Take a niacin "vacation"

I've been seeing a curious niacin phenomenon that has not, to my knowledge, been reported anywhere in the medical literature.

People with lipoprotein(a), or Lp(a), are best treated with niacin, particularly given the relative lack of other effective therapies. I now have seen approximately 10 people with great initial responses to niacin, only to observe Lp(a) levels slowly drift back up to the starting level over a period of 2-3 years.

In other words, if starting Lp(a) is 200 nmol/l (approximately 80 mg/dl), drops to 70 nmol/l on niacin. Then, over 2-3 years of treatment, it drifts back to 200 nmol/l. Very frustrating.

Somehow, your body's Lp(a) manufacturing mechanism circumvents the niacin, sort of like antibiotic resistance (without the bacteria, of course).

My response to this, though untested, is to have people take an occasional "niacin vacation". I don't mean take a trip to the Bahamas while on niacin. I mean take 2 weeks off from niacin every three months or so. My hope is that the occasional vacation from niacin will allow the body to continue to respond and suppress "resistance". When resuming niacin, you may have to escalate the dose gradually to avoid re-provoking the "flush".

The same "resistance" seems to develop to testosterone in males: an initial drop followed by a gradual increase. Curiously, I've not seen this in females with estrogens, which seems to generate a durable Lp(a) suppressing effect. For this reason, an occasional testosterone "vacation" might also be considered.

So far, I've advised several people to try this. The long-term success or failure, however, is uncertain. I know of no other solutions, however.

If you have Lp(a) and are on long-term niacin, you should consider talking about this issue with your physician. Like many aspects of Lp(a), while fascinating in its complexity, much remains uncertain. Stay tuned.

When LDL is more than meets the eye

Jerry wanted to know what to do with his LDL cholesterol of 112 mg/dl. "My doctor said that it's not high but it could be better."

So I asked him what the other numbers on his lipid panel showed. He pulled out the results:

LDL cholesterol 112 mg/dl

HDL 32 mg/dl

Triglycerides 159 mg/dl


I pointed out to Jerry that, given the low HDL and high triglycerides, his calculated LDL of 112 was likely inaccurate. In fact, if measured, LDL was probably more like 140-180 mg/dl. LDL particles were also virtually guaranteed to be small, since low HDL and small LDL usually go hand-in-hand (though small LDL can still occur with a good HDL).

So Jerry's LDL is really much higher than it appears. To prove it, Jerry will require an additional test, preferably one in which LDL is measured, such as LDL particle number (NMR), apoprotein B, or "direct" LDL.

It's really quite simple. Jerry likely has a high number of LDL particles that are too small. This pattern confers a three- to six-fold increased risk for heart disease.

Treatment requires more than just reducing LDL. Small LDL--an important component of this pattern, responds, for instance, to a reduction in processed carbohydrates like wheat products (breads, breakfast cereals, pretzels, etc.), NOT to a low-fat diet. Weight loss to ideal weight, especially loss of abdominal fat, will yield huge improvements in these numbers. Niacin may be a necessary component of Jerry's treatment program, since it increases LDL size and raises HDL.

For more discussion on measures superior to LDL cholesterol, see my upcoming editorial, Let Dr. Friedewald Lie in Peace (an expansion of a previous Heart Scan Blog). It will be posted on the Cardiologist on Call column on the Track Your Plaque website within the next week.)

Oil-based vitamin D


As time passes, I gain greater and greater respect for the power of restoring vitamin D blood levels to normal, i.e. 50-70 ng/ml. Just yesterday, I saw several people with blood levels of <10 ng/ml--severe deficiency.

Vitamin D deficiency this severe poses long-term risk for osteoporosis, arthritis, colon cancer, prostate cancer, inflammatory diseases, diabetes, and heart disease. Vitamin D appears to make coronary plaque reversal--reduction of your heart scan score--easier and faster.

But it is important that you take the right kind of vitamin D. Several of the people I saw yesterday with vitamin D levels of somebody living in total darkness were taking vitamin D, but they were taking tablets. Tablets are the wrong form. Powder-based tablets, in my experience, yield little or no rise in blood levels. Some preparations generate a small rise but the dose required is huge.

If you're going to take vitamin D, take a preparation that yields genuine and substantial rises in blood levels. This requires an oil-based capsule. I commonly see blood levels of 25-OH-vitamin D3 rise from, say, 10 ng/dl to 60 ng/ml when oil-based capsules are taken.

The most common dose I prescribe to patients is 2000 units per day to females, 3000-4000 units per day to males in non-sun exposed months. Ideally, your dose is adjusted to blood levels.

The Vitamin Shoppe preparation pictured here is one I've used successfully and generates bona fide rises in blood levels. And it costs around $5. Just be sure the preparation you buy is oil-based.

