Honey: More fructose than high-fructose corn syrup

Honey: It’s natural. Mom probably gave it to you, either straight or in tea for a sore throat when you were a kid. Even today, honey is touted as possessing almost supernatural qualities for promoting health.

Honey contains B vitamins, minerals, and a handful of antioxidants. It also contains . . . fructose. 60% of honey, in fact, is fructose.

While the average per capita intake of honey is only a modest 1.29 lb per year (National Honey Board; 2008) and therefore contributes only 0.77 lb of fructose per year, there are people who, believing honey to be healthy, use it to excess and use far more than 1.29 lb per year.

How does that compare to table sugar, or sucrose?

Sucrose is 50:50 glucose to fructose. How about high-fructose corn syrup, the sweetener found in virtually all processed foods that has replaced sucrose as the most common sweetener? Depending on the variety, high-fructose corn syrup is generally 42-55% fructose. Many of us (including me) believe that the proliferation of high-fructose corn syrup in processed foods is a big part of the reason Americans are fat and diabetic.

Yes: Judged by its fructose content, honey is worse than high-fructose corn syrup. It is also worse than sucrose.

It means that honey can also contribute to the adverse health effects of fructose, as detailed in this prior Heart Scan Blog post.

Sun, fish, and seaweed

Extraordinary heart health springs from three basic sources in our environment:

Sun, fish, and seaweed.

Sun: Sunlight exposure is nature's intended source of vitamin D. Humans were meant to run naked, or at least scantily clad, in tropical or sub-tropical climates. The large surface area of skin ensured plenty of skin activation of vitamin D, along with long days of intense sun (unlike the seasonal variation of day length and less intense sun further north).

Fish: Fish are the principal source of omega-3 fatty acids, as are, to a lesser degree, wild land animals. Humans as hunter-gatherers tracked, captured, and slaughtered fish and wild game, eaten immediately, since there was no means of storage. Omega-3-rich game was the principal source of fat for primitive cultures.

Seaweed: Seaweed is the world’s most concentrated source of iodine. While seafood like fish and shellfish also contain iodine, seaweed contains, on average, a thousand-fold greater quantity. Seaweed, like plants found on land, are also rich in phytonutrients.

The healthiest cultures on earth follow this simple recipe for health. The unhealthiest population on earth-meaning Americans (i.e., without benefit of bail-out medications and procedures that keep us alive, or vaccinations that protect us from infectious diseases)--neglect all three. Witness the Okinawans, whose daily meals nearly always contain some form of fish and seaweed, and whose sub-tropical climate provides greater sun exposure. It is not unusual for Okinawans to live to 100 years of age, not as an exception, but the rule. Heart disease was virtually unknown except in 90-year olds and older-that is, until the recent adoption of Western practices like fast food and snacks.

It's pretty incredible when you think about it: Simple practices can markedly reduce your likelihood of heart attack and developing heart disease.

Perhaps you’d rather not run naked along a semi-tropical beach, spear fish, and gather seaweed. You could always do the modern equivalents and achieve similar benefits.

Fructose is a coronary risk factor

As discussed in a previous Heart Scan Blog post, Say Goodbye to Fructose, a carefully-conducted University of California study demonstrated that, compared to glucose, fructose induces:

1) Four-fold greater intra-abdominal fat accumulation

2) 13.9% increase in LDL cholesterol, doubled Apoprotein B

3) 44.9% increase in small LDL, 3-fold more than glucose

4) Increased postprandial triglycerides 99.2%.


Other studies have shown that fructose:

--Increases uric acid--No longer is red meat the cause for increased uric acid; fructose has taken its place. Uric acid may act as an independent coronary risk factor and increases high blood pressure and kidney disease.

--Induces insulin resistance, the situation that creates diabetes

--Increases glycation (fructose linked to proteins) and protein cross-linking, processes that underlie atherosclerosis, liver disease, and cataracts.


Make no mistake: Fructose is a powerful coronary risk factor.
There is no doubt whatsoever that a diet rich in fructose from fruit drinks, honey, raisins and other dried fruit like cranberries, sucrose (table sugar), and high-fructose corn syrup is a high-risk path to heart disease.

Also note that many foods labeled "heart healthy" because of low-fat, low saturated fat, addition of sterol esters, or fiber, also contain fructose sources, especially high-fructose corn syrup.

Who lost weight?

The results of the latest Heart Scan Blog poll are in.


I went wheat-free and I . . .


Gained weight 6 (3%)

Lost no weight 41 (21%)

Lost less than 10 lbs 28 (14%)

Lost more than 10 lbs 34 (17%)

Lost more than 20 lbs 22 (11%)

Lost more than 30 lbs 28 (14%)

I'm still losing weight! 30 (15%)

(189 respondents)


This means that, by eliminating wheat:

24% had no success

31% had moderate success (less than 10 lbs or more than 10 lbs)

25% had extravagant results with 20 lbs or more lost


It would be interesting to know where along the weight-loss spectrum the last category, "I'm still losing weight," group falls. (Anyone with a good story please speak up!)

I believe we can conclude from this casual exercise that, as a simple strategy, wheat elimination is surprisingly effective.

Why would 3% gain weight? Well, without knowing the details, there are several possible explanations:

1) Weight gain developed through other foods. For instance, I've had people eliminate wheat only to replace it with fattening gluten-free alternatives. Remember: wheat-free is not gluten-free. Others load up on the wrong foods, e.g., Craisins and other dried fruit; overdo dairy; or snack on wheat-free but unhealthy foods like ice cream and chips.

