherts and her colleagues found a linear correlation between vitamin D and neuromuscular performance; scores were 78% better for those with vitamin D levels greater than 30 ng/ml compared to those with levels less than10 ng/ml.

Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, Dawson-Hughes B. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr. 2004 Sep;80(3):752-8.

Gerdhem P, Ringsberg KA, Obrant KJ, Akesson K. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA Study of Elderly Women. Osteoporos Int. 2005 Nov;16(11):1425-31.

Wicherts IS, et al. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metab. 2007 Mar 6; [Epub ahead of print]

Professor Heike Bischoff-Ferrari, now in Switzerland, did the largest study. She and her colleagues found a strong positive correlation and suggestion of a U-shaped curve with athletic performance on one test peaking with vitamin D levels of 50 ng/ml but deteriorating at higher levels. It is interesting to speculate that levels around 50 ng/ml may be optimal for athletic performance as such levels are common in humans living in a "natural" state of sun-exposure, such as lifeguards or tropical farmers.

Bischoff HA, Stahelin HB, Urscheler N, Ehrsam R, Vonthein R, Perrig-Chiello P, Tyndall A, Theiler R. Muscle strength in the elderly: its relation to vitamin D metabolites. Arch Phys Med Rehabil. 1999 Jan;80(1):54-8.

Interestingly, all three studies that looked for an association between mental abilities and vitamin D levels found one. A fourth study, unrelated to athletic function, also found an association. The obvious explanation for these findings is that cognitively impaired patients do not go outdoors as often as higher functioning patients and thus have lower vitamin D levels. However, Dhesi found the association after excluding all but mildly demented patients, making such an explanation more difficult. Flicker and - more recently - Przybelski and Binkley, found the association after controlling for outdoor activities, raising the possibility that the association of vitamin D levels with cognitive abilities is casual. Both the vitamin D receptor and the enzyme necessary to activate vitamin D are present in a wide-variety of human brain tissue. If vitamin D deficiency impairs cognitive abilities, it is likely that such deficiencies will also impair the brain's ability to process the complex circuits needed for peak athletic performance.

Dhesi JK, Bearne LM, Moniz C, Hurley MV, Jackson SH, Swift CG, Allain TJ. Neuromuscular and psychomotor function in elderly subjects who fall and the relationship with vitamin D status. J Bone Miner Res. 2002 May;17(5):891-7.

Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA. Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc. 2003 Dec;51(12):1762-7.

Flicker L, Mead K, MacInnis RJ, Nowson C, Scherer S, Stein MS, Thomasx J, Hopper JL, Wark JD. Serum vitamin D and falls in older women in residential care in Australia. J Am Geriatr Soc. 2003 Nov;51(11):1533-8.

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 Jan 8;

There can be no doubt that higher vitamin D levels are associated with improved athletic performance in the elderly. From what we know of physiology and pharmacology, the same associations should hold true in young people, including young athletes.

5. Numerous studies have found that vitamin D improves physical performance.

A. True
B. False.

True, but, again, most all the studies are in old persons, not young ones, and none of the studies are in world-class athletes. However, there is no medical reason why vitamin D would improve the athletic performance of vitamin D deficient old people but not vitamin D deficient young ones. Eleven studies found vitamin D improved physical performance, mainly on measures of balance and reaction time. The one study of younger subjects showed dramatic physical performance effects in 55 severely vitamin D deficient women.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Gloth FM 3rd, Smith CE, Hollis BW, Tobin JD. Functional improvement with vitamin D replenishment in a cohort of frail, vitamin D-deficient older people. J Am Geriatr Soc. 1995 Nov;43(11):1269-71.

Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H, Charles P, Eriksen EF. Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone involvement. Calcif Tissue Int. 2000 Jun;66(6):419-24.

Prabhala A, Garg R, Dandona P. Severe myopathy associated with vitamin D deficiency in western New York. Arch Intern Med. 2000 Apr 24;160(8):1199-203.

Verhaar HJ, Samson MM, Jansen PA, de Vreede PL, Manten JW, Duursma SA. Muscle strength, functional mobility and vitamin D in older women. Aging (Milano). 2000 Dec;12(6):455-60.

Pfeifer M, Begerow B, Minne HW, Abrams C, Nachtigall D, Hansen C. Effects of a short-term vitamin D and calcium supplementation on body sway and secondary hyperparathyroidism in elderly women. J Bone Miner Res. 2000 Jun;15(6):1113-8.

Bischoff HA, Stahelin HB, Dick W, Akos R, Knecht M, Salis C, Nebiker M, Theiler R, Pfeifer M, Begerow B, Lew RA, Conzelmann M. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003 Feb;18(2):343-51.

Dhesi JK, Jackson SH, Bearne LM, Moniz C, Hurley MV, Swift CG, Allain TJ. Vitamin D supplementation improves neuromuscular function in older people who fall. Age Ageing. 2004 Nov;33(6):589-95.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

In summary, five converging - but totally separate - lines of scientific evidence leave little doubt that vitamin D improves athletic performance. (I actually left out a sixth line of evidence, something a little more complicated, studies of muscle strength and vitamin D receptor polymorphisms; the two studies I could find were both positive.) Anyway, the scientific evidence that UVB radiation, either from the sun or from sunbeds, will improve athletic performance is overwhelming and the mechanism is almost certainly vitamin D production. Peak athletic performance will probably occur with 25(OH)D levels of about 50 ng/ml, whether from sun, sunbeds, or supplements.

All that is missing is a big-time professional or college team identifying and then treating their elite athletes who are vitamin D deficient. Can you imagine what such performance-enhancing effects would do for basketball players, most of who are African American and who practice and play indoors all winter? Or gymnasts? Or weight lifters?

However, a word of caution. The above studies suggest that taking too much vitamin D (more than 5,000 IU per day) may actually worsen athletic performance. Take the right amount, not all you can swallow. Take enough to keep your 25(OH)D levels around 50 ng/ml, year round. Easier yet, regularly use the sun in the summer and sunbeds in the winter - with care not to burn. Once a week should be about right.

When you think about it, none of this should surprise anyone. Every body builder knows that steroid hormones can improve athletic performance, certainly increase muscle mass. Barry Bonds knows they increase timing and power. Moreover, activated vitamin D is as potent a steroid hormone as exists in the human body. However, unlike other steroids, levels of activated vitamin D in muscle and nerve tissue are primarily regulated by sun exposure. That's right, the rate-limiting step for the cellular function (autocrine) of activated vitamin D is under your control. It depends on how much you put in your both or go into the sun. It's ironic that many athletes now avoid the sun, organized baseball is even promoting sun avoidance and sunblocks. The ancient Greeks knew better; they had there elite athletes train on the beach and in the nude.

The medical literature indicates vitamin D levels of about 50 ng/ml are associated with peak athletic performance. Of course, recent studies show such levels are ideal for preventing cancer, diabetes, hypertension, influenza, multiple sclerosis, major depression, cognitive impairments, etc. But who cares about all that disease stuff old people get, we're talking about something really important: speed, balance, reaction time, muscle mass, muscle strength, squats, reps, etc. And guess who's now taking 4,000 IU/day? Yes he is, and he tells me his timing is better, he can jump a little higher, run a little faster, and the ball feels "sweeter," whatever that means.

