Are there any alternatives to niacin?

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.

Is flaxseed oil a substitute for fish oil?


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.

If you have coronary artery disease . . . do you know why?

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.

Have you tried inulin yet?

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.

Fish oil update on Life Extension

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.

More on Vitamin D

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.

Why not just get "perfect" lipids and call it a day?

What if you achieved the Track Your Plaque lipid targets: LDL cholesterol 60 mg/dl, HDL 60 mg/dl, and triglycerides 60 mg/dl?

After all, these are pretty stringent standards. Compared to national guidelines (the ATP-III Guidelines of the National Cholesterol Educational Panel), the Track Your Plaque 60-60-60 goals are laughably ambitious. There's a lot of wisdom hidden in those numbers. The triglyceride level of 60, for instance, is a level at which triglycerides become essentially unavailable for formation of triglyceride-containing lipoprotein particles such as small LDL and VLDL.

If you get to the 60-60-60 target, isn't that good enough? What if you just held your values there and went about your business? Will coronary plaque stop growing and will your CT heart scan score stop increasing?

Sometimes it will. But, unfortunately, many times it will not. The experience generated through clinical trials bear this out. Studies like the St. Francis Heart Study and the BELLES Trial both showed that just reducing LDL cholesterol is insufficient to stop plaque growth. Beyond the Track Your Plaque experience, there's no clinical trial experience that shows whether the 60-60-60 approach does any better.

In our experience, achieving 60-60-60 is indeed better than just reducing LDL. That makes sense. Just raising HDL from the average of 42 mg/dl for a male, 52 mg/dl for a woman adds advantage. Compound this with triglyceride reduction from the plaque-creating equation, and you've doubled success.

But there's even more. What if you had hidden patterns not revealed by conventional lipids? How about lipoprotein(a)? Small LDL? Postprandial (after-eating) abnormalities? Hypertensive effects (more common than you think)!

In 2006, stopping the increase in your heart scan score is, for most of us, not just a matter of taking Lipitor or its equivalent and sitting back. For nearly all of us, stopping the progression of your score is a multi-faceted effort.

Hospitals: Then and Now

It's 1920. The hospital in your city is a facility run by nuns or the church. It's a place for the very ill, often without hope of meaningful treatment, but nonetheless a place where surgeries take place, babies are born, the injured and chronically ill can find care. No one has health insurance and there's no Medicare. Everyone pays what they can. The hospital is accustomed to doling out plenty of care without compensation. For that reason, they welcome donations and sometimes will build new additions or other facilities in honor of a major donor.

Volunteeers are common, since the wards are understaffed and generally suffering from a shortage of trained nurses and personnel associated with the church. Drugs, such as they are, are often prepared from basic ingredients in the hospital pharmacy. Product representatives hawking medicines and devices are virtually unheard of.

Though their therapeutic tools are limited, the physicians are a proud group, dedicating their careers to healing. The majority of the medical staff volunteer large portions of their time to care for the poor who come to the hospital with very advanced stages of disease: metastatic tumors, advanced heart failure, debilitating strokes, overwhelming septicemia, etc.

Hospitals are usually governed by a board of clergy and physicians who make decisions on how to apply their limited resources and continually seek charitable donations.


Fast forward to present day: Hospitals are high-tech, professional facilities with lots of skilled people, complicated equipment,and capable of complex procedures. While they still house people with advanced illnesses, the floors are also filled with people with much earlier phases of disease. In general, they do a good job, with quality issues scrutinized by a number of official agencies to police practices, incidence of hospital-related infections, medication errors, care protocols, etc.

The hospital of 2006 is a more more effective place than the hospital of 1920. But its aims and operations are different, also. Though some churches are still involved in hospitals, more and more are owned by publicly-traded companies that answer to shareholders--shareholders who want share value to increase. Though donations are still sought, much of the revenues are obtained by concentrating on profitable, large-ticket procedures. More procedures are often generated by advertising.

Because they operate to generate profits, several hospitals in a single city or region compete with one another. The 21st century has therefore witnessed the phenomenon of hospital-owned physicians: more and more practicing physicians are employees of their hospital. That way, the physician brings all his patients and procedures to his hospital, not to a competitor. The top of the funnel is the primary care physician, who tends to see all disease when it first occurs. The primary care physician then sends the patient to the specialist, who is obliged (by contract) to perform his/her procedure in the hsopital paying their salary.




Representatives from companies manufacturing and selling expensive hospital equipment and drugs are everywhere, falling over themselves to gain attention of the physicians using their equipment and the hospital buyers who make purchasing decisions. Millions of dollars can be transacted with just one sale.

The number of volunteers has dwindled. The poor and uninsured are commonly diverted elsewhere, often to a government-funded, and often second-rate, institution. Hospitals measure success by comparing annual revenues and numbers of major procedures.

The hospital of 2006 is a vastly different place than 1920. If you're expecting charitable treatment, compassion, and selfless care, you're in the wrong century. In 2006, the hospital is a business. You don't expect charitable treatment at Wal-Mart or from your car dealer. Don't expect it from your hospital. They are businesses and you are a customer. Recognize this fact, lose the nostalgia for the hospitals of yesterday, and a lot more will become clear to you.

The dreaded small LDL particle

Brian is a 59-year old landscape architect whose starting CT heart scan score was 276.

Brian's food choices at the start were deplorable: a pound of sausage per week, sometimes more; butter on anything and everything; up to two pounds of cheese per week; hot dogs; etc. His lipoproteins were accordingly just as miserable: low HDL, high triglycerides, excessive (postprandial, or after-eating) IDL. Small LDL was a particularly stand-out pattern, with 95% of all LDL particles in the small category.

Brian made a dramatic turnaround in lifestyle and corrected all of his patterns--except for small LDL. After one year, small LDL still occupied 95% of all LDL particles, even though the quantity of LDL had been reduced. In order to help convince Brian that correction of his small LDL was going to be necessary to achieve control oover coronary plaque, I suggested that he undergo another heart scan. His score: 435, or a 57% increase.