For rapid success, try the "fast" track

Have you tried fasting?

Before your eyes glaze over, let me tell you what I mean. I don't mean a water-only fast for two weeks while you drool over all the temptations around you and you feel sorry for yourself.

I also don't mean the juice fasts that some people use that turn into fruit juice fasts of pure sugar.

Here's another way to do it. Usually, 48 hours of doing this will yield several benefits:

--Weight loss of 1 lb. You will likely experience an even greater weight loss of 2-4 lbs, but much of this will be water loss.

--If you're like me and share a heightened sensitivity to sugars and carbohydrates (like wheat), you may find out just how awful you feel when you eat certain foods. Many people tell me they feel absolutely wonderful when they fast--clearer thinking, increased energy, improved mood. Not the constant gnawing urge to eat they expected.

--After your fast is over, you look back and realize just what large portions of food you were eating. You'll be content with smaller quantities--and enjoy it more.


The "fast" I've used successfully includes two foods:

1) Vegetable juices--that you either juice yourself or purchase. V8 or its equivalent works pretty well. Though purchased V8 is not the best, it's better than nothing and does work reasonably well. If you juice your own vegetable juices, watch out for the diarrhea if you're unaccustomed to vegetable juices. Four 8 oz glasses per day works well.

2) Soy milk--for a source of protein and modest quantity of sugar and fat. I like the Light Silk Soymilk (Vanilla) which contains 80 calories, 2 g fat (0.5 g monounsaturated), 7 g sugar, 6 g protein per 8 oz glass. Four 8 oz glasses of soymilk also work well. In my neighborhood, 8th Continent is another good choice.


Sip both of these throughout the day. Of course, drink water in unrestricted amounts.

What can you expect in your coronary plaque control/heart scan score reversal program? When the fast is over, a rise in HDL, reduction in small LDL, reduction in triglycerides, reduction in blood sugar and insulin, and a smaller tummy. This strategy can be useful to kick-start weight loss efforts or as a periodic way to maintain control over weight and lipid/lipoprotein patterns.


Nutritional Composition Silk Soymilk--Vanilla

Nutrition Facts
Serving Size 1 cup (240mL)
Servings per container 8 H/G OR 4 QT

Amount per Serving

Calories 70
Calories from Fat 20

% Daily Value
Total Fat 2g 3%
Saturated Fat 0g 0%
Trans Fat 0g
Polyunsaturated Fat 1g
Monounsaturated Fat 0.5g

Cholesterol 0mg 0%
Sodium 120mg 5%
Potassium 300mg 8%
Total Carbohydrates 8g 3%
Dietary Fiber 1g 4%
Sugars 6g
Protein 6g
Vitamin A 10%
Vitamin C 0%
Calcium 30%
Iron 6%
Vitamin D 30%
Riboflavin 30%
Folate 6%
Vitamin B12 50%
Magnesium 10%
Zinc 4%
Selenium 8%

No flush = No effect



"Inositol Hexanicotinate is the true 'flushless niacin.' Unlike 'sustained-release' niacin, which is just regular niacin in a pill which dissolves more slowly, Inositol Hexanicotinate is a niacin complex, formed with the B-vitamin-like inositol. When you take an IHN supplement, the central inositol ring gradually releases niacin molecules, one at a time delivering true niacin. This, like “sustained-release” niacin, allows you to take niacin at clinically-proven doses without going crazy with the itch."


That above bit of nonsense adorns one manufacturers sales pitch for its no-flush niacin. No-flush niacin is one of the biggest scams in the health food store.

Ordinarily, I love health food stores. There's lots of fun and interesting things available that pack real power for your health program. Unfortunately, there's also outright nonsense. No-flush niacin is absolute nonsennse.

No-flush niacin is inositol hexaniacinate, or an inositol molecule complexed with 6 niacin molecules. So it really does contain niacin. However, although it works in rats, it exerts no known effect in humans.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

The lack of any observable effect and no studies whatsoever showing a positive effect (there is one study demonstrating no effect), manufacturers continue to manufacture it and health food stores continue to push it as an alternative to niacin that causes the flush. It's quite expensive, commonly costing $30-$50 for 100 tablets.

Don't fall for this gimmick. Niacin is among the most helpful of treatments for gaining control over coronary plaque. It raises HDL, corrects small LDL, reduces triglycerides (along with its friend, fish oil, of course), reduces lipoprotein(a), and dramatically contributes to reduced heart attack risk. No-flush niacin does none of this. Track Your Plaque Members: For a thorough discussion of niacin--how to use it, what preparations work and which do not, read Niacin: Ins and outs, ups and downs on the www.cureality.com website.

"Black holes" on heart scan


Lots of smokers, especially younger smokers, rationalize their habit by telling themselves that they'll stop if and when any hint of adverse health effects develop.