John Cannell, MD

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The reason why I've been blogging lightly these past few days is because, as a favor, I'm covering the practice for some colleagues who I'm (very) loosely affiliated with. The time demands have been great.

Nonetheless, it is a good reminder to me just how far wrong conventional cardiology remains. Judging by what I see around me, there is a startling lack of restraint in proceeding to the catheterization laboratory. Curiously, the internists and family practitioners have been brainwashed into accepting this path. I suppose that all it takes is an occasional real "save" for these physicians to develop a fear of ever missing real disease.

What I'm seeing is just how many people presenting with chest pain or similar symptoms end up going to the cath lab. I would crudely estimate 80%. That is, once you make it past the emergency room, there's a four out of five chance that you'll end up with a heart catheterization to "be sure your heart is okay", "make certain you're not going to die of heart disease", "see if there's a ticking time bomb in your chest". You've heard all the clever, scary phrases that get tossed around to scare the pants off you and justify putting catheters in your groin.

Despite the fact that tools for heart disease prevention have improved dramatically, the volume of heart catheterizations continues to grow nationwide.

I find it shocking and unacceptable. We're currently working behind the scenes to help change this situation through education of the public. Persuade a $1 million a year cardiologist that he is overdoing procedures? Unlikely in my experience. Educate the public about the shocking over-reliance on high-revenue procedures? Perhaps more practical.

Garlic May Not Lower Cholesterol
Study Shows No Improvement in Cholesterol Levels From Raw Garlic or Garlic Supplements

Lots of reports continue to hit the press about a small study that hoped to determine whether garlic as whole cloves (4 to 6), an aqueous extract of garlic called Kyolic, or an oil extract called Garlicin (high in allicin), or placebo. No differences in lipid numbers including LDL cholesterol were observed.

(Full text at WebMD at http://www.webmd.com/cholesterol-management/news/20070226/garlic-may-not-lower-cholesterol?ecd=wnl_chl_030507. You may be required to log in or register.)

I believe that the researchers were sincere in their effort to follow an honest, scientfically sound clinical trial design. I'm personally not that surprised. The effect in prior studies has been modest, sometimes none. Does that mean that we should ignore the other studies that suggest there may be modest blood-thinning, anti-inflammatory, blood pressure-reducing, and cancer-preventing properties? No, it does not. Dr. Matt Budoff at UCLA even published a very small study in about 20 people that suggested a slowing of plaque growth by using Kyolic in persons tracked by CT heart scans.

Nonetheless, garlic is, at best, probably no more than a source of small benefits. The biggest fallout from this kind of report, however, is not the neutral results from garlic, but from the open door the drug companies sense when this happens.

If you read the WebMD report, you'll notice all sorts of advertisements from drug companies for statin cholesterol drugs ("Cholesterol health center"; "Understanding Cholesterol Numbers"; "There are two sources of cholesterol: food and family"), Niaspan (which I used to support but have been discouraged by the Kos companies excessively profiteering methods and recent big Wall Street sellout).

It doesn't follow. The failure of one nutritional strategy to reduce LDL does nothave to trigger a run to the drugs. Don't fall for it. Drugs have their place. So do supplements and food choices, which can be very powerful. Drug manufacturers and their marketing people salivate when something like this comes along, an open invitation to say, "If garlic doesn't work, _____ sure does."

Jason came to the office because of chest pain. At 34 years old, he works as manager of a (non-fast food) restaurant, but indulges in lots of the odds and ends. Among his indulgences: Diet Coke.

Every time he'd have a diet Coke, he'd have chest pain. Not drinking diet Coke--no chest pain. If Jason drank coffee, no chest pain. Other foods, no chest pain. Anyway, just eliminating the diet Coke seemed to do the trick. (Aspartame?)

Anyway, that's not why I tell you Jason's story. In the midst of his evaluation, an echocardiogram showed a mildly enlarged aorta, measuring 4.0 cm in diameter. So we obtained lipoproteins. Jason showed lipoprotein(a) and small LDL particles, the dreaded duo. We talked about how to correct this pattern. Among the strategies we discussed was niacin.

But what bothered me was that neither of Jason's parents had a diagnosis of heart disease. Jason had to have gotten Lp(a) from either his mother or father, since you obtain the gene from one or the other parent. You cannot acquire Lp(a). So one of Jason's parents was sitting on a genetic time bomb of unrecognized Lp(a) and hidden heart disease.

Because Jason's paternal grandfather had a heart attack at age 62, only Jason's Dad had the heart scan (though I urged both to get one). Score: 1483. Recall that heart scan scores >1000 carry a risk of death or heart attack of 25% per year if no preventive action is taken. Now, of course, we have to persuade Jason's Dad that a program of prevention--intensive prevention is in order, including a measure of Lp(a).

So that's the curious story of how Diet Coke probably saved Jason's Dad's life. The lesson is that if you or someone you know has Lp(a), think about their children as well as their parents, each of whom carry a 50% chance of having the pattern.

There's a widely-known (among cardiologists) problem with nuclear stress tests. It's called the "false positive." (Nuclear stress tests are known as stress Cardiolites, stress thalliums, stress Myoviews, persantine stress tests, adenosine stress tests)

Stress tests, nuclear and otherwise, are helpful for identifying areas of poor blood flow. If an area of poor blood flow is detected and the area is substantial, then there may be greater risk of heart attack and other undesirable events in the relatively near future.

What "false positive" means is a stress test that shows an abnormality but it's not true--it is falsely abnormal. There are a number of reasons why this can happen. The problem is that this phenomenon is very common. Up to 20% of nuclear stress tests are false positives.

There are indeed situations where there may an abnormality and it is not clear whether it is true or false. This may lead to a justifiable heart catheterization or CT coronary angiogram. But, given the extraordinary number of false positives, there's a lot of gray in interpreting these tests. Hospital staff, in fact, call nuclear medicine "unclear" medicine. It's common knowledge that you can often see just about anything you want to see on a nuclear image of the heart. Abnormalities in the bottom of the heart, the "inferior" wall, are especially common due to the overlap of the diaphragm with the heart muscle, yielding the appearance of reduced blood flow. Defects in the front of the heart heart are common in females with large breasts for the same reasons.

The problem: The uncertainty inherent in nuclear stress tests opens the door to the unscrupulous or lazy practitioner. Any blip, tick, or imperfection on the nuclear images serve as carte blanche to drag you into the hospital for procedures.

This abusive practice is, in my experience, shockingly common for two reasons: 1) It pays better to do heart catheterizations, and 2) Defensive medicine.

What's the disincentive? Only doing the right thing and maintaining a clear conscience. Slim reasons for many of my colleagues--and a lot less money.

If you are without symptoms and feel fine, and a nuclear stress test is advised by your doctor, followed by a discussion of an abnormality, insist on a discussion of exactly what is abnormal, just how abnormal, and what the alternatives might be. If you receive unsatisfactory or incomplete answers despite your best effort, it's time for another opinion.

Magnesium is kind of boring. So most people don't pay too much attention to it.