2) Too much alcohol

3) Hypothyroidism--A lot more common than you'd think. In fact, this has been the case with a majority of people who have done everything right, yet either failed to lose weight or gained weight.

Those are the biggies.

I'd like to hear your personal stories of wheat elimination--the ups and downs, your success or failure, how you felt during the process, how easy or difficult, your eventual results. Just post them as a response to this blog post.

A niacin primer

A reader of Life Extension reminded me of a piece I wrote about niacin a couple of years back.

Anyone desiring a primer on how and why to use niacin to correct lipid and lipoprotein patterns might find this useful.

While some people, no matter what they do, cannot tolerate niacin (about 10% of people), many others enjoy spectacular benefits.


Q: I recently had a cholesterol profile blood test and learned that I may be at risk of heart disease because my levels of beneficial HDL (high-density lipoprotein) are too low. I read that niacin could help increase my HDL, but my doctor said niacin is dangerous. Whom should I believe?

A: Your doctor would be right—if we were still living in 1985. Since then, however, we have learned how to use niacin (vitamin B3) safely and effectively. Unfortunately, many physicians have not yet caught up, or are still trapped by the idea that cholesterol-lowering statin drugs are the only way to decrease cardiovascular disease risk. I have personally prescribed niacin for thousands of patients as part of our program to reverse coronary disease. In fact, niacin is the closest thing we have available to a perfect treatment that corrects most of the causes of coronary heart disease.

Continued here.

What would life be like . . . ?

What if coronary heart disease could be prevented--no eliminated--applying methods that were accessible, easy, and cheap?

What if coronary heart disease and, thereby, angina, heart attack, sudden cardiac death, ventricular tachycardia, heart failure, and the cerebrovascular equivalent, stroke, could be eliminated using readily available tools available to virtually everyone in the U.S.? And, over a year, it cost less than a once-a-week latte at Starbucks?

How would the healthcare landscape change? What would become of hospitals, manufacturers of the billions of dollars of hospital equipment necessary to supply the cardiovascular hospital industry (e.g., stent manufacturers, catheter manufacturers, defibrillator and pacemaker manufacturers, pharmaceutical manufacturers who no longer have to produce the volume of antiplatelet agents, inotropic drugs, antiarrhythmic agents, etc.)?

How would our lives change? What would the end of life look like if people stopped dying of heart attack, sudden cardiac death, congestive heart failure at age 55, 65, or 75, but lived out their lives to die of something unrelated?

What if the solution had little or nothing to do with drugs but evolved from simple nutritional strategies, supplements meant to correct the deficiencies that accompany modern lifestyles, and a few unique strategies targeted towards the genetic predispositions that lead to heart disease?

What if all this were possible at a cost of a few hundred dollars per year?

It would certainly be a cataclysmic change. Hospitals would shrink to a small remnant of their current gargantuan, dozens-per-city presence. The need for hospital staff would be slashed by over half. The rare cardiologist would tend to congenital heart disease sufferers and other unusual forms of heart disease and he or she might have a colleague or two in all of a major city.

Healthcare costs would plummet, no longer having to sustain the enormous cardiovascular healthcare machine of hospitals, staff, industry, and long-term care. Health insurance, private or public, would drop by 50%.

It would free up nearly a trillion dollars that could be redirected towards other pursuits, like schools and research. Extraordinary leaps forward in quality of life and science would emerge, given that magnitude of funding.

It's not as grand a thought experiment as Alan Weisman's The World Without Us, in which he imagines what the world would be like without humans altogether.

How long would it take to recover lost ground and restore Eden to the way it must have gleamed and smelled the day before Adam, or Homo habilis, appeared? Could nature ever obliterate all our traces? How would it undo our monumental cities and public works, and reduce our myriad plastics and toxic synthetics back to benign, basic elements?

But I believe this thought experiment--what would life be like without heart disease because it was eliminated using inexpensive tools-- is more plausible, more likely to occur. In fact, it has already begun to occur.

See those vines growing up the side of the hospital?

Are jelly beans heart healthy?

Total Fat

3 g or less

Less than 6.5 g





Saturated Fat



1 g or less

1 g or less





Cholesterol

20 mg or less

20 mg or less





Sodium

480 mg or less per RACC* & labeled serving

480 mg or less per RACC* & labeled serving





Nutrients

Contain 10 percent or more of the daily value of 1 of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber



Contain 10 percent or more of the daily value of 1of 6 nutrients; vitamin A, vitamin C, iron, calcium, protein or dietary fiber





Trans fat

Less than 0.5 g per RACC* and labeled serving



Less than 0.5 g per RACC* and labeled serving





Whole Grain

N/A



51 percent by weight/RACC*







Minimum Dietary Fiber



N/A

1.7 g/RACC of 30 g

2.5 g/RACC of 45 g

2.8 g/RACC of 50 g

3.0 g/RACC of 55 g





(RACC=Reference Amount Customarily Consumed)

Thyroid correction: The woeful prevailing standard

Rich has been taking Synthroid or levothyroxine for many years.

When Rich came to my office for continuing management 10 years after his bypass surgery, I checked his thyroid panel:

TSH 7.44 uIU/L

Free T4 1.88 ng/dl (Ref range 0.80-1.90 ng/dl)

Free T3 2.0 pg/ml (Ref range 2.3-4.2 pg/ml)


Rich's thyroid hormone distortions--high TSH, low T3--are sufficient to account for a tripling of heart attack risk long-term.