The problem is that, even in the first decade of smoking, dramatic and profound effects can develop--but you won't know it.

One of the most graphic examples of this I see every day in people who have heart scans. While CT heart scans are, of course, for identification of coronary plaque/coronary disease, they're also great for visualizing the lungs.

This man is a light smoker. The lungs are the black tissues (that's normal) on either side of the (white) heart in the center. Now, note the holes in the lung tissue. That's what they literally are: holes left by the destrucive, tissue-eating effects of cigarette smoking.

How common are the holes (or emphysematous "blebs", as they're called in medical lingo)? Very common. You'll even see them in 30-somethings who've smoked only a few years.

These are holes that have nothing in them. The lung tissue that was destroyed to create the hole will never grow back, even when smoking stops. The holes in this example are actually small to average in size. I've seen much bigger. And this only represents the early stages of lung tissue destruction. A long-time heavy smoker shows all other sorts of abnormalities.

Whenever I show these "black holes" to people who smoke, they are horrified and I've actually gotten many people to quit. Take the opportunity to quit as soon as you can if you smoke.

Small LDL--a persistent bugger

Sometimes, small LDL is easy to get rid of. Take niacin, for instance, and it can simply disappear from your body.

But other times, it can be aggravatingly persistent. Several times every day, in fact, I need to run through the checklist of strategies to reduce small LDL with patients.

How important is small LDL? In my experience, it is among the most potent causes behind coronary plaque known. It's a big part of the explanation why some people at an LDL of cholesterol of X mg/dl will have heart disease, while others with the same X mg/dl of LDL will not. When present, small LDL particles are much more likely to trigger atherosclerotic plaque formation. Small LDL particles magnify Lp(a)'s ill-effects tremendously. The data vary but small LDL probably increases heart attack risk at least three-fold.



Here's a checklist of strategies that I advise patients to consider to minimize the small LDL pattern:


--Lose weight to ideal weight--This is very important and effective.


--Fish oil--A relatively small effect unless triglycerides are high to begin with.




--Reduction of wheat products--This can provide a BIG effect. More precisely, a reduction in high-glycemic index foods is effective. But the biggest day-to-day high-glycemic food culprits are wheat products like breads, pasta, crackers, chips, pretzels, and breakfast cereals. "You mean whole wheat bread makes small LDL?!" Yup.


--Reduction of sweets--For the same reasons as reducing wheat products.


--Add raw almonds and walnuts--1/4 to 1/2 cup per day.




--Replace wheat products with OAT products, especially oat bran. This does NOT mean oat-containing breakfast cereals with added sugar and wheat, e.g., Honey Nut Cheerios, Cracklin' Oat Bran Cereal, etc. You might as well eat candy. Buy oat bran as plain oat bran--nothing added. Use it as a hot cereal or added to yogurt, "breading" for chicken, etc.




--Vitamin D--A variable effect, likely resulting from its beneficial effects on "insulin resistance".


--Exercise


--Niacin--Very effective but not always enough.


Among the choices, my favorites are weight loss, niacin, and reduction of wheat products. Those will give you the biggest bang for your buck.

Red badge of courage

A group of 60- and 70-somethings were standing in the anteroom to the cardiac rehabilitation center. All (males) had their T-shirts pulled up, comparing their coronary bypass scars.

It reminds me of war veterans comparing their war wounds. The scars of suffering, of having "conquered" and won a war with a common enemy, a badge of courage.

This is part of the broad social acceptance of bypass surgery and other major procedures for heart disease. Hospitals support it. They do it for the psychological support for patients enduring a difficult process. Often, talking about a shared experience can be a helpful purge for the fears and frustrations of a traumatic event.

Curious thing, though. I've actually had people request bypass surgery simply because all their friends have had one. No kidding. "I just figure my time is coming. I might as well get it over with."

Get the picture? We've had a battle with heart disease and the hospitals have won. The enormous success of hospitals over the last 20 years is not because of delivering babies, it's not from psychiatric hospitalization, it's not from cancer treatment. It's from heart disease. The largest floors in the hospital are usually the cardiac floors. The bulk of revenues and profit are from heart disease.

If I manufacture widgets and each widget I sell makes me scads of money, guess what? I want to sell more and more widgets. I'll persuade people they need my widgets even if they don't. Perhaps I'll even persuade them that buying one is a noble cause. Maybe I'll subtly suggest that I am a charitable operation and I only sell my products for the public good. I could even name my company after a saint. Personal profit--absolutely not!

Ignore the hype. See hospitals and their "products" for what they are: A necessary service--some of the time; profitable products that they hope to sell to more and more people most of the time.

"We don't believe in heart scans"

Tim's CT heart scan score was an earth-shattering 3,447, clearly in the upper stratosphere of percentile rank. Risk of heart attack: 25% per year. At age 58, it was a wonder that nothing had happened yet.