Each day that passes, I gain more and more respect for small LDL as a cause for coronary plaque growth. Conventional thought among lipid experts is that small LDL should no longer be a factor if total LDL (e.g., LDL particle number) is reduced. But our experience suggests otherwise: when small LDL persists, we tend to see continued, sometimes frightening, plaque growth.

I therefore asked Brian to intensify his efforts: additional weight loss off his somewhat prominent abdomen (since visceral fat increases small LDL), further reduce wheat products and processed carbohydrates, increase niacin (to 1500 mg per day), and use more raw almonds and oat bran.

Don't let small LDL get the best of you. It is a nasty, sometimes persistent abnormality that has impressive effects on plaque growth.

Winning Through Intimidation

Do you remember the book, Winning Through Intimidation by author Robert J. Ringer?



In his 1984 bestseller, author Ringer details how to succeed in business by overwhelming clients and competition by appearing hugely successful and powerful. Rather than a business card, he'd hand out an elegant book to represent himself. He'd show up in a limousine to a meeting, even when he could barely afford it. He used these tactics, even when he was a small-fry, in commercial real estate and built a successful business following such techniques.

This reminds me a lot of what happens in conventional medical practice: The large and successful hospitals, filled with trained staff and technology, exude legitimacy and success. How can they possibly be wrong? Such overwhelming know-how and multiple levels of expertise mustbe right!

Let's be grateful that we do have access to such high-tech, capable care. Unfortunately, just as Mr. Ringer used deceptive practices to appear something he wasn't, this is also true in hospitals. Not all physicians have your best interests in mind. Their principal concern is how profitable your care can be for them--can you be persuaded to have your stent, bypass, etc.. After all, look around you: Aren't all this equipment and personnel impressive? Aren't you intimidated?

The patient that most recently drove home this issue for me recently was a smart and capable executive who came in for consultation. He had been told by his internist that a surgery (to replace his aorta, a HUGE procedure) was probably necessary. In my view, it was not--his process was simply not that far progressed. The risks for danger over the next several years was virtually nil. Unfortunately, this man, now confused and worried, sought an opinion from the chief of thoracic surgery (in the usual white coat and with professorial demeanor, I'm sure) in a major metropolitan hospital (in Chicago), who promptly rushed him off to the operating room.

The pathology report, cleverly not mentioned in any other of the hospital documentation, showed what I had suspected: this man had mild disease that wasn't even close to requiring surgery. But, with all that technology, $100,000 or so of costs, chief of surgery who looked the part, etc.--they must be right!

Robert Ringer's concepts only ring too true for hospitals and some of the unscrupulous physicians in practice. Don't allow yourself to be intimidated.

Bosom buddies

Male breast reduction surgery is a booming business. While most industries are in a downward tailspin, breast reduction surgery in men is growing at double-digit rates.

Other efforts, some legitimate, some not, are also cropping up, all intended to help men deal with this embarassing problem:

Exercise programs to reduce male breast size.

Liposuction--Not just for the belly!

Plastic surgery

Gynexin--a supplement that purportedly reduces male breast size.

Conventional medical treatment also includes estrogen blocking drugs, the same ones used to treat breast cancer, drugs like tamoxifen. There's even clothing intended to make breasts less obvious.


While male breast enlargement--"gynecomastia"--can occasionally occur due to rare endocrinologic problems, such as high prolactin hormone levels (hyperprolactinemia) or somewhat more commonly as failed testosterone production (hypogonadism), the vast majority of men who suffer with this problem simply have high estrogen levels.

Makes sense: Women develop larger breasts during development mostly due to increased levels of estrogen. A parallel situation in men likewise stimulates breast tissue.

So where does the excess estrogen come from?

Visceral fat converts testosterone to estrogen. Men with excess visceral fat therefore develop low levels of testosterone and high levels of estrogen. Estrogen levels can, in fact, be substantially higher compared to slender males.

So what foods cause the accumulation of visceral fat and, thereby, increased estrogen and decreased testosterone?

Foods that increase blood glucose and insulin to the greatest degree are the foods that begin this cascade. The common foods that increase blood sugar the most? Here's a list, starting with most blood glucose-insulin provoke at the top, least at the bottom:

Gluten-free foods (dried, pulverized cornstarch, rice starch, potato starch, tapioca starch)
Whole wheat bread
Sucrose
Milky Way bars
Snickers bars

So the whole wheat sandwiches you've been eating increase blood sugar and insulin, leading to visceral fat. (And, yes, whole wheat bread increases blood sugar higher than Milky Way bars and Snickers bars.) The more visceral fat grows, the more resistant to the effects of insulin you become, further escalating blood sugar. Estrogen increases, testosterone drops, mammary gland tissue grows, normal male breasts grow to B- or C-cup size.

Yet again, an entire industry is growing from the unintended consequence of conventional advice. In this instance, the advice to "eat more healthy whole grains" leads to this booming industry of male breast reduction efforts from surgery to medications to clothing. The REAL solution: Eliminate the foods that start the process in the first place.

Don't be a dipstick

If I want to know how much oil is in my car's engine, I check the dipstick.

The dipstick provides a gauge of the amount of oil in my engine. If the dipstick registers "full" because there an oil mark at one inch, I understand that there's more than one inch of oil in my engine. The dipstick provides an indirect gauge of the amount of oil in my engine.

That's what cholesterol was meant to provide: A gauge, a "dipstick," for the kind of lipoproteins (lipid-carrying proteins) in the bloodstream.

Lipoproteins are a collection of particles that are larger than a single cholesterol molecule but much smaller than a red blood cell. Lipoproteins consist of many components: various proteins, phospholipids, lots of triglycerides, as well as cholesterol. In the 1960s, methods to characterize lipoproteins were not widely available, so the cholesterol in lipoproteins were used as a "dipstick" to assess low-density lipoproteins ("LDL cholesterol") and high-density lipoproteins ("HDL cholesterol"). (Actually, even "LDL cholesterol" was not measured, but was derived from "total cholesterol," the quantity of cholesterol in all lipoprotein fractions.)