As Richs' thyroid was being managed by his primary care physician, I notified this doctor of Rich's panel. He therefore increased Rich's levothyroxine from 75 mcg per day to 100 mcg per day. Another thyroid panel several months later showed:

TSH 0.98 uIU/L

Free T4 2.38 ng/dl

Free T3 2.0 pg/ml



As you would expect, increasing the intake of the T4 hormone (levothyroxine) increased free T4 and suppressed TSH.

But what about T3? It's unchanged.

Indeed, Rich says that he feels no better and, in fact, wakes up in the morning foggy and requires a nap in the afternoon.

In my experience, the majority (approximately 70%, but not 100%) experience subjective improvement when T3 is added in some form and the free T3 level is increased. While the data (summarized here) are conflicted on whether there is objective benefit to T3 management and supplementation, there seems to be a poorly-quantified subjective improvement.

Rich's increased levothyroxine dose decreased (calculated) LDL cholesterol by 10 mg/dl. Based on my experience, I'll bet that his lipid panel would likely be further improved with T3 correction.

What I find incredible is the absolutely rabid resistance waged by primary care physicians and endocrinologists against this notion of T3, mostly due to fears of the remote likelihood of inducing atrial fibrillation and osteoporosis, while they are ready to prescribe lifelong statin drugs without a moment's hesitation.

Launch of new Track Your Plaque newsletter: Cardiac Confidential

Track Your Plaque has just launched a new version of our newsletter. We call it Cardiac Confidential.

Cardiac Confidential is meant to be a no-holds-barred, go-for-the-throat exposé of the world of heart disease. We will expose the dishonest, reveal what we view as the underlying truth. We'll even have an occasional "undercover" report of what goes on in hospitals and the go-for-the-money world of heart procedures.

Read the first issue here (open to everyone) in which "Laurie" describes her encounter with a sleazy, profiteering cardiologist. She survives, but not without paying a dear price.

Risks for coronary disease 2008

According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.


These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Food sources of vitamin K2



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

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

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

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

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

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











Feta cheese

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

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



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

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

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





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

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

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

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

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


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?



Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Appetite stimulants

Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.













Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.


How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

"Heart scans are experimental"

Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.

When meat is not just meat


The edgy nutrition advocate, Mike Adams, over at NewsTarget.com came up with this scary photo tour of a processed meat product from Oscar Mayer: Mystery Meat Macrophotography: A NewsTarget PhotoTour by Mike Adams







Along with increasingly close-up photographs of this meat-product, Adams lists the ingredients in Oscar Mayer's Cotto Salami:


Beef hearts
Pork
Water
Corn syrup
Beef

Contains less than 2% of:
Salt
Sodium lactate
Flavor
Sodium phosphates
Sodium diacetate
Sodium erythorbate
Dextrose
Sodium nitrite
Soy lecithin
Potassium phosphate
Potassium chloride
Sugar


As I reconsider the role of saturated fat in diet, given the startlingly insightful discussion by Gary Taubes of Good Calories, Bad Calories, I am reminded that not all meat is meat, not all saturated fat sources are equal.

I am concerned in particular about sodium nitrite content, a color-fixer added to cured meats that caused a stir in the 1970s when data suggesting a carcinogenic effect surfaced. The public's effort to remove sodium nitrite from the food supply was vigorously opposed by the meat council and it remains in cured meats like sausage, hot dogs, and processed meats like Cotto Salami. A 2006 meta-analysis (combined analysis of studies) of 63 studies did indeed suggest that sodium nitrite was related to increased risk of gastric cancer. This argument is plausible from animal models of cancer risk, as 40 animal models have likewise suggested the same carcinogenic association.

Also, fructose? This is most likely added for sweetness. Recall that fructose heightens appetite and raises triglycerides substantially.

I personally have a natural aversion to meat. I don't like the taste, the look, smell, and the thought of what the animal went through to make it to the supermarket. But, considered from the cold, carnivorous viewpoint of the question, "Is meat okay to eat?", among the issues to consider is whether the meat has been cured or processed, and does that process include addition of sodium nitrite.

Cotto Salami and similar products are not, of course, what carnivorous humans in the wild ate. This is a processed, modified product created from factory farm animals raised in cramped conditions and fed corn and other cheap, available foods. It is not created from free-ranging animals wandering their pastures or pens, eating diets nature intended. This results in modified fat composition, not to mention hormones and antibiotics added. These are not listed on the ingredients. Wild meat does not contain fructose or color-fixers, either.

So don't mistake "meat" in your grocery store for meat. It might look and smell the same--until you look a little closer.



Copyright 2007 William Davis, MD

Don't lament no OTC mevacor

After Merck's third go at FDA approval for over-the-counter (OTC) status for its statin cholesterol drug, Mevacor (lovastatin), the FDA advisory board suggested that its request be denied. They expressed concern that too many people would not understand how the drugs would be used and that misuse would be common.

Similar sentiments were echoed by Dr. Sidney Wolfe, director of the Health Research Group at Public Citizen; the American Medical Association (though the AMA always fights anything that threatens to erode physician control over health); and the de facto spokesman for cardiologists, Dr. Steven Nissen of the Cleveland Clinic.

Although I am a supporter for tools and legislation that yield greater self-empowerment in health care to the public, there is no need to lament the failed OTC status for Mevacor. For one, Merck had no plans to reduce the price on its OTC preparation. For many people, this would have meant an increase in cost, since health insurers would surely not cover a non-prescription agent.