Tim went to the Cleveland Clinic for an opinion, long a powerful bastion of heart procedures. The consulting cardiologist told Tim, "We don't believe in heart scans. They're wrong too often."

An opinion from a widely-respected cardiovascular center. If they don't "believe" in heart scans, does that mean they "believe" in stents and bypass surgery? Does it mean that the thousands of research studies that have now been published on the value of heart scanning are pure fiction? Is there a choice to believe or not believe?

I continue to be shocked at the extraordinary ignorance on the topic of heart scanning among my colleagues. The number one killer of Americans and you still rely on stress tests?

Why this perception that heart scans are "wrong too often"? What this cardiologist means, I believe, is that when people are taken to the cath lab for catheterization, a substantial number of those with positive heart scan scores don't have "blockage". But I could have told him that even before the heart catheterization.

There is an expected and well-documented likelihood of finding significant "blockage" based on your heart scan score. At Tim's scary score of 3,447, what is the likelihood of "blockage" of 50% or more? It's around 40-50%. That means that half the people at this score will have a blockage sufficient to justify inserting stents or undergoing bypass surgery, half will not. There will indeed be many plaques, but none severe enough to block flow.

Does that make the heart scan wrong? I don't think it does. Just because you don't need a major procedure to "fix" blockages does not mean that no heart disease is present. Without preventive efforts, Tim's heart attack risk remains an alarming 25% per year--whether or not he gets stents or bypass. The only treatments that substantially reduce this risk (in an asymptomatic person) are preventive efforts, not procedures.

Yet cardiologists like the one Tim consulted at the Cleveland Clinic regard heart scans as something "he doesn't believe in". I would suggest a return to the textbooks and published literature and re-thinking how heart disease should be managed.

Heart scans should provide an opportunity for prevention, not an opportunity for profit.

More on the “Rule of 60”

Despite its apparent simplicity, there’s a lot of thought and wisdom in the Rule of 60.

What if you achieve only a single value in the Track Your Plaque “Rule of 60”? What if, for instance, you got LDL down to 60 mg/dl, but ignored the fact that your HDL was 41 mg/dl and triglycerides were up to 145 mg/dl? Can you still do pretty well?

Probably not. In fact, this specific combination of low HDL and high triglycerides tells me several things:

1) LDL is really much higher than suggested by the 60 mg/dl, which is a calculated value, often much higher. Recall that calculated LDL is prone to immense inaccuracy. When measured, the LDL is commonly somewhere between 120 and 160 mg/dl. However, when you raise HDL to 60 and reduce triglycerides to 60, much of the inaccuracy is removed, i.e., calculated LDL becomes more accurate. LDL can be measured as LDL particle number (NMR), apoprotein B, or direct LDL.

2) LDL particles are small. This is yet another reason why the weight-based LDL measures can be inaccurate. Imagine you have two identical glass jars full of marbles. One jar has small marbles, the other has large marbles, but both jars have the same weight in marbles. Which jar has more marbles? The one with small marbles, of course. The same phenomenon occurs with LDL particles: at the same weight, you can have different numbers of LDL particles. It’s the number of particles that better determine risk for heart disease, not the weight.

3) Triglycerides of 145 mg/dl is actually below the target advised by the National Cholesterol Education Panel Adult Treatment Panel-III guidelines, i.e., you’re okay by conventional standard. But look beneath the surface, and you’ll find that triglycerides at 145 mg/dl are associated with flagrant excesses of VLDL lipoprotein particles and a greater likelihood of a postprandial (after-eating) disorder (increased IDL or postprandial triglycerides), both of which add to coronary plaque.

4) This pattern is also commonly associated with higher blood sugar, higher blood pressure, increased inflammation (e.g., C-reactive protein), increased fibrinogen—all the facets of the metabolic syndrome, or pre-diabetes.

In fact, some of the most aggressive plaque growth—increasing heart scan scores—will occur with this specific pattern. So just achieving one facet of the Track Your Plaque Rule of 60 does not suffice. It’s the whole package that really stacks the odds in your favor of stopping or dropping your heart scan score.

Lessons from the 20-year statin experience

Readers of the Heart Scan Blog know that, while I recognize that statins are useful in a small segment of the population with genetically-determined disorders, they are wildly overused, misused, and abused. In my view, the majority of people taking statins have no business doing so and could, in fact, obtain superior results by following some of the strategies advocated in these pages.

Nonetheless, the 30-year long statin experience has taught us some important lessons. Statin drugs have enjoyed more "research" than any other class of drugs ever conceived. They have received more media attention and embraced by more physicians than any other class of drugs. Combine these social phenomena and I believe that several lessons can be learned:

Small LDL particles and increased HbA1c--An evil duo

Small LDL particles are triggered by consumption of carbohydrates. Eat more "healthy whole grains," for instance, and small LDL particles skyrocket.