Magnesium can be important, however. I saw an interesting phenomenon recently. A type I diabetic patient of mine (that is, an adult who developed diabetes as a child), Mitch, was experiencing wide swings in blood sugar: low low's and very high high's (300-400 mg/dl). Mitch's magnesium was only marginally low at 2.0 mEq/L. (Ranges for normal magnesium blood levels are usually 1.3–2.1 mEq/L or 0.65–1.05 mmol/L.) Note that Mitch's blood levels fall within "normal." I do not agree with these "normal" ranges. I shoot for 2.1 to 2.4 mEq/L, which I think is the truly normal range.

In addition to eating plenty of raw nuts and green vegetables, Mitch began supplementing magnesium with magnesium citrate, 200 mg twice a day (our preferred supplement form). He reported that the wide swings in blood sugar were nearly eliminated.

Mitch's dramatic benefit is just a great illustration of how magnesium can help control blood sugar metabolism. A type I diabetic is more sensitive to the effects, but anyone with type II (adult) diabetes, metabolic syndrome, or just a slightly high blood sugar could benefit from magnesium supplementation.

There's a number of ways to accomplish getting sufficient magnesium in your daily regimen. Track Your Plaque members, Be sure to read:

Your water may be killing you at
http://www.cureality.com/library/fl_03-002magnesium.asp

Magnesium: Water to the rescue! at http://www.cureality.com/library/fl_03-010magnesium2.asp

It struck me recently that, for many people, it's not the second but the third heart scan that more commonly shows a reduction in score.

I think this is because many people's reaction to their first heart scan is "This can't be. There's no way my arteries have that much plaque." They then follow a half-hearted program to correct their patterns.

When the second heart scan shows a significantly higher score, that really catches their attention. This is when they finally buckle down and give it their all.

Only the occasional person will, after the first heart scan, seize full control and take their program very seriously. These tend to be highly motivated people.

Don't feel too bad if your second heart scan score shows an increase. Look at it for what it represents: feedback on the adequacy of your program.

Peter started out at age 59 at 248 lbs, standing 6 ft tall (BMI = 33.6!).

Along with his weight, Peter had the entire panel of phenemena of the so-called "metabolic syndrome", or pre-diabetes:

--Triglycerides 238 mg/dl and associated with extremes of excess VLDL and IDL
--High blood pressure
--Blood sugar 115 mg/dl
--High c-reactive protein
--Small LDL particles 99% of total LDL

Interestingly, Peter's HDL was a surprisingly favorable 58 mg/dl (HDL is usually low in this syndrome). However, when broken down by size, he had nearly zero large, healthy HDL (sometimes called HDL2b). Though total HDL was favorable, most of it was simply ineffective.

Peter eliminated snacks and processed foods, particularly bread; increased his reliance on healthy oils and lean proteins; incorporated soy protein; increased vegetables. He added 30 minutes of a rapid walk on a treadmill every day. He added vitamin D to achieve a blood level of 50 ng/dml. He added a magnesium supplement.

Peter has lost 31 lbs. in the last year. Weight 207 lbs., BMI 28.1 (desirable <25). Blood sugar: 96 mg/dl; triglycerides: 56 mg/dl; HDL 71 mg/dl with 35% in the large fraction; small LDL 45% of total. Not perfect, but a damn site better.

Control of metabolic syndrome is an achievable goal for over 90% of people, just with these simple efforts. We haven't yet had a chance to assess the effect on the progression or regression of Peter's heart scan score, but he has, at the very least, spared himself a future of diabetes and all its complications.

This is a "slice" from a normal heart scan in a 58 year old woman. Heart scan score zero. Look at the lungs, the dark areas left and right of the heart in the center. The lungs are also normal. Black represents normal density, healthy lung tissue. The white streaking is just normal lung blood vessels. This person doesn't smoke.

This woman smokes a pack of cigarettes a day and has done so for 45 years ("45 pack-years"). She had a surprisingly low heart scan score (at age 64) of only 71, despite the smoking. However, look at this woman's lungs. It's a little tough to make out, since the computer graphics loses some of the resolution. But you can see the near absence of lung tissue on both sides. This is an advanced phase of the destructive lung disease, emphysema, from smoking. Even if she quit smoking today, the destroyed lung tissue never grows back. She literally has huge gaps or holes in her lungs where lung tissue used to be.

Smoking is among the most destructive, terrible things you can do to your body, short of swallowing strychnine or jumping off a building. Stay as far the heck away from cigarettes as you possibly can. If you are exposed to "secondary" smoke, insist that the person never smoke in your presence. It's not the smell that destroys your lungs or causes coronary plaque (though it is indeed foul), it's the actual smoke.

Do you need to become a vegetarian in order to reduce your heart scan score?

No. Plain and simple. We’ve had many non-vegetarians drop their scores.

That said, are there still advantages to following a vegetarian diet, or some variation on the vegetarian theme?

Yes, there are. Let’s put aside the moral or religious arguments in favor of not eating animals—the need to eliminate killing animals for food, elimination of suffering common in modern livestock practices, Kosher considerations, etc. (Not that there aren’t real arguments here. Our focus for this conversation is not, however, the moral dilemma, but the health argument.)

Some of the most unhealthy people I’ve ever met, mostly males, are proud carnivores who boast of their prodigious capacities to eat meat. Unfortunately, it’s hard to tease out the ill-effects of excessive meat eating, since these same men also tend to be substantially overweight, smoke, drink excessively, and fail to get exercise unless their job is physically demanding. You know the type.

What advantages does a vegetarian obtain? A number of studies have suggested that the reduced saturated fat, reduced exposure to parasites, as well as reduced exposure to the antibiotics and hormones now used routinely in livestock-raising practices, do indeed provide benefits to the vegetarian. Thus, vegetarians tend to be substantially thinner, experience less bowel cancer, have less diabetes and heart disease, and live longer.

(If you are interested in reading or seeing more about just how inhumane modern livestock practices are, take a look at the video, "Meet Your Meat" at meat.org. Be sure not to view this after dinner.)

Of course, some of the disadvantages of eating animal products diminish when free-range livestock are eaten, i.e., livestock not raised in the inhumane cramped, filthy conditions of livestock factories, but in the open, grazing or rooting freely. These animals tend to have different fat compositions and taste different.

The advantages of vegetarianism, however, have blurred in recent years, since many so-called vegetarians have failed to maintain the distinction between naturally-occurring foods and processed foods. So, Ritz Crackers, Oreo cookies, whole wheat bread, and Raisin Bran fit into a vegetarian program, but they’re awful for your health. I’ll occasionally meet a self-proclaimed vegetarian who looks every bit as unhealthy as a conventionally eating American, that is, overweight, pre-diabetic person with a developing heart scan score.

So it is not necessary to be vegetarian to reduce your score. You might consider vegetarianism for other reasons, such as moral considerations, or to reduce your risk for cancer. But it is not necessary to drop your heart scan score. A non-processed food diet? Now that's is worth giving serious consideration.

A Heart Scan Blog reader posted the link to this very excellent presentation by Dr. David Diamond, a neuroscientist at the University of South Florida.