Second, OTC status sends the implicit message that cholesterol is the most common cause of heart disease; it is not. (Small LDL particles are the number one cause, a pattern only partially addressed by any statin drug and a pattern largely responsible for the failure of statin drugs to "cure" heart disease despite pharmaceutical manufacturer's attempts to increase doses to take up any slack in effect.)

Thirdly, you can achieve the same effect--no, a superior effect--by incorporating several simple strategies into your life. These strategies are superior to Mevacor because they do more than just reduce LDL cholesterol. You can achieve similar LDL-reducing effect to Mevacor, 20 mg, just by adding:

--2 tablespoons oat bran or ground flaxseed per day (choose flaxseed if you have sugar problems or small LDL; flaxseed contains no digestible sugars, only protein and fiber)
--Raw almonds or walnuts--at least a handful, though more is fine and will not make you fat. (It's nuts like party mixes, mixed nuts roasted in unhealthy oils, and honey-roasted nuts that make us fat, not raw.)
--Soy protein sources--probably the weakest effect of all foods listed, but a contributor that can be obtained in a variety of forms, such as tofu, soy protein powders, and soy milk.
--Other foods that reduce LDL include pectin sources (e.g., citrus rind), flavonoids (e.g., green tea); stanol esters found in butter substitute Benecol (recall that sterol-containing products like Take Control and the flood of new products on the market like HeartWise orange juice might have potential for allowing sterol esters to enter the blood, so I do NOT recommend them); and, of course, niacin.

Many of these strategies also reduce small LDL, raise HDL, reduce triglycerides, and reduce blood sugar, effects that go beyond that achieved with Mevacor. Of course, a combination strategy is not as easy as popping one pill a day, it's better for you.

I will certainly not shed any tears for Merck and its relentless efforts to gain a stronger foothold in the "transform conditions into diseases" marketing strategy, the same strategy that classifies shyness, toe fungus, and sadness into medical conditions necessitating medication. While I do generally support efforts to increase public access to strategies that increase their health care power, this one was not necessarily all good.

Members of Track Your Plaque can read the complete report, Unique nutritional strategies to Reduce cholesterol naturally on the Track Your Plaque website.



Copyright 2007 William Davis, MD

Damage control

Medical device manufacturer, Cordis, is launching a new marketing program to promote its Cypher drug-coated stent. You can view the details at www.CypherUSA.com , including the slick TV commercial that HeartHawk posted a blog about.

The campaign opens with:

When you open up your heart, you open up your life.

Lives hampered by angina. By shortness of breath. By restricted blood flow. These lives are changing. Because of a state-of-the-art advancement. One that can have a huge impact on arteries around your heart. The CYPHER® Stent. It can open up your arteries. Increase flow of blood and oxygen. And change your restricted life. To an active life worth living. Your new life is...

Life Wide Open


Direct-to-consumer drug advertising has been around for a few years. While it has increased awareness of drugs and the "conditions" they are supposed to treat, it has also highlighted the aggressive profit-motive of the drug industry. This is not health care for the needy and sick, but health care for profit.

So now we're beginning to see the emergence of direct-to-consumer (DTC) advertising for medical devices. There was also a brief, though unsuccessful, foray into DTC advertising for implantable defibrillators, of all things, by Medtronic a couple of years ago, also.

What is the purpose of Cordis' marketing effort? Is it to educate and inform the public who might unknowingly receive non-drug coated stents and be deprived of the restenosis-inhibiting advantage of a drug-coated device? Is it meant to right a systematic wrong, a failure of cardiologists to insert the technologically, biologically, and ethically superior coated stents?

I find that doubtful. A more likely motive is damage control. With some of the (both deserved and undeserved) negative press the drug-coated stents have received lately, Cordis, eager to protect their $20 billion (annual revenues, 2006) medical device franchise, came up with this DTC strategy. After viewing the smiling faces of people , elated because of their "wide open" arteries and lives, Cordis hopes to see people going to their doctors insisting on the stent that is "opening millions of lives," since, "when your arteries narrow, so does your life."

Cool, trendy, liberating. That's the message they wish to deliver. Cool music, beautiful people, flashy high-tech images. Who wouldn't want a Cypher stent?

Beyond damage control, it's a familiar marketing theme: You're slender, glamorous, and sexy if you drink Coke, you're a caring mother if you feed your children Jif peanut butter, you're health conscious and smart if you eat Total cereal . . . you're cool and know what you want from life if you insist on a Cypher stent.

I don't object to advertising. It's part of the capitalistic economic system. It drives awareness and grows businesses. I do get concerned when advertising is so slick and effective that the people who are not properly armed with information can be duped into thinking that they need something that they don't really need.

Or, for which there are powerful, viable alternatives. Even hear about "prevent the disease in the first place?"

Low expectations

The Framingham Risk Calculator is a standard method used by many physicians to predict risk for heart attack or death from heart disease over a 10-year period. Low-risk is defined as <10% risk of heart attack or cardiac death over 10 years; high-risk is defined as 20% or more over 10 years; intermediate-risk is in between.

Let's put it to the test:

Amy is a 53-year old businesswoman. She is 5 ft 4 inches, weighs 150 lbs. Her father had a heart attack in his early 50s followed by the usual list of hospital procedures including bypass surgery at age 60.