Increased hemoglobin A1c, HbA1c, a reflection of the last 60-90 days' blood sugars, is likewise a reflection of carbohydrate consumption. The greater the carbohydrate consumption and/or carbohydrate intolerance, the greater the HbA1c. Most regard a HbA1c of 6.5% or greater diabetes; values of 5.7-6.4% pre-diabetes. However, note that any value of 5.0% or more signifies that the process of glycation is occurring at a faster than normal rate. Recall that endogenous glycation, i.e., glucose modification of proteins, ensues whenever blood sugars increase over the normal range of 90 mg/dl (equivalent to HbA1c of 4.7-5.0%). Glycation is the fundamental process that leads to cataracts, arthritis, and atherosclerosis.

Put the two together--increased quantity of small LDL particles along with HbA1c of 5.0% or higher--and you have a powerful formula for heart disease and coronary plaque growth. This is because small LDL particles are not just smaller; they also have a unique conformation that exposes a (lysine residue-bearing) portion of the apoprotein B molecule contained within that makes small LDL particles uniquely glycation-prone. Compared to large LDL particles, small LDL particles are 8-fold more prone to glycation.

So glycated small LDL particles are present when HbA1c is increased above 5.0%. Small, glycated LDL particles are poorly recognized by the liver receptor that ordinarily picks up and disposes LDL particles, unlike large LDL particles, meaning small LDL particles "live" much longer in the bloodstream, providing more opportunityt to do its evil handiwork. Curiously, small LDL particles are avidly taken up by inflammatory white blood cells that can live in the walls of arteries, where they are oxidized--"glycoxidized"--and add to coronary atherosclerotic plaque.

The key is therefore to tackle both small LDL particles and HbA1c.

Unforgiving small LDL particles

Small LDL particles are triggered by carbohydrates in the diet: Eat carbohydrates, small LDL particles go up. Cut carbohydrates, small LDL particles go down.

A typical scenario would be someone starts with, say, 2000 nmol/L small LDL (by NMR) because they've been drinking the national Kool Aid of eating more "healthy whole grains" and consuming somewhere around 200 grams carbohydrates per day, including the destructive amylopectin A of wheat. This person slashes wheat followed by limiting other carbohydrates and takes in, say, 40-50 grams per day. Small LDL: 200 nmol/L.

In other words, reducing carbohydrate exposure slashes the expression of small LDL particles, since carbohydrate deprivation disables the liver process of de novo lipogenesis that forms triglycerides. Abnormal or exaggerated postprandial (after-eating) lipoproteins that are packed with triglycerides are also reduced. Because triglycerides provide the first lipoprotein "domino" that cascades into the formation of small LDL particles, carbohydrate reduction results in marked reduction in small LDL particle formation.

So let's say you are doing great and you've slashed carbohydrates. Small LDL particles are now down to zero--no small LDL whatsoever. What LDL particles you have are the more benign large variety, say, 1200 nmol/L (LDL particle number), all large, none small. You are due for some more blood work on Thursday. On Tuesday, however, you have four crackers because, what the heck, you've been doing great, you've lost 43 pounds, and have been enjoying dramatic correction of your lipoprotein abnormalities.

Your next lipoprotein panel: LDL particle number 1800 nmol/L, small LDL 700 nmo/L--substantially worse, with a major uptick in small LDL.

That's how sensitive small LDL particles can be to carbohydrate intake. And the small LDL particles can last for up to several days, since small LDL particles are not just smaller in size, they also differ in conformation, making them unrecognizable by the normal liver receptor. The small LDL particles triggered by the 4 crackers therefore linger, outlasting the normal-conformation large LDL particles that are readily cleared by the liver.

This phenomenon is responsible for great confusion when following lipoprotein panels, since a 98% perfect diet can yield dismaying results just from a minor indulgence. But, buried in this simple observation is the notion that small LDL particles are also extremely unforgiving, being triggered by the smallest carbohydrate indulgence, lasting longer and wreaking their atherosclerotic plaque havoc.

I eliminated wheat . . . and I didn't lose weight!

Elimination of wheat is a wonderfully effective way to lose weight. Because saying goodbye to wheat means removing the gliadin protein of wheat, the protein degraded to brain-active exorphins that stimulate appetite, calorie consumption is reduced, on average, 400 calories per day. It also means eliminating this source of high blood sugar and high blood insulin and the 90-minutes cycles of highs and lows that cause a cyclic need to eat more at the inevitable low. It means that the high blood sugar and insulin phenomena that trigger accumulation of visceral fat are now turned off. It may possibly also mean that wheat lectins no longer block the leptin receptor, undoing leptin resistance and allowing weight loss to proceed. And weight loss usually results effortlessly and rapidly.