Some other component of lipoproteins could have been measured instead of cholesterol, such as apoprotein B, apoprotein C, or others, all meant to act as the "dipstick" for various lipoproteins.

Relying on cholesterol to characterize lipoproteins provides a misleading picture. Imagine watching cars go by at high speed while standing on the side of the highway. You want to count how many people--not cars, but people--go by in a given amount of time. Because you cannot make out the detail of each and every car whizzing by, you count the number of cars and assume that each car carries two people. Whether it's rush hour, Sunday morning, late evening, rainy, sunny, or snowing, you make the same assumption: two people per car.

That's what cholesterol does: It is assuming that each and every lipoprotein particle (car) carries the same amount of cholesterol (people).

But that may, obviously, not be true. A bus goes by carrying 25 people. Plenty of cars may carry just the driver. People carpooling may be in cars carrying 3 or 4 people. Assuming just 2 people per car can send your estimates way off course.

That is precisely what happens when your doctor tries to use conventional cholesterol values (total cholesterol, LDL cholesterol) to gauge the lipoproteins in your bloodstream. Measuring cholesterol can also provide the false impression that cholesterol is the cause of heart disease, even though it was originally meant to simply serve as a "dipstick."

What we need to do is to characterize lipoproteins themselves. We can distinguish them by size, number, density, charge, and the type and form of proteins contained within. It provides greater insight into the composition of lipoproteins in the blood. It provides greater insight into the causes underlying coronary atherosclerotic plaque. It can also tell us what dietary changes trigger different particle patterns and how to correct them.

Until you have a full lipoprotein analysis, you can never know for certain 1) if you will have heart disease in your future, or 2) how your heart disease was caused.

Unfortunately, the vast majority of doctors are perfectly content to just count cars going by and assume two people per car, i.e., confine assessment of your heart disease risk using cholesterol . . . just as drug industry marketing has instructed them.

It's not your job to educate your doctor. If he or she refuses to provide access to lipoprotein testing to better determine your heart disease risk, then consider going out on your own. Many of our Track Your Plaque program followers have obtained lipoprotein testing on their own through Direct Labs.

The ultimate insurance company cost savings

I had a very disturbing conversation with a physician who is employed by an insurance company last week.

I admitted a patient in the hospital for very clear-cut reasons. She is one of my few non-compliant patients, doing none of the strategies I advocate--no fish oil, no vitamin D, no correction of her substantial lipoprotein abnormalities, not even medication. Much of this was because of difficult finances, some of it is because she is from the generation (she is in her late 70s) that tends to ignore preventive health, some of it is because she is a kind of happy-go-lucky personality. So her disease has been progressive and, now, life-threatening, including an abdominal aneurysm near-bursting in size (well above the 5.5 cm cutoff). The patient is also a sweet, cuddly grandmother. I have a hard time bullying nice little old ladies.

While she was in the hospital, the social worker told me that her case was being reviewed by her insurer and would likely be denied. Their medical officer wanted to speak to me.

So the medical officer called me and started asking pointed questions. "Why did you do that test? You know that she's not been compliant. Are you sure you want to do that? I don't think that's a good idea." In other words, this was not just a review of the case. This was an opportunity for the insurance company to intervene in the actual care of the patient.

Then the kicker: "Have you considered not doing anything and . . . just letting nature take its course?"

At first, I was stunned. "You mean let the patient die?"

Expressed in such blatant terms, while he was trying to be diplomatic, made him back down. "Well, uh, no, but she is a high-risk patient."

Anyway, this was the first instance I've encountered in which the insurance company is not just in the business of reviewing a case, but actually trying to intervene during the hospital stay, to the point of making the ultimate healthcare cost savings: Letting the patient die.

Unfortunately, never having had an experience like this before, I did not think to record the conversation or take notes. I am wondering if this is an issue to be taken up by the Insurance Board . . . or is this a taste of things to come as the health insurers fall under increasing pressure with the legislative changes underway?

Salvation from halogenation

Iodine is a halogen.

On the periodic table of elements (remember the big chart of the elements in science class?), the ingenious table that lays out all known atomic elements, elements with similar characteristics are listed in the same column. The elegant genius of the periodic table has even allowed prediction of new, undiscovered elements that conform to the "laws" of atomic behavior.

Column 17 (also called "group VIIa") contains all the halogens, of which iodine is one member. Other halogens include fluorine, chlorine, and bromine.

Odd phenomenon in biologic systems: One halogen can often not be distinguished from another. Thus, a chlorinated compound can cleverly disguise itself as an iodinated compound, a brominated compound can mimic an iodinated compound, etc.

What this means in thyroid health is that, should sufficient iodine be lacking in the body, i.e., iodine deficiency, other halogens can gain entry into the thyroid gland.

While a polychlorinated biphenyl (PCB) molecule may be recognized as an iodinated compound, it certainly doesn't act like an iodinated compound once it's in the thyroid's cells and can disrupt thyroid function (Porterfield 1998). Another group of chlorine-containing compounds, perchlorates, that contaminate groundwater and are found as pesticide residues in produce, are extremely potent thyroid-blockers (Greer 2002). Likewise, bromine-containing compounds, such as polybrominated diphenyl ethers (PBDEs), widely used as flame retardants, also disrupt thyroid function (Zhou 2001). Perfluorooctanoic acid (PFOA), found in Teflon non-stick cookware and stain-resistant products,  has been associated with thyroid dysfunction (Melzer 2010). PFOA, incidentally, can disrupt thyroid dysfunction that will not show up in the TSH test used by primary care physicians and endocrinologists to screen for thyroid dysfunction. (In fact, the presumed champions of thyroid health, the endocrinology community, have proven a miserable failure in translating and implementing the findings from  toxicological science findings to that of preserving or restoring thyroid health. They have largely chosen to ignore it.)