What is Amy's risk for heart attack or death from heart disease over the next 10 years? If we enter her data into the Framingham risk calculator, the following result is returned:

Information about your risk score:
Age: 53
Gender: female
Total Cholesterol: 198 mg/dL
HDL Cholesterol: 74 mg/dL
Smoker: No
Systolic Blood Pressure: 120 mm/Hg
On medication for HBP: No
Risk Score: 1% Means 1 of 100 people with this level of risk will have a heart attack in the next 10 years.


So, according to the Framingham calculation, Amy has <1% risk for heart attack or death from heart disease over the next 10 years. Most primary care physicians would, at most, prescribe a statin drug and talk about a reduction in saturated fat.

Thankfully, Amy didn't fall for that bit of conventional mis-information. She instead got a CT heart scan, principally because of her father's history. Her score: 117. At age 53, this put her into 90th percentile, in the worst 10% of scores for women in her age group (50-55). By heart scan criteria, her risk for heart attack is probably more like 4-5% per year, or approximately 40-50% over the next 10 years.

Let's do just a bit more math. If Amy hadn't known about her heart scan score and no preventive action was taken, the expected progression of her heart scan scores would likely be:

Start: 117
Year 1: 152
Year 2: 198
Year 3: 257
Year 4: 335
Year 5: 436
Year 6: 567
Year 7: 737
Year 8: 958
Year 9: 1245
Year 10: 1618

In fact, given Amy's starting heart scan score of 117, it is highly unlikely that she survives the next 10 years without heart attack or a fatal heart event. Yet the Framingham risk calculator puts Amy's risk at less than 1%. Could anything be more wrong?

The folly of the Framingham calculator was highlighted by a recent publication from the large Multi-Ethnic Study of Atherosclerosis (MESA), in which 3600 women (45-84 years), all of whom fell into the "low-risk" category by the Framingham calculator--just like Amy--were tracked over approximately 3 3/4 years. This study generated several observations:

1) 30% of the "low-risk" women had positive heart scan scores.
2) 5% of the "low-risk" women had scores of 300 or greater (very significant for a woman). 8.6% of these women experienced a cardiovascular event like heart attack or death over the period. Women with a heart scan score of 300 or greater had a 22-fold greater event risk compared to women with zero heart scan scores.
3) Women with heart scan scores of 1 to 299 had a cardiovascular event risk of approximately 5-fold greater risk over the period.


Across the U.S., 90% of women younger than 70 years old fall into the Framingham "low-risk" category. Yet this fiction is accepted as the prevailing standard, along with LDL and total cholesterol, for determination of risk in women and men.

In my view, using the Framingham risk calculator is a misguided, misleading path, one that will mis-classify a substantial number of women who could otherwise be spared from heart attack and catastrophe.

By the way, Amy is also the Track Your Plaque program record holder (by percentage drop), with a 63% drop in heart scan score over a 15 month period.

60-year old man dies of high cholesterol

Never saw a headline like this? Neither have I. That's because it doesn't happen.

Cholesterol doesn't harm, maim, or kill. It is simply used as a crude--very crude--marker. It is, in reality, a component of the body, of the cell wall, of lipoproteins (lipid-carrying proteins) in the bloodstream. It is used a an indirect gauge, a "dipstick," for lipoproteins in the blood to those who don't understand how to identify, characterize, and quantify actual lipoproteins in the blood.

Cholesterol itself never killed anybody, any more than a bad paint job on your car could cause a fatal car accident.

What kills people is rupture of atherosclerotic plaque in the coronary arteries. For all practical purposes, you must have atherosclerotic plaque in order for it to rupture (much like a volcano erupts and spews lava). It's not about cholesterol; it's about atherosclerotic plaque. Plaque might contain cholesterol, but cholesterol is not the thing itself that causes heart attack and death.

So why do most people obsess about cholesterol? Good question. It is, at best, a statistical marker for the possibility of having atherosclerotic plaque that ruptures. High cholesterol = higher risk for heart attack, low cholesterol = lower risk for heart attack. But the association is weak and flawed, such that people with high cholesterol can live a lifetime without heart attack, people with low cholesterol can die at age 43.The same holds true for LDL cholesterol, you know, the calculated value based on flawed assumptions about LDL's relationship to total cholesterol, HDL cholesterol, and VLDL cholesterol.

A crucial oversight in the world of cholesterol: There are many other factors that cause atherosclerotic plaque and its rupture, such as inflammatory phenomena, calcium deposition, artery spasm, hemorrhage within the plaque itself, degradative enzymes, etc., none of which are suggested by cholesterol measures.

But one observation has held up, time and again, over the past 40 years of observations on coronary disease: The greater the quantity of coronary atherosclerotic plaque, the greater the risk of atherosclerotic plaque rupture. An increasing burden of atherosclerotic plaque along the limited confines of coronary arteries, just a few millimeters in diameter and a few centimeters in length, is like a house of cards: It's bound to topple sooner or later, and the bigger it gets, the less stable it becomes.

If you are concerned about future potential for heart disease and heart attack, don't get a cholesterol panel. Get a measure of coronary atherosclerotic plaque.

Back to basics: Coronary calcium

After having my attentions pulled a thousand different directions these past 6 months, with the release of Wheat Belly and all the wonderful media attention it has attracted, I've decided to pick up here with a series of discussions about the fundamental issues important to the Track Your Plaque program and prevention and reversal of coronary atherosclerotic plaque.