But not always. Why? Why are there people who, even after eliminating this appetite-stimulating, insulin-triggering, leptin-blocking food, still cannot lose weight? Or stall after an initial few pounds?

There are a list of reasons, but here are the biggies:

1) Too many carbohydrates--What if I eliminate wheat but replace those calories with gluten-free breads, muffins, and cookies? Then I've switched one glucose-insulin triggering food for another. This is among the reasons I condemn gluten-free foods made with rice starch, cornstarch, tapioca starch, and potato starch. Or perhaps there's too many potatoes, rices, and oats in your diet. While not as harmful as wheat, they still provoke phenomena that cause weight loss to stall. So cutting carbohydrates may become necessary, e.g., no more than 12-14 grams per meal.

2) Fructose--Fructose has become ubiquitous and has even assumed some healthy-appearing forms. "Organic agave nectar" is, by far, the worst, followed by maple syrup, honey, high-fructose corn syrup, sucrose,and fruit--yes, in that order. They are all sources of fructose that causes insulin resistance, visceral fat accumulation or persistency, prolongation of clearing postprandial (after-meal) lipoproteins that antagonize insulin, and glycation. Lose the fructose sources--as much of it as possible. (Fruit should be eaten in very small portions.) Watch for stealth sources like low-fat salad dressings--you shouldn't be limiting your fat anyway!

3) Thyroid dysfunction--A real biggie. Number one cause to consider for thyroid dysfunction: iodine deficiency. Yes, it's coming back in all its glory, just like the early 20th century before iodized salt made it to market shelves. Now, people are cutting back on iodized salt. Guess what's coming back? Iodine deficiency and even goiters. Yes, goiters, the disfiguring growths on the neck that you thought you'd only see in National Geographic pictures of malnourished native Africans. Number two: Exposure to factors that block the thyroid. This may include wheat, but certainly includes perchlorate residues (synthetic fertilizer residues) on produce, pesticides, herbicides, polyfluorooctanoic acid residues from non-stick cookware, polybrominated diphenyl ethers (flame retardants), and on and on. If you are iodine-deficient, it can even include goitrogenic iodine-blocking foods like broccoli, cauliflower, and soy. Thyroid status therefore needs to be assessed.

4) Cortisol--Not so much excess cortisol as disruptions of circadian rhythm. Cortisol should surge in the morning, part of the process to arouse you from sleep, then decline to lower levels in the evening to allow normal recuperative sleep. But this natural circadian cycling is lost in many people represented, for instance, as a flip-flopping of the pattern with low levels in the morning (with morning fatigue) and high levels at bedtime (with insomnia), which can result in stalled weight loss or weight gain. Cortisol status therefore needs to be assessed, best accomplished with salivary cortisol assessment.

5) Leptin resistance--People who are overweight develop an inappropriate resistance to the hormone, leptin, which can present difficulty in losing weight. This can be a substantial issue and is not always easy to overcome. It might mean assessing leptin levels or it might mean taking some steps to overcome leptin resistance.

Okay, that's a lot. Next: More on how to know when thyroid dysfunction is to blame.

Do the math: 41.7 pounds per year

Consumers of wheat take in, on average, 400 calories more per day. Conversely, people who eliminate wheat consume, on average, 400 calories less per day.

400 calories per day multiplied by 365 days per day equals 146,000 additional calories over the course of one year. 146,000 calories over a year equals 41.7 pounds gained per year. Over a decade, that's 417 pounds. Of course, few people actually gain this much weight over 10 years.

But this is the battle most people who follow conventional advice to "cut your fat and eat more healthy whole grains" are fighting, the constant struggle to subdue the appetite-increasing effects of the gliadin protein of wheat, pushing your appetite buttons to consume more . . . and more, and more, fighting to minimize the impact.

So, if you eat "healthy whole grains" and gain "only" 10 pounds this year, that's an incredible success, since it means that you have avoided gaining the additional 31.7 pounds that could have accumulated. It might mean having to skip meals despite your cravings, or exercising longer and harder, or sticking your finger down your throat.

400 additional calories per day times 365 days per year times 300,000,000 people in the U.S. alone . . . that's a lot of dough. Is this entire scenario an accident?

Or, of course, you could avoid the entire situation and kiss wheat goodbye . . . and lose 20, 30, or 130 pounds this year.

We got the drug industry we deserve

A biting commentary on just who is writing treatment guidelines for diabetes and cardiovascular disease was published in the British Medical Journal, summarized in theHeart.org's HeartWire here.

"About half the experts serving on the committees that wrote national clinical guidelines for diabetes and hyperlipidemia over the past decade had potential financial conflicts of interest (COI), and about 4% had conflicts that were not disclosed.