We therefore navigate through a world teeming with halogenated thyroid blocking compounds. We should all therefore avoid such exposures as perchlorates in produce by rinsing thoroughly or purchasing organic, avoid non-stick cookware, avoid use or exposure to pesticides and herbicides.

Another crucial means to block the entry of various halogenated compounds into your vulnerable thyroid: Be sure you are getting sufficient iodine. While it doesn't make your thyroid impervious to injury, iodine circulating in the blood in sufficient quantities and residing in sufficient stores in the thyroid gland provides at least partial protection from the halogenated impostors in your life.

I make this point in the context of heart disease prevention, since even the most subtle degrees of thyroid dysfunction can easily double, triple, or quadruple heart disease risk. See related posts, Is normal TSH too high? and Thyroid perspective update.

Lipitor-ologist

One of the things I do in practice is consult in complex hyperlipidemias, the collection of lipoprotein disorders that usually, but not always, lead to atherosclerosis.

First order of business: Make the diagnosis--familial combined hyperlipidemia, hypoalphalipoproteinemia, lipoprotein(a), familial heterozygous hypercholesterolemia, familial hypertriglyceridemia, hyperapoprotein B with metabolic syndrome, etc. These are the disorders that start with a genetic variant, e.g., a missing or dysfunctional enzyme or signal protein, such as lipoprotein lipase or apo C3.

I then ask: What can be done that is easy and safe and preferably related to diet and lifestyle?

By following an effective diet, many of these abnormalities can be dramatically corrected, sometimes completely. Familial hypertriglyceridemia, for instance, an inherited disorder of lipoprotein lipase in which triglyceride levels can exceed 1000 mg/dl, high enough to cause pancreatic damage, responds incredibly well to carbohydrate restriction and over-the-counter fish oil. I have a number of these people who enjoy triglyceride levels below 100 mg/dl--unheard of in conventionally treated people with this disorder.

Then why is it that, time after time, I see these people in consult, often as second or third opinions from lipidologists (presumed lipid specialists) or cardiologists, when the only solutions offered are 1) Lipitor or other statin drug, and 2) a low-fat diet? Occasionally, an aggressive lipidologist might offer niacin, a fibrate drug (Tricor or fenofibrate), or Lovaza (prescription fish oil).

Sadly, the world of lipid disorders has been reduced to prescribing a statin drug and little else, 9 times out of 10.

I don't mean to rant, but I continue to be shocked at the incredible influence the drug industry has over not just prescribing patterns, but thinking patterns. Perhaps I should say non-thinking patterns. The drugs make it too easy to feel like the doctor is doing something when, in truth, they are doing the minimum (at best) and missing an opportunity to provide true health-empowering advice that is far more likely to yield maximum control over these patterns with little to no medication.

All in all, I am grateful that there is a growing discipline of "lipidology," a specialty devoted to diagnosing and treating hyperlipidemias. Unfortunately, much of the education of the lipidologist is too heavily influenced by the pharmaceutical industry. Not surprisingly, the drug people favor "education" that highlights their high-revenue products.

Seeing a lipidologist is still better than seeing most primary care physicians or cardiologists. Just beware that you might be walking into the hands of someone who is simply the unwitting puppet of the pharmaceutical industry.

Robb Wolf's new Paleo Solution

The Paleo Solution: The Original Human Diet


The Paleo Solution: The Original Human Diet

I have to say: I'm impressed. If you would like insight into why a "Paleo" nutritional approach works on a biochemical level--why you lose weight, burn fat, and gain overall better health--then Robb's book is worth devoting a few hours to, of not a reread or two.

Robb has a particular knack for organizing and presenting information in a way that makes it immediately accessible. You will gain an appreciation for how far American nutritional habits have veered off course.

Because Robb brings expertise from his academic biochemistry background, as well as personal trainer and educator running a successful gym in northern California, NorCal Strength and Conditioning, he delivers a book packed with information that is extremely easy to convert to immediate action in health and exercise. He seems to anticipate all the little problems and objections that people come up with along the way, dealing with them in his characteristic lighthearted way, providing practical, rational solutions.

Robb's book nicely complements what Dr. Loren Cordain has written in his The Paleo Diet: Lose Weight and Get Healthy by Eating the Food You Were Designed to Eat and The Paleo Diet for Athletes: A Nutritional Formula for Peak Athletic Performance. (My wife is now reading The Paleo Diet for Athletes and loves it. I'm going to add Robb's book to her reading list for her to read next.)

If nutrition has you stumped, if the USDA food pyramid still sounds like a reasonable path, or if you just would like to understand nutrition a little bitter, especially its biochemical ins and outs, Robb's book is a wonderful place to start.

Human foie gras

If you want to make foie gras, you feed ducks and geese copious quantities of grains, such as corn and wheat.

The carbohydrate-rich diet causes fat deposition in the liver via processes such as de novo lipogenesis, the conversion of carbohydrates to triglycerides. Ducks and geese are particularly good at this, since they store plentiful fats in the liver to draw from during sustained periods of not eating during annual migration.

Modern humans are trying awfully hard to create their own version of foie gras-yielding livers. While nobody is shoving a tube down our gullets, the modern lifestyle of grotesque carbohydrate overconsumption, like soft drinks, chips, pretzels, crackers, and--yes--"healthy whole grains" causes fat accumulation in the human liver.

Over the past few years, there has been an explosion of non-alcoholic fatty liver disease and non-alcoholic steatosis, two forms of liver disease that result from excess fat deposition. The situation gets so bad in some people that it progresses to cirrhosis, i.e., a hard, poorly-functioning liver that paints a very ugly health picture. The end-result is identical to that experienced by longstanding alcoholics.



While Hannibal Lecter might celebrate the proliferation of human fatty livers with a glass of claret, fatty liver disease is an entirely preventable condition. All it requires is not eating the foods that create it in the first place.