I fear the discussions at times have drifted off into the exotic. This is great because this is how we learn new lessons, but we can never lose sight of the basics, else we risk losing control over this disease.

Imagine you've got a beautiful new car. You wax it, gap the spark plugs, rotate the tires, etc. and it looks brand-new, just like it came off the dealer's lot. 50,000 miles pass, however, and you realize you've forgotten to change the oil. Ooops! In other words, no matter how meticulous the attention to transmission, tires, and paint job, neglect of the most basic responsibility can ruin the whole thing. We can't let that happen with heart health.

If we propose to reverse coronary atherosclerotic plaque, we've got to have something to measure. First, it tells us whether we have atherosclerotic plaque in the first place, the stuff that accumulates and blocks flow and causes anginal chest pains, and ruptures like a little volcano and causes heart attacks. Second, it gives us something to track over the years to know whether plaque has grown, stopped growing, or been reduced. Without such a measure, you will be driving without a speedometer or odometer, just guessing whether or not you've gotten to your destination.

Of course, the conventional approach to heart disease and heart attack is not to track atherosclerotic plaque in your coronary arteries, but to track some distant "risk factor" for atherosclerotic plaque, especially LDL cholesterol. But LDL cholesterol is flawed at several levels. First, it is calculated, not measured. The nearly 50-year old Friedewald equation used to calculate LDL cholesterol is based on several flawed assumptions, yielding a value that can be 20, 30, or 50% inaccurate as a rule, only occasionally generating a value close to the real value. (No point in publicizing this problem, of course: Why compromise a $27 billion annual cash cow?) It also ignores the effect of diet. (No, cutting fat does not reduce LDL for real, only the calculated value. Cutting carbohydrates, especially wheat--"healthy whole grains"--slashes measured LDL values like NMR LDL particle number and apoprotein B.)

But all risk factors are, at best, snapshots of the situation at that moment in time. They change from day to day, week to week, month to month, year to year. If you do something dramatic in health, like lose 50 pounds, you can substantially change your risk factors values, like LDL cholesterol and HDL cholesterol. But you may not modify the amount of atherosclerotic plaque in your heart's arteries.

Measuring the amount of atherosclerotic plaque in your heart's arteries is, in effect, a cumulative expression of the effects of risk factors up until the moment of measurement.

There are several stumbling blocks, however, in the concept of measuring coronary atherosclerotic plaque. We cannot measure all the unique components of plaque, such as fibrous tissue like collagen, or degradative enzymes like collagenases, or inflammatory proteins like matrix metalloproteinase, or the debris of hemorrhage and inflammation. We struggle to contemporaneously mix in measures of bloodborne inflammation, coagulation and viscosity, and physiological phenomena of the artery itself, like endothelial dysfunction, medial (muscle) tone, and adventitial fat.

So we are left with semi-static measures of total coronary atherosclerotic plaque like coronary calcium, obtainable via CT heart scans as a calcium "score." No, it is not perfect. It does not reflect that moment's blood viscosity, it does not reflect the inflammatory status of the one nasty plaque in the mid-left anterior descending, nor does it reflect the irritating sheer effects of a blood pressure of 150/95.

But it's the best we've got.

If anyone has something better, I invite you to speak up. Carotid ultrasound, c-reactive protein, ankle-brachial index, stress nuclear studies, myoglobin, skin cholesterol, KIF6 genotype . . . none of them approach the value, the insight, the trackability of actually measuring coronary atherosclerotic plaque. And the only method we've got to gauge coronary atherosclerotic plaque that is non-invasive and available in 2012? Yup, a good old CT heart scan calcium score.

Myocardial infraction

I've seen a few heart attacks this past year . . . but none in the people who follow this program.

I saw a heart attack in a priest, a wonderful man who was unable to say "no" to his parishioners who insisted on bringing pies, cakes, and cookies every day.

I saw an impending heart attack in a 74-year old man, a football coach who thought the whole wheat-free, low-carb thing was some wacko trend. Four stents later, he's changed his mind.

A 69-year old woman had to be hospitalized for heart failure due to partial closure of an artery. She repeatedly told me that she simply could not follow the diet because it was "too restrictive."

There were a few others. Interestingly, all felt they were eating healthy, minimizing junk foods and avoiding fatty foods. None were wheat-free nor restricted carbohydrates.

In other words, in the people who follow the basic advice of the Track Your Plaque program to do such simple things as eliminate wheat, don't indulge in junk carbohydrates, normalize vitamin D status, supplement omega-3 fatty acids, supplement iodine and correct any thyroid dysfunction . . . well, they have no heart attacks.

Diet is superior to drugs

Might-o’chondri-AL left this wonderful record of his lipoprotein experience in the comments to the last Heart Scan Blog post. It is a great example of what is achievable with diet and a few supplements . . . without drugs.