ATP-3, or Adult Treatment Panel-3, is the set of cholesterol treatment guidelines as established by the National Cholesterol Education Panel, the guidelines used by practicing physicians nationwide. They are also the metric by which the "quality" of care is being judged by agencies like Medicare, health insurers, and other parties interested in policing healthcare. Dr. Diamond ably recounts how we ended up in this mess, the conflagration of "cut your fat, reduce cholesterol, and take a statin drug."

I was very impressed that, in his closing comments, he briefly discusses the pivotal role of glycation in heart disease causation. You will see in coming conversations how important an understanding of glycation is to create a healthy diet and lifestyle.

Conventional thinking is that high LDL cholesterol causes heart disease. In this line of thinking, reducing cholesterol by cutting fat and taking statin drugs thereby reduces or eliminates risk for heart disease.

Here's an (extreme) example of just how far wrong this simpleminded way of thinking can take you. At age 63, Michael had been told for the last 20 years that he was in great health, including "perfect" cholesterol values of LDL 73 mg/dl, HDL 61 mg/dl, triglycerides 102 mg/dl, total cholesterol 144 mg/dl. "Your [total] cholesterol is way below 200. You're in great shape!" his doctor told him.

Being skeptical because of the heart disease in his family, had a CT heart scan. His coronary calcium score: 4390. Needless to say, this is high . . . extremely high.

Extremely high coronary calcium scores like this carry high likelihood of death and heart attack, as high as 15-20% per year. So Michael was on borrowed time. It was damn lucky he hadn't yet experienced any cardiovascular events.

That's when Michael found our Track Your Plaque program that showed him how to 1) identify the causes of the extensive coronary atherosclerosis signified by his high calcium score, then 2) correct the causes.

The solutions, Michael learned, are relatively simple:

--Omega-3 fatty acid supplementation at a dose sufficient to yield substantial reductions in heart attack.
--"Normalization" of vitamin D blood levels (We aim for a 25-hydroxy vitamin D level of 60-70 ng/ml)
--Iodine supplementation and thyroid normalization
--A diet in which all wheat products are eliminated--whole wheat, white, it makes no difference--followed by carbohydrate restriction.
--Identification and correction of all hidden causes of coronary plaque such as small LDL particles and lipoprotein(a)

Yes, indeed: The information and online tools for health can handily exceed the limited "wisdom" dispensed by John Q. Primary Care doctor.

Our new recipes, such as New York Style Cheesecake and Chocolate Coconut Bread, are wheat-free and low- or no-carbohydrate. They fit perfectly into the New Track Your Plaque Diet for gaining control over coronary atherosclerotic plaque, not to mention diabetes, pre-diabetes, hypertension, small LDL particles, high triglycerides, high inflammation (c-reactive protein) and other distortions of metabolism.

However, there's one compromise: We include use of non-nutritive sweeteners. It's therefore important to know that artificial sweeteners are not all created equal.

One common tripping point: maltodextrin.

Maltodextrin is composed of polymers (repeating subunits) of glucose, as few as 3 or as many as 20 or more glucose subunits. So maltodextrin is glucose sugar. While it lacks the especially destructive pentose sugar, fructose, maltodextrin is metabolized to glucose and thereby increases blood sugar substantially.

Many artificial sweeteners are bulked up with maltodextrin. For instance, granulated Splenda and Stevia in the Raw, two sweeteners billed as low-calorie and sugar-free that is used on a cup-for-cup basis like sugar, are primarily maltodextrin--with only a teensy bit of Splenda or stevia.

The best artificial sweeteners, i.e., the most benign without a load of maltodextrin, are:

Liquid stevia--Just the extract from stevia leaves and water. It can be a bit pricey, e.g., $10 for a 2 oz bottle, but a little goes a long way.

Truvia--While I'm not too fond of the manufacturer (Cargill), I believe that Truvia is among the better sweeteners around. It is a mixture of the natural sugar, erythritol, that generates little to no blood sugar effects and rebiana (rebaudioside), an isolate of stevia. Some people aren't too fond of the mild menthol-like cooling effect of the erythritol nor the slight aftertaste. I find it works pretty well in most recipes.

Be aware that, no matter which artificial sweetener you use, it has the potential to stimulate appetite. I therefore like to not eat foods sweetened with liquid stevia or Truvia in isolation but as part of a meal. That way, any appetite stimulation that results is substantially quelled by the proteins and fats ingested.

Former Men's Health editor, Jeff O'Connell, has just released his new book, Sugar Nation.

Back in 2009, Jeff contacted me to obtain some background insights into diabetes and its relationship with diet. He recently sent me a copy of his new book that contains some brief quotes from me.

Jeff is a writer, not a physician nor scientist. But I think that you will find his grasp of diabetes and the nutritional and lifestyle events that led him there far exceed the insights held by most practicing physicians. Like many of us, Jeff discovered how to find his way back from pre-diabetes through lessons he had to learn on his own, but not from his doctor.

Jeff tells this story as reporter, son of an estranged diabetic father with whom he reconnects as he approaches the end of his life, and as fellow sufferer of the pre-diabetic/diabetic mess that modern habits and "official" dietary advice have given us. Jeff's book is worth a read to see yet another dimension of the human stories that are emerging from this incredible nutritional tangle we find ourselves in.

Here's a unique YouTube video about Jeff's story.

. . . but not in a good way.

The September, 2011 issue of Consumer Reports showcases their Protect Your Heart discussion. Third paragraph: "The website Track Your Plaque warns, 'The old tests for heart disease were wrong--dead wrong.' It says heart scans are 'the most important health test you can get.'"

They go on to expose the overuse of heart procedures like angioplasty and stent implantation and offer their advice on how to manage heart disease risk: lower BP, reduce LDL cholesterol, lose weight, stop smoking, take aspirin. They quote Dr. Paul Ridker who declares heart scans are not useful because the "deposits cardiologists worry about are the less stable plaques that CT scans routinely miss."

I thought I'd been transported back to 1995. Not only is it clear that the Consumer Report writers never looked beyond the homepage of Track Your Plaque, but somehow saw our heart disease prevention and reversal program as promoting heart procedures. Incredible.

Of course, the Track Your Plaque program does the exact opposite: Advocates an approach that virtually eliminates the need for procedures and returns control over heart disease to the participant. That's a critical difference.

And, as I've had to remind my colleagues time and time again, what we are really after is an index of total coronary atherosclerotic plaque. Even in 2011, that index remains the simple coronary calcium score, a gauge of total plaque, not just of "hard," stable plaque. Perhaps in 10 years we will be using a better tool to gauge progression and regression of all the components of coronary atherosclerotic plaque, but today it remains the simple, accessible, mammogram-like coronary calcium score.

Consumer Reports does for the idea of heart disease prevention what food manufacturers do for health and weight loss: Echo conventional wisdom of the sort that generally makes us fatter, more diabetic, leads us to more heart procedures and needless deaths. I might use Consumer Reports to rate MP-3 devices or toasters, but I certainly would not rely on them for insightful health advice.

A 23-year old man came to my office having experienced weeks of extreme anxiety, palpitations, and 19 pounds of weight loss triggered by an overactive thyroid.