Let go of my love handles

When is fat not just fat?

When it's visceral fat. Visceral fat is the fat that infiltrates the intestinal lining, the liver, kidneys, even your heart. It's the stuff of love handles, the flabby fat that hangs over your belt, or what I call "wheat belly."

Unlike visceral fat, the fat in your thighs or bottom is metabolically quiescent. Thigh and bottom fat may prevent you from fitting into your "skinny jeans," but its mainly a passive repository for excess calories.

Visceral fat, on the other hand, is metabolically active. It produces large quantities of inflammatory signals ("cytokines"), such as various interleukins, leptin, and tumor necrosis factor, that can trigger inflammatory responses in other parts of the body. Visceral fat also oddly fails to produce the protective cytokine, adiponectin, that protects us from diabetes, cancer, and heart disease.

Visceral fat also allows free fatty acids to leave and enter fat cells, resulting in a flood of fatty acids and triglycerides (= 3 fatty acids on a glycerol "backbone") in the bloodstream. This worsens insulin responses ("insulin resistance") and contributes to fatty liver. The situation is worsened when the very powerful process of de novo lipogenesis is triggered, the liver's conversion of sugar to triglycerides.

Visceral fat is also itself inflamed. Biopsies of visceral fat show plenty of inflammatory white blood cells (macrophages) infiltrating its structure.

So what causes visceral fat? Anything that triggers abnormal increases in blood glucose, followed by insulin, will cause visceral fat to grow.

It follows logically that foods that increase blood glucose the most will thereby trigger the greatest increase in visceral fat. Eggs don't lead to visceral fat, nor do salmon, olive oil, beef, broccoli, or almonds. But wheat, cornstarch, potato starch, rice starch, tapioca starch, and sugars will all trigger glucose-insulin that leads to visceral fat accumulation.

Fructose is also an extravagant trigger of visceral fat. Fructose is found in sucrose (50% fructose), high-fructose corn syrup, agave syrup, maple syrup, and honey.

Increased visceral fat can be suggested by increased waist circumference. The inflammatory hotbed created by excess visceral fat has therefore been associated with increased likelihood of heart attack, cardiovascular mortality, diabetes, cancer, and total mortality.

So I'm not so worried that you can't squeeze your bottom into your size 8 jeans. I am worried, however, when you need to let your belt out a notch . . . or two or three.

Surviving a widow maker

Gwen came to me 5 years ago. In her late 60s, she'd been having feelings of chest pressure for the past 4 weeks with small physical efforts, such as climbing a flight of stairs or lifting her grandchildren.

She sat in my office, heaving small sobs, accompanied by her daughter.

Gwen had already undergone a heart catheterization at a hospital near home by a cardiologist who I knew to be honest and competent. She'd been told that she had a 90% stenosis ("blockage") of her proximal left anterior descending (LAD) coronary artery. He called it a "widow maker," since closure of the artery at this point can be fatal within minutes. He advised bypass surgery as soon as possible. Though a stent could be placed at this location, he felt that its proximity to the left main stem (i.e., the "trunk" that divides into the LAD and circumflex arteries) might be jeopardized by expanding a stent in this bulky plaque, what I felt was a reasonable concern.

I reviewed the images that she brought with her. Yes, indeed: a widow maker. The portion of the left ventricle (heart muscle) fed by the LAD was also impaired ("hypokinetic"), reflecting reduced flow through the artery.

I advised Gwen that her first cardiologist's advice was sound: This was a potentially dangerous and severe condition. Either a bypass or stent should be performed near-future, the less delay the better.

But Gwen and her daughter would have no talk of any more procedures. She'd come to me because she heard about the (then rudimentary) effort I'd been making at reversing coronary plaque. "I admire your commitment, Gwen, but I am concerned that there may not be sufficient time to implement a program of prevention or reversal. Prevention is very powerful, but very slow. When symptoms like yours are active, also, it can mean that we won't have full control over the plaque causing the symptoms. This risks closure of the vessel, since flow characteristics in the plaque are abnormal. I think that you should go through a stent or bypass. We can then start your prevention/reversal program once we know you're safe."

Gwen would still have none of it. I asked her to return in a few days after thinking it over. In the meantime, we drew her lipoprotein blood samples while she added fish oil, l-arginine (back then I used a lot of l-arginine for its endothelial health effects), and began the Track Your Plaque diet a la 2004. This was in addition to the aspirin, beta blocker, and statin prescribed by the first cardiologist.

Several days later, Gwen and her daughter returned, as committed as ever to not having a procedure and proceeding with our prevention/reversal efforts.

So off we went. I was nervous about Gwen's safety, but she had clearly made her mind made up. Gwen's lipoprotein analysis revealed a severe small LDL pattern along with markers for prediabetes (high insulin, high blood glucose, hypertension, along with the loose tummy of visceral fat). So I counseled her intensively in diet and added niacin.

Within 2 weeks, Gwen no longer had chest pain. Whether this was due to her efforts or to some resolution of an intraplaque phenomenon (e.g., resorption of internal plaque hemorrhage), I don't know. But her symptoms did not return.

As the program evolved, we added the new strategies along the way--vitamin D supplementation; elimination of all wheat along with other changes in diet; iodine and thyroid normalization; as well as discontinuing l-arginine after the initial two years. She also got rid of the statin drug after losing around 20 lbs on the diet.

It's now been six years with her "widow maker" and Gwen has been fine: no recurrence of her symptoms, all stress tests performed have been normal, reflecting normal blood flow in her coronary arteries.

Should ALL people with symptomatic widow makers undergo such an effort and avoid procedures? No, not yet. Prevention and reversal efforts are indeed powerful, but slow. Some people just may not have sufficient time to accomplish what Gwen did. The fact that Gwen showed evidence for reduced flow in the LAD worried me in particular. There is no question that mortality benefits for stenting or bypass of this location are not as large as previously thought (see here, for instance), but each case needs to be viewed individually, factoring in flow characteristics in the artery, appearance of "stability" or "instability" of the plaque itself, not to mention commitment of the person.