"Five of the guidelines did not include a declaration of the panel members' conflicts of interest, but 138 of the 288 panel members (48%) reported conflicts of interest at the time of the publication of the guideline. Eight reported more than one conflict. Of those who declared conflicts, 93% reported receiving honoraria, speaker's fees, and/or other kinds of payments or stock ownership from drug manufacturers with an interest in diabetes or hyperlipidemia, and 7% reported receiving only research funding. Six panelists who declared conflicts were chairs of their committee.

"Of the 73 panelists who had a chance to declare a conflict of interest but declared none, eight had undeclared COI that the researchers identified by searching other sources. Among the 77 panel members who did not have an opportunity to publicly declare COI in the guidelines documents, four were found to have COI.
"

The closing quote by Dr. Edwin Gale of the UK is priceless:
"Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve."

It's like having Kellogg's tell us what to each for breakfast, or Toyota telling us what car to drive. The sway of the drug industry is huge. Even to this day, I observe colleagues kowtow to the sexy sales rep hawking her wares. But that's the least of it. Far worse, even the "experts" who we had trusted to have objectively reviewed the evidence to help the practitioner on Main Street appears to be little more than a hired lackey for Big Pharma, hoping for that extra few hundred thousand dollars.

Wheat "debate" on CBC

"Many Canadians plan warm buns, stuffing and pie for their Thanksgiving meals tonight. But I'll speak with a cardiologist who thinks we have no reason to be thankful for any food that contains wheat. William Davis says our daily bread is making us fat and sick."

That's the introduction to my recent interview and debate on CBC, the Canadian public radio system, aired on the Canadian Thanksgiving. Arguing the other side was Dr. Susan Whiting, an academic nutritionist. (I use the word "arguing" loosely, since she hardly argued the issues, certainly hadn't read the book, but was content to echo the conventional line that whole grains are healthy and cutting out a food group is unhealthy.)

I do have to give credit to the Canadian media, including the CBC, who have been hosting some rough-and-tumble discussions about the entire wheat question despite Canada being a world exporter of wheat. I recently participated in another debate with a PhD nutrition expert from Montreal who, in response to my assertion that the genetically-altered high-yield, semi-dwarf strains have changed the basic composition of wheat, argued that the creation of the 2-foot tall semi-dwarf strain was a convenience created so that farmers could see above their fields--no kidding. I stifled my laugh. (The semi-dwarf variants were actually created to compensate for the heavy seed head that develops with vigorous nitrate fertilization that buckles 4 1/2-foot tall wheat stalk, making harvesting and threshing impossible, a process farmers call "lodging." The 2-foot tall semi-dwarf thick, stocky stalk is strong enough to resist lodging.)

In short, debating the nutrition "experts" on this question has been tantamount to arguing with a school age child on the finer points of quantum physics. There has not yet been any real objection raised on the basic arguments against modern genetically-altered wheat. Modern semi-dwarf wheat is, and remains, an incredibly bad creation of the genetics laboratories of the 1970s. It has no business on the shelves of your grocery store nor on the cupboards in your home.

Carrot Cake

This is among my favorite recipes from the Wheat Belly book. I reproduce it here for those of you who read the Kindle or audio version and therefore didn't get the recipes.

I made this most recently this past weekend. It was gone very quickly, as even the 13-year old gobbled it up.

(I reduced the sour cream in this version from 8 to 6 oz to reduce cooking time. Also, note that anyone trying to avoid dairy can substitute more coconut milk, i.e., the thicker variety, in equivalent quantities.)

Makes 8-10 servings



 

 

 

 

 

 

Ingredients:
Cake:
2 cups carrots, finely grated
1 cup chopped pecans
1 cup coconut flour
1 tablespoon ground flaxseed
2 teaspoons ground cinnamon
1 teaspoon allspice
1 teaspoon nutmeg
1 teaspoon baking powder
2 tablespoons freshly grated orange peel
Sweetener equivalent to ½ cup sugar (e.g., 4 tablespoons Truvia)
½ teaspoon sea salt
4 eggs
1/2 cup butter or coconut oil, melted
2 teaspoons vanilla extract
½ cup coconut milk
6 ounces sour cream

Icing:
8 ounces cream cheese or Neufchâtel cheese, softened
1 teaspoon lemon juice
1 tablespoon Truvía or 1/8 teaspoon stevia extract powder or ¼ cup Splenda

Preheat oven to 325° degrees F. Grate carrots and set aside.

Combine coconut flour, flaxseed, cinnamon, nutmeg, baking powder, orange peel, sweetener, and salt in large bowl and mix by hand.

Put eggs, butter or coconut oil, vanilla coconut milk, and sour cream in mixing bowl; mix by hand. Pour liquid mixture into dry pecan/coconut flour mixture and blend with power mixer until thoroughly mixed. Stir carrots and pecans in by hand with spoon. Pour mixture into greased 9- or 10-inch square cake pan.