It all happened because of a large dose of iodine received during a CT scan using iodine-containing x-ray dye. (X-ray dyes are made visible on x-ray due to the iodine content.) This is a reaction first described in the 19th century by German physician, Karl Adolph von Basedow. (Jod is German for iodine.)[caption id="attachment_4313" align="alignleft" width="217" caption="Dr. von Basedow. Image courtesy Wikipedia"]

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Now, here's the kicker: Jod-Basedow only occurs when there is pre-existing iodine deficiency. Indeed, this young man had an enlarged thyroid, signaling longstanding iodine deficiency (a goiter).

This example is among the more flagrant examples of something I have been witnessing: the return of iodine deficiency. As Americans cut back on their intake of iodized salt and fail to obtain iodine in sufficient quantities from seafood, seaweed, or supplementation, goiters and iodine deficiency are making a return in all its glory, reminiscent of the early 20th century, pre-iodized salt.

This young man's frightening experience is yet another way iodine deficiency can show itself, by the overenthusiastic thyroid response to a large dose of iodine when iodine deficiency has been present for a prolonged period.

Iodine deficiency and goiters have been lost to memory for most people. Even the FDA, in its advice for Americans to reduce salt and sodium intake, have forgotten to remind everyone to obtain iodine from an alternative source. "Those who cannot remember the past are condemned to repeat it."

Get your iodine.

In the recent Heart Scan Blog post, Can I eat quinoa, I discussed how non-wheat carbohydrate sources like quinoa, amaranth, black beans, brown rice, fruit, etc. do not exert the inflammation-provoking, appetite-increasing effects of wheat (since gliadin and gluten are not present), nor do they increase blood glucose as enthusiastically as the amylopectin A of wheat--but non-wheat grains can still increase blood sugar quite substantially.

Of course, any food that triggers blood sugar also trigger hepatic de novo lipogenesis, thereby increasing triglyceride levels and postprandial particles (e.g., chylomicron remnants), which, in turn, triggers formation of small LDL particles.

So these non-wheat carbohydrates, or what I call "intermediate carbohydrates" (for lack of a better term; low-glycemic index is falsely reassuring) still trigger all the carbohydrate phenomena of table sugar. Is it possible to obtain the fiber, B-vitamin, flavonoid benefits of these intermediate carbohydrates without triggering the undesirable carbohydrate consequences?

Yes, by using small portions. Small portions are tolerated by most people without triggering all these phenomena. Problem: Individual sensitivity varies widely. One person's perfectly safe portion size is another person's deadly dose. For instance, I've witnessed many extreme differences, such as 1-hour blood sugar after 6 oz unsweetened yogurt of 250 mg/dl in one person, 105 mg/dl in another. So checking 1-hour blood sugars is a confident means of assessing individual sensitivity to carbs.

Some people don't like the idea of checking blood sugars, however. Or, there might be times when it's inconvenient or unavailable. A useful alternative: Count carbohydrate grams. (Count "net" carbohydrate grams, of course, i.e., carbohydrates minus indigestible fiber grams to yield "net" carbs.) Most people can tolerate around 40-50 grams carbohydrates per day and deal with them effectively, provided they are spaced out throughout the day and not all at once. Only the most sensitive, e.g., diabetics, apo E2 people, those with familial hypertriglyceridemia, are intolerant to even this amount and do better with less than 30 grams per day. Then there are the genetically gifted from a carbohydrate perspective, people who can tolerate 50-60 grams, occasionally somewhat more.

People will sometimes say things like "You don't know what the hell you're talking about because I eat 200 grams carbohydrate per day and I'm normal weight and have perfect blood sugar and lipids." As in many things, the crude measures made are falsely reassuring. Glycation, for instance, from postprandial blood sugars of "only" 140 mg/dl--typical after, say, unsweetened oatmeal--still works its unhealthy magic and will lead long-term to cataracts, arthritis, and other conditions.

Humans were not meant to consume an endless supply of readily-digestible carbohydrates. Counting carbohydrates is another way to "tighten up" a carbohydrate restriction.

Diabetics are instructed to monitor blood glucose first thing in the morning and two hours after eating. This helps determine whether blood sugar is controlled with medications like metformin, Januvia, Byetta injections, or insulin.

But that's not how you use blood sugar to use to prevent or reverse diabetes. Two-hour blood sugars are also of no help in deciding whether you have halted glycation, or glucose modification of proteins the process that leads to cataracts, brittle cartilage and arthritis, oxidation of small LDL particles, atherosclerosis, kidney disease, etc.

So the key is to check one-hour after-eating (postprandial) blood sugars, a time when blood glucose peaks after consumption of carbohydrates. (It may peak somewhat sooner or later, depending on factors such as how much fluid was in the meal; protein, fat, and fiber content; presence of foods like vinegar that slow gastric emptying; the form of carbohydrate such as amylopectin A vs. amylopectin B, amylose, fructose, along with other factors. Once in a while, you might consider constructing your own postprandial glucose curve by doing fingersticks every 15 minutes to determine when your peak occurs.)

I reject the insane notion that after-eating blood sugars of less than 200 mg/dl are acceptable, the value accepted widely as the cutoff for health. Blood sugars this high occurring with any regularity ensure cataracts, arthritis, and all the other consequences of cumulative glycation. I therefore aim to keep one-hour after-eating glucoses 100 mg/dl or less. If you start in a pre-diabetic or diabetic range of, say, 120 mg/dl, then I advise people to not allow blood glucose to go any higher. A pre-meal blood glucose of 120 mg/dl would therefore be followed by an after-eating blood glucose of no higher than 120 mg/dl.

No doubt: This is strict. But people who do this:

--Lose weight from visceral fat
--Heighten insulin sensitivity
--Drop blood pressure
--Drop HbA1c and fasting glucose over time
--Reduce small LDL and other carbohydrate-sensitive measures

By the way, if you inadvertently trigger a high blood sugar like I did when I took my kids to the all-you-can-eat Indian buffet, go for a walk, bike, or burn the sugar off with a 30-minute or longer physical effort. Check your blood sugar again and it should be back in desirable range. But then learn from your lesson: Eliminate or reduce portion size of the culprit carbohydrate food.

Anyone following the conversations on these pages know that I have some very serious concerns about this thing being sold to us called "wheat"--cause it ain't wheat! It is the result of incredible genetics shenanigans inflicted on this plant, mostly in the name of increased yield per acre.

I now classify wheat as "Public Enemy #1," the prime nutritional culprit underlying obesity, heart disease, "cholesterol" abnormalities, hypertension, arthritis, psychiatric illness, and on and on. Once you read the full story, I believe that you will agree: Modern Triticum aestivum, the plant that now serves as the source for virtually all the wheat flour products now consumed--organic, whole grain, multigrain, sprouted . . . it makes no difference--does not belong in the human diet. So many people, searching for solutions for their fatigue, weight gain, leg edema, incurable rashes, joint pain, etc., will find their answers here.

Wheat Belly: Lose the wheat, lose the weight and find your path back to health will be on bookstore shelves including Barnes and Noble August 30, 2011 or is available for preorder here at Amazon. Wheat Belly will also be available as a downloadable Kindle book and as unabridged audio CDs.

You can also follow the Wheat Belly conversations on my Wheat Belly Blog. One of my recent posts discusses the herbicide-resistant semi-dwarf wheat strain, Clearfield, that is now making its way to more and more supermarket shelves.