But it can be done.

Fred Hahn's Slow Burn

I just had a workout with personal trainer and fitness expert, Fred Hahn. After a workout that quickly taught me that I had a lot to learn about exercise and strength training, Fred and I had a nice low-carbohydrate dinner at a Manhattan restaurant and shared ideas.

Fred is coauthor of Slow Burn Fitness Revolution: The slow motion exercise that will change your body in 30 minutes a week, written in collaboration with the Drs. Eades, Michael and Mary Dan. Fred also blogs here.

I had heard about Fred's "slow-burn" concept in past, but made little of it. I then met Fred on Jimmy Moore's low-carb cruise this past year, where I gave a talk on how carbohydrate-reduced diets reduce small LDL particles. Fred provided a group demonstration on his slow-burn techniques. I watched the demonstration, even tried it a few times back home in the gym, but never really applied them, losing patience most of the time and just going back to my usual routine.

Well, Fred showed me today how to do his slow-burn. In a nutshell, it is the slow, methodical use of weight resistance until the muscle is exhausted. It involves slow movement--e.g., 5 seconds for a lat pulldown from top to bottom--repeated until exhaustion using a weight that allows, perhaps, 6 repetitions over a 60-second effort.

I've been strength training since I was a teenager. I've seen lots of bad training techniques, injuries, and hocum when it comes to how to use resistance training techniques. But I believe that Fred Hahn's slow-burn technique really provides something unique that I hadn't experienced before.

For one, the burn is nothing like I've felt before. Two, there appears to be nearly zero risk for injury, since the usual momentum-driven, herky-jerky motion often employed with weight machines is entirely gone. Three, if what Fred is seeing is true--enhanced visceral (abdominal) fat loss, reduced blood glucose, increased HDL, decreased LDL/total cholesterol--then there's something really interesting going on here.

I also discovered that Fred is no ordinary personal trainer. He has insights into metabolism that I found truly impressive. After all, he's been hanging around with Mike Eades, who's a pretty sharp guy. What Mike Eades is to metabolic insights is what Fred Hahn is to exercise physiology.

I'm going to take Fred's slow burn training insights home with me. I'll let you know how it goes. Some aspects I'd like to explore: Will strength, muscle mass, and blood sugar responses change?



Fred Hahn's latest book, adapting slow burn techniques for kids.

Unexpected effects of a wheat-free diet

Wheat elimination continues to yield explosive and unexpected health benefits.

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

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

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

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

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

--Reduction or elimination of irritable bowel syndrome

--Reduction or elimination of gastroesophageal reflux

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

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

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


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

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

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

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

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

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

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

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

Do "Heart Healthy" sterols cause heart disease?

The sterol question continues to pop up.

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

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


Sterols should be outlawed

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

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


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

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

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

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

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




Though the data are mixed:

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

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




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

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




Each Nature Valley Healthy Heart Bar contains 400 mg sterols.












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













Promise SuperShots contains 400 mg sterols per container.














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














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














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










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

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

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


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

Why obese people can't fast

Why do obese people claim it is impossible to fast?

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

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

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

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

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

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

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

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

Test your own thyroid

134 people responded to the latest Heart Scan Blog poll:


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

Accommodates me without question 45 (33%)

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

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

Refuses without explanation 4 (2%)

Ridicules your request 16 (11%)



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

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

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

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

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

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

You could:

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

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

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

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

Trains, planes, and heart scans

A Heart Scan Blog reader posted the following question:

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

Good question. Think of it this way:

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

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

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

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

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

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


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

D2 and D3 are two different things

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

(Edited slightly for clarity.)

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

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

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

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

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

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

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

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

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

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

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

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

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

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



Incredible.

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

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

Humans need human vitamin D. Plain and simple.

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

Weight loss: Different causes, different solutions

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

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


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

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

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

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

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

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

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

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

Calling all losers!

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

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

It would be helpful to hear and see these results.

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

Weight loss and vitamin D

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

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

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

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

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

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

Some references on this effect:

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

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

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

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

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

You've come a long way, baby

In 1945, the room-sized ENIAC vacuum tube computer was first turned on, women began to smoke openly in public, and a US postal stamp cost three cents. And this was the US government's advice on healthy eating:



 

 

 

 

 

 

 

 

 

 

 

 

 

Green and yellow vegetables; oranges, tomatoes, grapefruit; potatoes and other vegetables and fruits; followed by milk and milk products; meat, poultry, fish, or eggs; bread, flour, and cereals, butter and fortified margarine.

In 2011, the computing power of the ENIAC can be performed by a microchip a few millimeters in width, smoking is now banned in public places, and a first class postage stamp has increased in price by 1466%. And this is the new USDA Food Plate for Americans:



 

 

 

 

 

Have we made any progress over the past 65 years? We certainly have in computing power and awareness of the adverse effects of smoking. But have US government agencies like the USDA kept up with nutritional advice? Compare the 2011 Food Plate with the dietary advice of 1945.

It looks to me like the USDA has not only failed to keep up with the evolution of nutritional thought, but has regressed to something close to advising Americans to go out and buy stocks on the eve of the 1929 depression. Most of us discuss issues like the genetic distortions introduced into wheat, corn, and soy; the dangers of fructose; exogenous glycoxidation and lipoxidation products yielded via high-temperature cooking; organic, free-range meats and the dangers of factory farming, etc. None of this, of course, fits the agenda of the USDA.

My advice: The USDA should stay out of the business of offering nutritional advice. They are very bad at it. They also have too many hidden motives to be a reliable source of unbiased information.

 

 

Fasting with green tea

I've been playing around with brief (18-24 hour) fasts with the use of green tea. Of the several variations on fasting, such as juice "fasts,"  I've been most impressed with the green tea experience.