(A) Jan. 2011 1st ever NMR lipo-protein analysis was done after 4 months of consistent home food prep of pretty low fat (only olive oil and 1 tablespoon coconut oil daily) but plenty of whole wheat and half potatoes:
* LDL # of particles (P) = 1,676 in nmol/L————being a LDL cholesterol (C) reading of 139 mg/dL
* small LDL # P = 1,021 nmol/L —————yikes! you advise smLDL be less than 117 nmol/L
* HDL # of particles = 28.8 umol/L ————–being a HDL C reading of 45 mg/dL
* Triglycerides = 90 mg/dL ————– true, I never struggled with my weight

(B) May 2011 2nd NMR after another 4 months but added in more fat (1 teaspoon highly concentrated fish oil daily, 90% chocolate, handfulls of nuts, more olive oil and kept coconut oil at 1 tablespoon daily for a controlled experiment), added 500 mg Niacin 3 times a day (in stages up to1,500 mg. total daily), 6000 IU daily vitamin D, deliberately cut out all grains except for social politeness and substituted in daily Koji fermented brown rice (rustic Amazake):
** LDL # P……………= 976 nmol/L ——————————– being LDL C of 100 mg/dL
** small LDL # P …. = 96 nmol/L ——————————– nice surprise
** HDL # P ………… = 27.3 umol/L ——————————being an increase to HDL C of 64 mg/dL
** Triglycerides …… = 42 mg/dL ——————————– despite daily carbs over 150 gr. daily

(C) Dec. 2011 3rd NMR after another 7 more months thinking Doc’s advice is worthwhile I added in yet more fat (mainly daily 2 tablespoons of coconut oil, more 90% chocolate), bumped Niacin up to 1,000 mg twice a day (2,000 mg. total daily), cut out the Amazake, kept up the vitamin D adding daily vitamin K & daily ate main mid-day meal out as lunch on spicy Thai & Chinese fish/shrimp/soup/rice meals (my next control):
*** LDL # P ………. = 764 nmol/L ————— being LDL C of 107 mg/dL ( 2x coconut’s saturated fat)
***small LDL # P… = less than 90 nmol/L ——–surprised me NMR can’t count lower
***HDL # P ……… = 41.4 umol/L ——————– being an increase to HDL C of 88 mg/dL
*** Triglycerides ….= 43 mg/dL ——————- daily carbs below ~ 120 gr. & lost too much weight

Isn't that great? Spectacular job, Might!

MIght achieved values that are superior to that achievable with, say, a high-dose statin strategy. Statins only reduce total LDL particles, reducing small LDL in a non-selective way. And, of course, this diet does not cause muscle aches, memory loss, nor liver problems.

Something to consider: As the diet has become so effective, we can reduce our reliance on niacin. In fact, the benefits of niacin diminish substantially, as small LDL is reduced, HDL increased, triglycerides decreased, and postprandial lipoproteins subdued with the diet only.

Low-carb is heart healthy

Anybody following the discussions in these pages know that: Limiting carbohydrate intake reduces risk for coronary heart disease and heart attack.

First of all, why do conventional diets advocate restricting saturated and total fat? From the standpoint of surrogate markers of cardiovascular risk, cutting saturated and total fat reduces total cholesterol; reduces calculated LDL cholesterol; and may reduce c-reactive protein modestly (an index of inflammation). It also increases blood sugar and HbA1c (reflecting the prior 60 days blood sugars), increases glycation of the proteins of the body leading to cataracts, arthritis, and hypertension.

Problem: Total cholesterol is a combination of HDL cholesterol, an estimate of VLDL cholesterol (triglycerides), and LDL cholesterol. It is a composite of both "good" things (HDL) and "bad" things (LDL and VLDL). Cutting saturated and total fat results in reduced HDL, increased VLDL/triglycerides, and a reduction in calculated LDL. Pretty weak stuff. The last item, i.e., reduction in calculated LDL, is not even a real phenomenon. In fact, the net effect in most genotypes (genetic types) may be negative: increased heart disease risk.

In contrast, what is the effect of reducing carbohydrate without restricting fat? (In the approach I use, we start with elimination of the most destructive of carbohydrates, wheat, followed by reducing exposure to other carbohydrates, especially cornstarch and corn products, sugar, and oats.) If, say, we cut carbohydrate intake into the range of a truly low-carbohydrate diet of 10-15 grams per meal ("net" carbs, or total carbohydrates minus fiber), then we witness a number of metabolic transformations:

Reduced fasting triglycerides and VLDL
Reduced postprandial (after-eating) triglycerides, chylomicrons, and chylomicron remnants
Increased HDL and shift towards large HDL particles (presumably more protective)
Reduced small LDL particles
Reduced glycation and oxidation of small LDL particles
Reduced hemoglobin A1c
Reduced c-reactive protein and other inflammatory markers
Reduced blood pressure

By slashing carbohydrates, we also witness weight loss from visceral fat, reversal of pre-diabetes and diabetes, and reduced phenomena of glycation. And, if the wheat-free part of low-carb is maintained, you can also see marked improvement in gastrointestinal health, relief from joint pains, relief from leg edema, relief from migraine headaches, improved behavior and ability to concentrate in children with impaired learning, ADHD, and autism, better mood, deeper sleep. You will see multiple inflammatory and autoimmune diseases improve or completely relieved, such as rheumatoid arthritis and ulcerative colitis.

Having personally gone down the diabetic path and back by cutting the fat in my diet, now maintaining a HbA1c of 4.8% with fasting glucose 84 mg/d; (without medications), there should be no remaining doubt: Low-carb diets, especially if wheat-free, dramatically reduce the factors leading to heart disease; low-fat diets worsen the factors leading to heart disease.

Mocha Walnut Brownies

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.


Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)


Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.

Are you hungry?

Eliminate modern high-yield semi-dwarf Triticum aestivum . . . and what is the effect on appetite?

A reduction in appetite is among the most common and profound experiences resulting from wheat elimination. I know that I have personally felt it: Wake up in the morning, little interest in breakfast for several hours. Lunch? Maybe I'll have a few bites of something. Dinner . . . well, I'd like to exercise first.