You'll also find more conversation on the Wheat Belly Facebook pages.

I witness spectacular results restricting carbohydrates, both in the office as well as in my online experiences, such as those in Track Your Plaque. Of course, the diet I advocate is not just low-carb; it starts with elimination of wheat (for a long list of reasons). So the diet is wheat-free in the setting of low-carbohydrate.

What does this accomplish? Here's a partial list:

--Weight loss-Specifically, loss of visceral fat, the kind hinted at on the surface as "love handles" or what I call "wheat belly."
--Reduced blood sugar and HbA1c (reflecting prior 60-90 days glucose)
--Marked reduction in small LDL and triglycerides, increased HDL
--Reduced inflammatory measures like c-reactive protein
--Reduced leptin and leptin resistance, increased adiponectin
--Reduced estrogen and prolactin in men, accompanied by shrinkage or loss of enlarged breasts ("man boobs"); reduced estrogen in females accompanied by reduced risk for breast cancer

Pretty impressive. But there's one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.

Everybody has two genes for apo E; the most common type is apo E 3/3. Around 1 in 4 people have 1, less commonly 2, genes for apo E4.

I hate apo E4. I hate apo E4 because it means I've got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that's what apo E4 people have to do. But it doesn't end there.

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.

So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

It still gives me the creeps to tell an apo E4 person that they've got to watch their fats, worse than watching Starsky and Hutch reruns.

John received a coronary stent in 2003 following a small heart attack. The artery causing the heart attack was a diagonal artery, a branch of the important left anterior descending coronary artery (in the front of the heart). His cardiologist at the time advised him, "Take Lipitor and we'll do stress tests every year. Come back if you have any more chest pain." That was the full extent of John's preventive care.

He came to me for a second opinion and, naturally, we enrolled him in our program. We began by obtaining a CT heart scan score, though we had to exclude the stented diagonal artery. His score: 471. At age 51 and physically active, John had 7 additional abnormal lipoprotein patterns identified. We counseled John on better approaches to food choices, his weight target, fish oil, and correction of all lipoprotein patterns.

Two years later, John's repeat heart scan score: 511 . John was initially disappointed with the increase. But a closer look yielded something entirely different: the right coronary artery and circumflex (no stents) showed 20-30% reduction in their scores. The increase in total score was entirely due to substantial increase in score just outside the stent, in the left anterior descending artery. In other words, all of the increase in score was due to growth of a plaque at the mouth of the stent in the diagonal artery.

This is curious: profound regression of plaque with a big drop in score in the "un-instrumented" arteries, but tremendous growth of plaque and an increase in score in the "instrumented", or stented, artery, all in the same person's heart.

I don't know how controllable this specific situation in the left anterior descending and stented diagonal will be, and I'm unaware of any specific strategies to impact on this situation. The whole world of tissue growth within or around stents is littered with high hopes followed by failures. The drug-coated stents have been the only partial solution to this problem, though that's precisely the sort of stent John received.

Is there a message here? The message I take from this is that you and I should work like mad to keep from receiving a stent. Once they're implanted, we have less control over our coronary future. We can indeed regress ("reverse") coronary plaque. But we may not be able to regress the sort of tissue that grows in response to a stent implantation.

Imagine two people.

Tom is a 50-year old man. Tom's initial heart scan score is 500--a bad score that carries a 5% or more risk for heart attack per year.

Harry is also 50 years old. His heart scan score is 100--also a concerning score but not with the same dangers of Tom's much higher score.

Tom follows a powerful heart disease prevention program like the Track Your Plaque program. He achieves the 60:60:60 lipid targets; chooses healthy foods; takes fish oil; raises his blood vitamin D level to >50 ng/ml, etc. One year later, Tom's heart scan score is 400, a 20% reduction from his starting score.

Harry, on the other hand, doesn't understand the implications of his score. Neither does his doctor. He's casually provided a prescription for a cholesterol drug by his doctor but nothing else. One year later, Harry's heart scan score is 200, a doubling (100% increase) of the original score.

At this point, we're left with Tom having a score of 400, Harry with a score of 200. That is, Tom has twice the score, or 200 points higher, compared to Harry. Who's better off?

Tom is better off. Even though he has a significantly higher score, Tom's plaque is regressing. It is therefore quiescent with its components being extracted, inflammation subsiding, the artery is in a more relaxed state, etc.

Harry's plaque, in contrast, is active and growing: inflammatory cells are abundant and producing enzymes that degrade supportive tissue, excessive constrictive factors are constantly causing the artery to pinch partially closed, fatty materials are accumulating and triggering a cascade of abnormal responses.

This is therefore a peculiar situation in which a higher score is actually better than a lower score. It reflects the power of adhering to a preventive program. It also demonstrates how two scans are better than one because they show the rate of increase given a particular preventive approach.

Warren had a moderately high LDL cholesterol for years and took a statin drug sporadically over the past 7 years. Finally retired from a successful real estate investment business, he had a CT heart scan to assess his heart disease status.

Warren's score: 49. At age 59, this put him in the lowest 25%, with an estimated heart attack risk of 1% per year or less--a relatively low risk. At this heart scan score, the likelihood of an abnormal stress test was less than 3%, or a 97% likelihood of a normal stress test. Most would argue that a stress test would be unproductive, given its low probability of yielding useful information. In other words, there would be a 97% probability of normal blood flow through Warren's coronary plaque, and less than 3% likelihood that a stent or bypass surgery would be necessary.

Warren was also without symptoms. He hiked and biked without any chest discomfort or breathlessness. A prevention program like Track Your Plaque to gain control over future coronary plaque growth was all that was necessary and Warren had high hopes for a life free of heart attack and major heart procedures.

Then why did he go through a heart catheterization?

Warren did indeed undergo a heart catheterization on the advice of his cardiologist. When I met Warren for another opinion, it became immediately obvious that the heart catheterization was completely unnecessary. Then why was this invasive procedure done? There can only be a few reasons:

--The cardiologist didn't truly understand the meaning of the heart scan score. "We need to do a 'real' test."

--The cardiologist was terrified of malpractice risk for underdiagnosing or undertreating any condition, no matter how mild.

--The cardiologist wanted to make more money. Talking about heart disease prevention is a money-saving, not a money-making, approach.

Regardless of which of the three motivations was at work here, they're all inexcusable. A disservice was done to this man: he had an unnecessary procedure, incurred some risk of complication in the process, and gained nothing.

An ignorant or profit-seeking cardiologist is worse than the unscrupulous car mechanic who, when presented with an unknowing car repair customer, proceeds to replace the carburetor and rebuild the engine when a simple 5-minute adjustment would have taken care of the problem.

I estimate that no more than 10% of my colleagues follow such practices, but it's often hard to know who is in that 10%. Ask pointed questions: Why is the catheterization necessary? What is the likelihood of finding information useful to my health? What are the alternatives? (By the way, the emerging CT coronary angiograms can be a useful alternative in some situations like this.)

Track Your Plaque is your source for credible information. Be well armed.

Art undeniably had high blood pressure.

At age 53, he had all the “footprints” of high blood pressure that’d been present for at least several years: abnormal patterns by EKG, abnormally thick heart muscle, and an enlarged aorta by an echocardiogram. These sorts of changes require many years to develop. Art’s blood pressure was 140/85 sitting quietly in the office.