While the weight loss effects of daily green tea consumption are modest, there seems to be a specific satiety effect that has now been demonstrated in multiple studies, such as this and this. In other words, green tea, through an uncertain mechanism, reduces hunger. The effect is not just due to volume, since the effect cannot be reproduced with hot water alone.

I therefore wondered whether green tea might be a useful beverage to consume during a fast, as it might take the "edge" off of hunger. While hunger during a fast in the wheat-free is far less than wheat-consuming humans, there is indeed an occasional twinge of hunger felt.

So I tried it, brewing a fresh 6-8 oz cup evert two hours or so. I brewed a pot in the morning while at home, followed by brewing single cups using my tea infuser at the office. Whenever I began to experience a hunger pang, I brewed another cup and sipped it. I was pleasantly surprised that hunger was considerably reduced. I sailed through my last 18 hours, for instance, effortlessly. The process was actually quite pleasant.

I brew loose Chinese bancha, sencha, and chunmee teas and Japanese gyokuro tea. Gyokuro is my favorite, but also the most expensive. Bancha is more affordable and I've used that most frequently.

If anyone else gives this a try, please report back your experience.

Dreamfields pasta is wheat

An active question on the blogosphere and elsewhere is whether Dreamfields pasta is truly low-carb. Dr. Andreas Eenfeldt of Diet Doctor detailed his high blood glucose experience with it. Jimmy Moore of Livin' La Vida Low Carb had a similar experience, observing virtually no difference when compared to conventional pasta.

The Dreamfields people make the claim that "Dreamfields' patent-pending recipe and manufacturing process protects all but 5 grams of the carbohydrates per serving from being digested and therefore lessens post-meal blood glucose rise as compared to traditional pasta." They call the modified carbohydrates "protected" carbs.



In other words, they are making the claim that they've somehow modified the amylopectin A and amylose molecules in durum wheat flour to inhibit conversion to glucose.

I'd like to add something to the conversation: Dreamfields pasta is wheat. It is a graphic demonstration that, no matter how you cut it, press it, sauce it up, "protect" it, it's all the same thing: wheat. (It reminds me of a bad girlfriend I had in my 20s: She'd put on makeup, a pretty dress, I'd take her out someplace nice . . . She was still an annoying person who whined about everything.)

Wheat is more than a carbohydrate. It is also a collection of over 1000 proteins, including gliadins, glutens, and glutenins. Gliadins, for instance, are degraded to polypeptide exorphins that underlie the addictive potential of wheat, as well as its withdrawal phenomenon on halting consumption. Gliadin-derived exorphins are also the triggers of auditory hallucinations and paranoid delusions in schizophrenia, as well as behavioral outbursts in children with ADHD and autism.

Wheat is a source of lectins that have the curious effect of "unlocking" the proteins of the intestinal lining, the oddly-named "zonulin" proteins, that protect you from ingested foreign molecules. Ingest wheat lectins and all manner of foreign molecules gain entry into your bloodstream. Cholera works by a similar mechanism. (How about a love story: Bread in the time of cholera?)

Glutens, of course, are responsible for triggering celiac disease, the devastating small intestinal disease that now afflicts 3 million Americans, although 2.7 million don't even know it. Glutens are also responsible for neurologic conditions like cerebellar ataxia, peripheral neuropathy, and dementia ("gluten encephalopathy") and the skin condition, dermatitis herpetiformis.

Then there are the conditions for which the active wheat components have not been identified, including acid reflux, irritable bowel syndrome, asthma (excepting "bakers' asthma), rheumatoid arthritis, edema and fluid retention, and a long list of skin conditions from alopecia to gangrene.

My point: Yeah, Dreamfields pastas, from these instructive experiences, acts a lot like conventional durum wheat pasta. But, even if Dreamfields or somebody else perfects the low-carb aspect of it, it's still wheat. Modern wheat is the genetically tarted-up version of Triticum aestivum, the product of genetic shenanigans from the 1960s and 1970s.

Bet you can't fast

People who continue to consume the world's most destructive grain, i.e., wheat, can rarely endure fasting--not eating for an extended period--except by mustering up monumental willpower. That's because wheat is a powerful appetite stimulant through its 2-hour cycle of exaggerated glycemia followed by a glucose low, along with its addictive exorphin effect. Wheat elimination is therefore an important first step towards allowing you to consider fasting.

Why fast? I regard fasting as among the most underappreciated and underutilized strategies for health.

In its purest form, fasting means eating nothing while maintaining hydration with water alone. (Inadequate hydration is the most common reason for failing, often experienced as nausea or lightheadedness.) You can fast for as briefly as 15 hours or as long as several weeks (though I tell people that any more than 5 days and supervision is required, as electrolyte distortions like dangerously low magnesium levels can develop).

Among its many physiological benefits, fasting can:

  • Reduce blood pressure. The blood pressure reducing effect can be so substantial that I usually have people hold some blood pressure medications, especially ACE inhibitors and ARB agents, during the fast since blood pressure will drop to normal even without the drugs. (A fascinating phenomenon all by itself.)

  • Reduce visceral fat, i.e., the fat that releases inflammatory mediators and generates resistance to insulin.

  • Reduce inflammatory measures

  • Reduce liver output of VLDL that cascades into reduced small LDL, improved HDL "architecture," and improved insulin responsiveness. (The opposite of fasting is "grazing," the ridiculous strategy advocated by many dietitians to control weight. Grazing, or eating small meals every two hours, is incredibly destructive for the opposite reason: flagrant provocation of VLDL production.)

  • Accelerate weight loss. One pound per day is typical.


Beyond this, fasting also achieves unique subjective benefits, including reduced appetite upon resumption of eating. You will find that as single boiled egg or a few slices of cucumber, for example, rapidly generate a feeling of fullness and satisfaction. Most people also experience greater appreciation of food--the sensory experience of eating is heightened and your sense of texture, flavors, sweetness, sourness, etc. are magnified.