The wheatless report that:

--Appetite diminishes to the point where you can't remember whether you've eaten or not. It is not uncommon to miss a meal, perfectly content. Calorie intake drops by 400 calories per day, on average, calories you otherwise would not have needed but all went to . . . you know where.
--Hunger feels different: It's not the gnawing, rumbling hunger that plagues you every 2 hours. In its place, you will find that hunger feels like a soft reminder that, gee, maybe it's time to have something to eat because you haven't had anything in--what?--4 to 6 hours. And it's a subtle reminder, not a desperate hunt that makes you knock people aside at the food bar, steal coworkers' lunches stored in the refrigerator, salivating at the mere thought of food.
--The simplest foods satisfy--It no longer requires an all-you-can-eat buffet to satisfy, but a few small pieces of healthy food. (Yeah, but what happens to revenues at Kraft, Nabisco, and Kelloggs, not to mention the revenues at agribusiness giants ADM and Monsanto? Slash consumption by, say, 30%, you likewise slash revenues by 30%. What would shareholders say?)
--Even prolonged periods of not eating, i.e., fasting, is endured with ease.

Hunger and the relentless search for something to eat disappear for most people. By eliminating the appetite-stimulating properties of wheat, we return to a natural state of eating for sustenance, to satisfy physiologic need. We are no longer victims of this incredibly powerful appetite-stimulant called gliadin from wheat.

This is why many diets fail: They fail to remove this powerful appetite stimulant. You might eat only lean meats, limit your calories, and exercise 90 minutes per day, but as long as the gliadin protein is pushing your appetite button, you will want to eat more or you will have to mount monumental willpower to resist it. You can lose 20 pounds on phase 1 of the South Beach diet, for instance, only to regain it in phases 2 and 3 when "healthy whole grains" are added back.

So the key is to remove the gliadin protein from your life, i.e., eliminate all things wheat.

 

Chocolate . . . for adults only

If you've got a serious chocolate addiction and you'd like to make it as healthy as possible, give this X-rated dark chocolate a try.
I call it X-rated because it is certain to not satisfy young, sugar-craving palates, but is appropriate for only the most serious chocolate craver. This is a way to obtain the rich flavors and textures of cocoa, the health benefits (e.g., blood pressure reduction, antioxidation) of cocoa flavonoids, while obtaining none of the sugars/carbohydrates . . . and certainly no wheat!

It is easy to make, requiring just a few ingredients, a few steps, and a few minutes. Set aside and save for an indulgence, e.g., dip into natural peanut or almond butter.

Ingredients:
8 ounces 100% unsweetened cocoa
5 tablespoons coconut oil, melted
1/2 cup dry roasted pistachios
1/4 cup whole flaxseeds or chia seeds
Truvia or other non-aqueous sweetener

Using double-boiler method, melt cocoa. Alternatively, melt cocoa in microwave in 15-20 second increments. Stir in coconut oil, pistachios, and flaxseeds or chia seeds. Stir in sweetener, mixing thoroughly. (Note that the sweetener must be non-aqueous, as water-based sweeteners will separate in the oils.)

Lay a sheet of parchment paper out on a large baking pan. Pour chocolate mixture slowly onto paper, tilting pan carefully to spread evenly until thickness of thick cardboard obtained. Place pan in refrigerator or freezer for 20 minutes.

Remove chocolate and break by hand into pieces of desired size.

"Friday is my bad day"

At the start, Ted had a ton of small LDL particles. His starting (NMR) lipoprotien values:

LDL particle number: 2644 nmol/L

Small LDL: 2301 nmol/L

In other words, approximately 85% of all LDL particles were abnormally small. I showed Ted how to use diet to markedly reduce small LDL particles, including elimination of wheat, limiting other carbohydrates, and even counting carbohydrates to keep the quantity no higher than 15 grams per meal ("net" carbs).

Ted comes back 6 months later, having lost 14 pounds in the process (and now with weight stabilized). Another round of lipoproteins show:

LDL particle number: 1532 nmol/L

Small LDL: 799 nmol/L

Better, but not perfect. small LDL persists, representing nearly 50% of total LDL particle number.

So I quiz Ted about his diet. "Gee, I really stick to this diet. I have nothing made of wheat, no sugars. I count my carbs and I almost never go higher . . . except on Fridays."

"What happens on Friday?" I asked.

"That's when I'm bad. Not really bad. Maybe just a couple of slices of pizza. Or I'll go out for a big custard cone or something. That wouldn't do it, would it?"

That's the explanation. Your liver is well-equipped to recognize normal, large LDL particles. Large LDL particles therefore "live" for only a couple of days in the bloodstream. But the human liver does not recognize the peculiar configuration of small LDL particles, so it lets them pass--over and over and over again. The result: Once triggered by, say two slices of pizza, small LDL particles persist for 5 days, sometimes longer.

So Ted's one "bad" day per week is enough to allow a substantial quantity of small LDL particles to persist. While a fat indulgence (if there is such a thing) pushes large LDL up, the effect is relatively short-lived. Have a carbohydrate indulgence, on the other hand, and small LDL particles persist for up to a week. It means that Ted's one "bad" day per week is enough to allow his small LDL particles to persist at this level, preventing him from gaining full control over coronary plaque.

It also means that, if you have blood drawn for lipoprotein analysis but had a carbohydrate goodie within the previous week, small LDL particles may be exaggeratedly high.

HDL 80 mg/dl

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.