“That’s about what my primary care doc gets, too. Whenever it’s high, he takes it again after a few minutes and it always comes down.”

Art tried to persuade me that his blood pressure was high today only because of the traffic on the way into the office. When I dismissed this as a cause, he insisted that stress he’d been suffering because of his teenage son was the cause. “I just know I don’t have high blood pressure!”

Who’s right here? Well, Art is not here to defend himself. But one fact is crystal clear: you cannot develop complications of high blood pressure unless you truly have high blood pressure!

In other words, Art’s abnormal changes in heart structure (thickened heart muscle and enlarged aorta) are serious changes that develop only with years and years of sustained blood pressure at least as high as the one in the office. His blood pressure almost certainly ranged much higher at other times, particularly during stressful situations like waiting in the check-out line at the grocery store, watching a suspenseful TV show, petty irritations at his job, and on and on.

Blood pressure does not have to be high all the time to generate complications of high blood pressure. It can be sporadic, variable, even occasional. Clearly, sustained high blood pressure is the worst situation that creates adverse consequences more quickly. But blood pressure that wavers from low to high only some of the time can still, given sufficient time, cause the very same unwanted effects.

Control of blood pressure is crucial to your coronary plaque control program. Blood pressure may be boring: not as exotic, say, as lipoproteins, and not as fun as talking about nutritional supplements. But neglect blood pressure issues and you will not gain full control over coronary plaque growth—-your heart scan score will increase.

Watch for an upcoming Special Report on the Track Your Plaque Membership website, a full detailed discussion of how to recognize when blood pressure is an important issue, along with a full discussion of nutritional methods to reduce it, often sufficient to minimize or eliminate the need for medication.

In the Track Your Plaque program, we tend to rely a great deal on niacin. When used properly, 90-95% of people will do just fine and achieve their lipid and lipoprotein goals with the help of niacin, along with their other efforts.

Unfortunately, around 5% of people simply can't take niacin without intolerable "hot flush" effects, or occasionally excessive skin sensitivity--itching, burning, etc.

Why does this happen? These 5% tend to be "rapid metabolizers" of niacin, i.e. they convert niacin (nicotinic acid, or vitamin B3) into a metabolite called nicotinuric acid. Nicotinuric acid is the compound responsible for the skin flush. Most people can slow or reduce the effects of nicotinuric acid by:

--Taking niacin with dinner, so that food slow tablet dissolution.

--Taking with plenty of water. Two 8-12 oz glasses usually eliminates the flush entirely in most people.

--Taking with an uncoated 325 mg tablet of aspirin in the first few weeks or months. Eventually, you will need to revert back to a better stomach tolerated dose of 81 mg, preferably enteric coated. But a full 325 mg uncoated can really help in the beginning, or when you have any niacin dose increases, e.g., 500 mg to 1000 mg.

But even with these very effective strategies, some people still struggle. That's when the question arises: Are there any alternatives to niacin?

Well, it depends on why niacin is being used. If you and your doctor are using niacin for:

Raising HDL--Then weight loss to your ideal weight; reduction of processed carbohydrates, especially wheat products; avoidance of hydrogenated ("trans") fats; a glass or two of red wine per day; dark chocolates (make sure first ingredient is chocolate or cocoa, not sugar), 40 gm per day; fish oil; exercise; other prescription agents (fibrates like Tricor; TZD agents for diabetes; cilostazol (Pletal)). Niacin is by far the most effective agent of all, but, if you're intolerant, raising HDL is still possible through a multi-faceted effort.

Reduction of small LDL--The list of effective strategies is the same as for raising HDL, but add raw almonds (1/4-1/2 cup per day), oat bran and other beta-glucan rich foods like oatmeal. Reduction of processed carbohydrates is especially important to reduce small LDL.

Reduction of Lipoprotein(a)--This is a tricky one. For men, testosterone and DHEA are effective alternatives; for women, estrogen and perhaps DHEA. Hormonal preparations of testosterone and estrogen are stricly prescription; DHEA is OTC. I have not seen the outsized benefits on lipoprotein(a) claimed by Rath et al by using high-dose vitamin C, lysine, and profile, unfortunately. We are clearly in need of better alternatives to treat this difficult and high-risk disorder.

Reduction of triglycerides/VLDL/IDL--I lump these three together since they all respond together. If you're niacin intolerant, maximixing your fish oil can be crucial for reduction of these patterns using doses above the usual starting 4000 mg per day (providing 1200 mg EPA+DHA). Reduction of processed carbohydrates, eimination of processed foods that contain high-fructose corn syrup, and weight loss to ideal weight are also very effective. "Soft" strategies with modest effects include green tea (>6 cups per day) or theaflavin 600-900 mg/day; raw nuts like almonds, walnuts, and pecans; exercise; soy protein.

Reduction of LDL--Lots of alternatives here including oat bran (3 tbsp per day), ground flaxseed (3 tbsp per day), soy protein (25 grams per day), Benecol butter substitute (for stanol esters), soluble fibers like pectin, psyllium, glucomannan; raw nuts like almonds, walnuts, and pecans.

In future, should torcetrapib become available (by prescription), this will add to our available tools for these areas when niacin can't be used. Until now, the alternatives to niacin depend on what you and your doctor are trying to achieve. In the vast majority of cases, HDL, small LDL, triglyceride, etc. goals for heart scan score control can be achieved, even when niacin is not well tolerated.

This question comes up so frequently that it's worth going over.

Flaxseed oil is a wonderful oil rich in linolenic acid, which may provide health benefits all by itself. Some authorities have speculated that the substantial reduction in heart attack seen in the Lyon Heart Study, the study that demonstrated the healthy power of the Mediterranean diet, is due to linolenic acid.

Flaxseed oil is also rich in monounsaturates and low in saturates, both desirable qualities. Of course, I'm talking here about flaxseed oil, to be distinguished from flaxseed , which are the intact seeds. The seeds themselves also contain the same oils, but contain other components, specifically lignan, a plant fiber with suspected health benefits like reduction in cancer risk.

Despite all flaxseed oil's wonderful properties, it is definitely not a substitute for fish oil. Why do we use fish oil for our coronary plaque control program (trying to reduce your heart scan score)? Several reasons. Fish oil:

--Dramatically reduces triglycerides, usually by 50% or more.
--Dramatically reduces specific lipoprotein classes like VLDL
--Dramatatically reduces, often eliminates, abnormal postprandial (after-eating) lipoprotein patterns, like IDL (intermediate-density lipoprotein)
--Has been conclusively shown to reduce risk of heart attack and death from heart attack (GISSI Prevenzione Trial).
--Has been shwon to reduce risk of stroke.
--Modifies blood clotting parameters, particularly a 20% reduction in fibrinogen.

Flaxseed oil, or linolenic acid concentrate for that matter, do not accomplish any of these effects, all crucial if you are to gain control over your coronary plaque.

Flaxseed oil and flaxseed remain wonderful nutritional agents for their own reasons. But they will not substitute for fish oil in your program. Only fish oil--the real thing--does the job.

This conversation is aimed primarily at non-followers of the Track Your Plaque program, because if you were a follower, you’d already know the answer!