After decades of the sense-deadening effects of processed foods--over-sugared, over-salted, reheated, dehydrated then just-add-water foods--fasting reawakens your appreciation for simple, real food. On breaking one of my fasts, I had a slice of green pepper. Despite its simplicity, it was a veritable feast of flavors and textures. Just a few more bites and I was full and satisfied.

Once you've fasted, I believe that you will see why it is often practiced as part of religious ritual. It has an almost spiritual effect.

More on fasting to come . . .

Total cholesterol 220

Talking about total cholesterol is like wearing a tie-dyed t-shirt with the peace sign emblazoned on the front: So totally 60s and out of date.

But talk of total cholesterol somehow keeps on coming back. After I spend 45 minutes discussing a patient's lipoprotein patterns, for instance, they'll asking something like, "But what's my total cholesterol?"

To help put this ridiculous notion of total cholesterol to rest, let me paint several pictures of what total cholesterol can tell you. Let's start with a theoretical, but very common, total cholesterol value of 220 mg/dl. Recall that:

LDL cholesterol = total cholesterol - HDL cholesterol - triglycerides/5

Note that LDL cholesterol is nearly always a calculated value. (Yes, your doctor has been treating a calculated, what I call "fictitious," value.)

Rearranging the equation:

Total cholesterol = LDL cholesterol + HDL cholesterol + Triglycerides/5

This relationship means that a great many variations are possible, all under total cholesterol = 220 mg/dl. For example:

LDL 95 mg/dl + HDL 105 mg/dl + Triglycerides 100 mg/dl

(a relatively low-risk pattern for heart disease)

LDL 160 mg/dl + HDL 50 mg/dl + Triglycerides 50 mg/dl

(an indeterminate risk pattern, potentially moderate risk)

LDL 120 mg/dl + HDL 30 mg/dl + Triglycerides 350 mg/dl

(a potentially high-risk pattern)

LDL 60 mg/dl + HDL 25 mg/dl + Triglycerides 675 mg/dl

(an indeterminate risk pattern)

 

That's just a sample of the incredible variation of patterns that can all fall under this simple observation, total cholesterol 220 mg/dl.

Total cholesterol is an outdated concept, one ready long ago for the junk heap of outdated ideas. It's time to throw total cholesterol out in the trash along with beliefs like high-fat intake causes diabetes, whole grains are healthy, and the tooth fairy will leave you money when you leave your molars under the pillow.

Scientists are freakin' liars

So says Tom Naughton, referring to the frequent misinterpretations or misrepresentations of data that characterize much medical research. Dr. Andreas Eenfeldt posted Tom Naughton's recent wonderfully engaging and hilarious talk from Jimmy Moore's Low-Carb Cruise on his Diet Doctor blog.

Comedian and blogger Tom Naughton, also the filmmaker of the movie Fat Head, has brought humor and personality into the low-carb movement. I told my wife to watch it and I could hear her laughing from 30 feet away while watching her laptop.

Dr. Eenfeldt is a sensation of sorts himself, making a big low-carb splash in Sweden. While I missed the cruise this year (due to time pressures), it's clear that Eenfeldt and Naughton have contributed substantially to helping people understand the nonsense that passes as dietary advice in the U.S. and the world.

I watched Naughton's talk while eating my three eggs scrambled with ricotta cheese. I almost spit my eggs out at the computer screen I was laughing so hard.

 

Tell me your wheat elimination story and receive a copy of my new book, Wheat Belly

I'm looking for interesting wheat-free experiences.

For the past year, I have been writing my new book, Wheat Belly . After many, many late nights and soccer games missed, it's now finished. The book will be out in fall, 2011, to be published by Rodale, the Prevention Magazine people.

Wheat Belly will provide, in excruciating detail, the discussion of how wheat was transformed from innocent wild grass to incredible genetically-altered Frankengrain and why it has become such a health nuisance.

I am looking for interesting stories of wheat elimination for the online and special editions of the book. If you have an interesting tale of wheat-elimination successes, woes, or drama, I'd like to hear about it. Even better, if you would agree to be interviewed by phone (not for live use, just for comments and detail), the editors at Rodale will help tell your story.

If we use your story, I will have a free copy of the new Wheat Belly sent to you when it becomes available.

Please post your story in the comments here. I will then need to obtain your contact info, which we will do privately.

 

Real men don't eat carbs

Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen levels; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone and high estrogen, a cause for depression, emotionality, weight gain, and low libido.

--Sugar-provoking carbohydrates like wheat cause visceral fat to accumulate which, in turn, triggers prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and persistent lipoproteins, like chylomicron remnants and VLDL particles, that impair endothelial function literally within minutes to hours of ingestion. Impaired endothelial function underlies erectile dysfunction. This is why Internet spammers so enthusiastically send you offers for discounted Viagra.

--Carbohydrates increase blood sugar which provokes the process of glycation, glucose modification of proteins, that also contributes to endothelial dysfunction followed by erectile dysfunction.

Real men therefore avoid carbs.

Real men don't eat carbs

Real men don't eat carbs. At least they don't eat them without eventually paying the price.

How do carbohydrates, especially those contained in "healthy whole grains," impair maleness? Several ways:

--Consume carbohydrates, especially the exceptional glucose-increasing amylopectin A from wheat, and visceral fat grows. Visceral fat increases estrogen; estrogen, in effect, opposes the masculinizing effects of testosterone. Overweight males typically have low testosterone, high estrogen, a cause for depressions, emotionality, and weight gain.

--Consume carbohydrates like wheat and visceral fat causes prolactin to be released. Increased prolactin in a male causes growth of breasts: "man boobs,""man cans," "moobs," etc. This is why male breast reduction surgery is booming at double-digit growth rates. In cities like LA, you can see billboards advertising male breast reduction surgery.

--Carbohydrates increase visceral fat that sets the stage for postprandial abnormalities, i.e., markedly increased and prolonged lipoproteins like chylomicron remnants and VLDL particles that impair endothelial function. Impaired endothelial function underlies erectile dysfunction. Eat a bagel, become impotent.