Bake for 60 minutes or until toothpick withdraws dry. Allow to cool 30 minutes.

Place Neufchâtel cheese in bowl. Add lemon juice and sweetener and mix thoroughly. Spread on cake.

Why wheat makes you fat

How is it that a blueberry muffin or onion bagel can trigger weight gain? Why do people who exercise, soccer Moms, and other everyday people who cut their fat and eat more "healthy whole grains" get fatter and fatter? And why weight gain specifically in the abdomen, the deep visceral fat that I call a "wheat belly"?

There are several fairly straightforward ways that wheat in all its varied forms--whole wheat bread, white bread, multigrain bread, sprouted bread, sourdough bread, pasta, noodles, bagels, ciabatta, pizza, etc. etc.--lead to substantial weight gain:

High glucose and high insulin--This effect is not unique to wheat, but shared with other high-glycemic index foods (yes: whole wheat has a very high-glycemic index) like cornstarch and rice starch (yes, the stuff used to make gluten-free foods). The high-glycemic index means high blood glucose triggers high blood insulin. This occurs in 90- to 120-minute cycles. The high insulin that inevitably accompanies high blood sugar, over time and occurring repeatedly, induces insulin resistance in the tissues of the body. Insulin resistance causes fat accumulation, specifically in abdominal visceral fat, as well as diabetes and pre-diabetes. The more visceral fat you accumulate, the worse insulin resistance becomes; thus the vicious cycle ensues.

Cycles of satiety and hunger--The 90- to 120-minute glucose/insulin cycle is concluded with a precipitous drop in blood sugar. This is the foggy, irritable, hungry hypoglycemia that occurs 2 hours after your breakfast cereal or English muffin. The hypoglyemia is remedied with another dose of carbohydrate, starting the cycle over again . . . and again, and again, and again.

Gliadin proteins--The gliadin proteins unique to wheat, now increased in quantity and altered in amino acid structure from their non-genetically-altered predecessors, act as appetite stimulants. This is because gliadins are degraded to exorphins, morphine-like polypeptides that enter the brain. Exorphins can be blocked by opiate-blocking drugs like naltrexone. A drug company has filed an application with the FDA for a weight loss indication for naltrexone based on their clinical studies demonstrating 22 pounds weight loss after 6 months treatment. Overweight people given an opiate blocker reduce calorie intake 400 calories per day. But why? There's only one food that yields substantial quantities of opiate-like compounds in the bloodstream and brain: wheat gliadin.

Leptin resistance--Though the data are preliminary, the lectin in wheat, wheat germ agglutinin, has the potential to block the leptin receptor. Leptin resistance is increasingly looking like a fundamental reason why people struggle to lose weight. This might explain why eliminating, say, 500 calories of wheat consumption per day yields 3500 calories of weight loss.

And, as in many things wheat, the whole is greater than the sum of the parts. Despite all we know about this re-engineered thing called wheat, eliminating it yields health benefits, including weight loss, that seem to be larger than what you'd predict with knowledge of all its nasty little individual pieces.

Just who is "Real Facts 2000"?

This is an example of what seems to be developing over at Amazon.com, posted as a "book review":

The author has no credentials, no credibility, just a small cult of terribly misinformed followers. Don't be fooled by the high volume screech against wheat and grains. Allegations of "secret ingredients in wheat" to make you eat more, or comparisons to cigerettes. Seriously?! For over 8000 years wheat has sustained and grown human kind, oh and it tastes good when mixed with a little water and yeast. Every nutritionist and serious medical professional will tell you that bread is the most economical and safe source of essential nutrients. In fact, bread is handed out in natural disasters because it sustains life without food safety issues or requiring refrigeration. And now, suddenly it will kill you. Comical! This book is such a bone headed, misinformed way to just scare people into not eating.

As for secret ingredients, humm, apparently the author is ignorant of the food laws that regulate everything that goes into food and on food labels. Unlike some enforcement agencies, the FDA has some serious teeth behind its enforcement. As for frankenwheat, again seriously?! Wheat, due to its ubiquitous presence in the world is treated as sacrosant from any GMO research or development.

If you need real, science based information on healthy eating, check out [...] and leave this book and its cult in the compound.


If you recognize the wording and tone, you will readily recognize the footprints of the Wheat Lobby here. "Terribly misinformed followers"? . . . Hmmm. "Food laws"? I didn't realize that eating more "healthy whole grains" was a . . . law?

Make no mistake: There are people and organizations who have a heavy stake in your continued consumption of the equivalent of 300 loaves of bread per year. There are people and organizations (read: pharmaceutical industry) who have a big stake on the "payoff" of your continued consumption of "healthy whole grains."

This is not a book review; this is part of a concerted, organized campaign to discredit a message that needs to be heard.

Anybody from the media listening?