I saw a woman in the hospital today. She’d just survived her second heart attack one week earlier. At 51 years old, she was understandably shaken, perhaps terrified. She felt that her future was uncertain and, in fact, had discussed with her husband what he should do to prepare for a future without her.

One week earlier, she’d received three stents that successfully aborted her heart attack. But, as is always the case, the modest delays of ambulance transport, the emergency room preliminaries, then of mobilizing an available cardiologist and catheterization laboratory team, totaled nearly two hours before her stent procedure. Inevitably, a moderate amount of damage had been done to her heart.

Her first “event” had been very similar: very little warning, then 911 and the flurry of activity. Both times, the cardiologists (two different physicians) complimented the patient on her prompt action. Both also called her heart attacks “close calls”.

She defied the odds with two near-death events. So, when I met her a week after her last heart attack, I asked an obvious question: “Has anyone told you why you’re having these heart attacks?”

She looked completely puzzled at first. She then said, “No, not really. I just assumed it was genetic. My mother went through the same thing when she was my age. But she didn’t get as far as I have, since they didn’t have these procedures back then.”

To me, this seems inexcusable: This woman had experienced two brushes with death and no doctor had established a cause. Could this woman’s belief be true, that it’s just genetic?

While there are, indeed, genetic causes for heart disease, the vast majority of these genetic causes are 1) identifiable, and 2) correctable. Genetic does not necessarily mean hopeless. It just means that the usual equation of heart disease risk management (heart disease = LDL cholesterol = need for Lipitor) has limited value. It would be like giving penicillin to people for any and all infections. It will work occasionally, but it will fail miserably in a great many cases. Treating LDL cholesterol with statin drugs is just like that.

Perhaps this woman has lipoprotein(a), a serious genetic trait that predicts heart disease at a young age and is largely unaffected by statin drugs. Or, she may have a severe excess of small LDL, only partially suppressed by statins. If she has the combined pattern of lipoprotein(a) and small LDL, that means she has two statin-unresponsive and significant genetic traits. But they respond to niacin, specific nutritional strategies, and several other agents.

The message: If you have coronary disease, you need to insist on knowing why. “It’s genetic” is not an acceptable answer. “There’s no proof of any heart disease causes beyond cholesterol” is also nonsense. “Everyone gets heart disease, or “hardening of the arteries”, eventually. You just got it a little before everyone else” is also patently ridiculous.

Identifying the causes of your coronary disease (or coronary plaque if you’ve had a CT heart scan) is the first step in developing a program of treatment that provides you with control over this disease.

If you haven't yet tried it to facilitate weight loss, it's really worth giving the new inulin-containing product, Fiber Choice "Weight Management", a try.

Recall (from a prior Heart Scan Blog) that inulin is a vegetable-based fiber found in celery, green peppers, etc. that, when exposed to water, expands to many times original volume. This simple phenomenon yields satiety--a feeling of fullness.

The manufacturer of the product has also added green tea, which has been shown in two small clinical studies to enhance weight loss, though by a different route.

We've been advising patients to chew two of the strawberry flavored tablets one hour before every meal (or with breakfast if you eat immediately in the morning). You'll be satisfied with less food and you'll experience less intense food cravings.

Though no one so far has achieved a huge drop in weight, it does seem to enhance a slow, gradual weight loss larger than achieved by diet and exercise alone. And it's very safe and inexpensive. If you give it a try to help you lose weight, let us know what kind of results you've obtained.

An article of mine came out in Life Extension Magazine and is available on the online version at:

http://www.lef.org/magazine/mag2006/sep2006_report_omega1_01.htm

This is an update on the heart health applications of fish oil.

Or, go to to www.lef.org and put fish oil into your on-site search and you'll come back to it in future.

Of course, it comes with Life Extension's promotion of its supplements.

Although it's not yet available online, the hard copy version of an article I wrote on homocysteine is available in the October, 2006 Life Extension Magazine. If you're not a member of their program, they'll send you a free copy just for signing up for it without obligation. Go to the home page of www.lef.org to do so. Or, Life Extension is available at newstands if you're in a rush or don't want to sign up for a free copy.

If you haven't done so already, you should subscribe to Dr. John Cannell's free newsletter on vitamin D issues. His newest issue is available at:

http://www.vitamindcouncil.com/newsletter/2006-aug.shtml

A sign-up to subscribe is available on the same page.

I continue to be shocked and amazed at the prevalence and magnitude of vitamin D deficiency in the people I see every day. It's been a beautiful summer with very little rain. Most days have been in the 70-80 degree range--very comfortable to be outdoors in the sun and getting skin expoxure to activate vitamin D in the skin.

Yet, in the vast majority of people I see, summer blood levels of vitamin D are virtually indistinguishable from winter levels. Both hover around the 30 ng/ml range. Summer levels in Wisconsin people seem to be no more than 10 ng/ml higher than winter levels. This remains true even in people who spend a lot of their day outdoors gardening, walking, etc. wearing shorts and a short-sleeved shirt, i.e. with plenty of skin surface area exposed.

I'm at a loss to explain precisely why. Yes, it is Wisconsin. But a direct sun overhead, 75 degree day should be providing plenty of sun. My suspicious is that a combination of factors are at work: people are not spending as much time outdoors as they claim; they often seek shade; use sunscreen; and they're overweight. (Excess weight decreases vitamin D blood levels dramatically, yet another reason not to get fat!)

Read more about vitamin D by checking out Dr. Cannell's insightful comments on the unfolding vitamin D story. He holds nothing back.

How long should it take to stop or reverse coronary plaque growth? How long will it require to stop your heart scan score of, say, 350, from increasing at the expected rate of 30% per year, slow it down (we say "decelerate") to less than 30%, or stop it altogether? Or, actually reduce your score?

It can vary widely. Several simple patterns do seem to emerge, however. Our experience is that lower scores, particularly less than 100 at the start, are easier to gain control over. Scores of 50 or less, in fact, commonly can return to zero.

Higher scores, particularly those >1000, are more difficult to slow or reduce, though we've done it many times. You'll generally have to try harder and it may take longer. It's not uncommon to not stop plaque growth with a starting score this high until your 2nd or 3rd year of effort.

Sometimes it may take even longer. An occasional person requires four or five years to gain control. And there are, unfortunately, some people who never really gain complete control. They slow plaque growth compared to what it would have been with conventional efforts, but never completely halt growth. Why? Sometimes it's a matter of less than full commitment. Other times, we just don't know. Thankfully, these especially difficult cases are few and the majority enjoy substantial slowing or reversal.

Since, in some people, success may take time, you've got to stick it out. Have you ever gotten lost in a strange city only to find out later that the place you were looking for was right around the corner? It can be the same way with stopping coronary plaque growth. If you start with a score of 1000 and, after two years of effort, you've only slowed growth to 11% per year and then give up in frustration, you may have missed the opportunity to have stopped growth entirely in your third year.

All we can do is tip the scales heavily in your favor. We provide you with the best tools known. You've got to provide the commitment, the consistent effort of taking your supplements or medication, making the lifestyle changes, choosing the right foods and avoiding the wrong ones. But you've got to go the distance and not give up too easily.