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?

Almonds are the new wheat

Once you eliminate this genetically-altered Frankengrain called modern wheat, the diet should center around vegetables, nuts, healthy oils like olive and coconut, fish, meats, cheese, olives, avocados and other real whole foods. This is, in fact, the diet that I have advocated in my heart disease prevention practice, as well as my online program for prevention and reversal of heart disease.

But what if you'd like a piece of cheesecake or a nice slice of dessert bread---but you don't want to gain two pounds, spend 48 hours in the bathroom suffering with diarrhea and cramps, 3 weeks of joint pains and leg swelling, wade through mental "fog," anxiety, and rage just because you had that momentary indulgence---as you would with wheat?

That's why I've been focusing on recipes that allow you to have something familiar, e.g., chocolate coconut bread or biscotti, but using ingredients that will not generate the metabolic contortions triggered by wheat.

On perusing these recipes, you will notice that there are recurring ingredient themes. Many of the same ingredients pop up time and again. Among the most frequent, versatile, user-friendly, and tasty: Almonds.

You can use almonds as ground whole almonds, ground blanched almonds for a finer texture, ground roasted almonds, almond butter (though, for maximum health benefits, I prefer the ground whole almonds). Ground almonds allow you to recreate muffins, breads, scones, pizza crust, pie crust, biscotti, and cookies with health benefits that exceed that of whole wheat---but with none of the downside: no weight gain, no high blood sugar, no triggering of small LDL particles (#1 cause of heart disease in the U.S.), no accumulation of visceral fat, no appetite stimulation.

In short, you just have your chocolate almond biscotti or mocha cupcake and enjoy it, no health price to pay. So I call almonds the new wheat, except better.

Being regular is dangerous to your health

No, I'm not referring to your daily morning ritual in the bathroom. I'm talking about heart rate.

Counterintuitively, a perfectly regular heart rate is a marker of poor health. People with perfect regularity of heart rate have more heart attacks, for instance.

Regularity of heart rate occurs more commonly in people with hypertension and other metabolic derangements, and it signals increased risk for both heart attack and death. A perfectly regular heart rate, i.e., no variation in the time interval from beat to beat, suggests that the parasympathetic nervous system, the component of automatic ("autonomic") nervous system control that is associated with the relaxation response, feelings of well-being, quiet, and relaxation, is weak. It also means that the opposing sympathetic nervous sytem that regulates the "fight or flight," adrenaline-like response is allowed to be dominant. Dominance of the sympathetic over the parasympathetic system generates regularity of heart rate. Heart rate also tends to be faster, e.g., 85 beats per minutes rather than 55 or 60 beats per minute. So perfect regularity, as well as increased rate, is undesirable.

What we want is irregularity of heart rate. But not irregularity that occurs chaotically with no rhyme or reason. More precisely, we want variability in heart rate. And we want variability to occur in synchrony with breathing, i.e., the respiratory cycle.

The ideal response is:

1) increase in heart rate with inspiration

2) decrease in heart rate with expiration.

Heart rate in healthy people typically varies 15-20 beats per minute within the respiratory cycle, e.g., 60 bpm at end-exhalation, 80 bpm at end-inspiration.

Restoration of increased heart rate variability is associated with reduced blood pressure, reduced blood sugars (HbA1c), reduced inflammatory markers and cortisol (associated with stress), even an increase in DHEA levels. Feelings of well-being and calm also develop.

Among the strategies to consider to restore heightened heart rate variability and slowed heart rate include:

--Omega-3 fatty acid supplementation
--Exercise
--Weight loss
--Deep breathing exercises
--Meditation, prayer, and biofeedback

For our Track Your Plaque purposes, we are folding in the HeartMath strategies, i.e., use of a heart rate monitor that calculates heart rate variability in the context of respiratory cycle. If you've not already done so, take a look at the two Special Reports devoted to this topic on the Track Your Plaque website.

You mean weight loss is hazardous to your health?

In my last Heart Scan Blog post, What is this wacky thing called weight loss?, I discussed how weight loss is associated with distortions in cholesterol and blood sugar values that can be very confusing, often leading your doctor to wrongly and unnecessarily prescribe drugs--since he/she likely rarely sees weight loss.

Blog reader, Donald K., posted his enlightening story:

I experienced this very thing.

After losing serious weight from the eliminating wheat, processed, and sugary foods (1 year in total) I lost 130 pounds. When I was nearly finished I went to see my doctor. He wanted to put me on statins. I explained to him how the data does not support application to me (no evidence of heart disease) and I got the mantra about standards of practice, etc, etc. I held my ground and decided I am much happier eating dairy, eggs, grass fed beef, wild caught fish, and as much raw foods (nuts, veggies, fruits) as my body desires to treat my health parameters.

Maintaining weight, it is easy. My BMI (23 down from 40) has remained constant for a few months now. You are right: metabolic processes definitely change. I no longer have sensations of glucose fluctuations or an uncontrolled appetite. I can only imagine the improved hormone regulation and metabolic communication going on inside my body.

The symptoms from obesity, all gone. Goodbye sleep apnea, hypertension, hemorrhoids, arrhythmias, gastroinestinal disruptions, smelly body, chaffing thighs, and others not mentioned. The positive effects are just as dramatic, but I don’t want to ramble on.

Weight loss? What is it? Getting your life back!


Brace yourself: If you are following the nutrition advice posted here and in the Track Your Plaque program, or the discussion I've initiated in Wheat Belly, then you may find yourself in the very same health predicament as Donald. Arm yourself to protect yourself against the drug-wielding ways of doctors. No, weight loss to achieve ideal weight is definitely not bad for health. But your doctor's misinterpretation of its effects can be!

What is this wacky thing called "weight loss"?

I've discussed this before, but it has proven such an (encouragingly!) frequent issue that I thought it was worth discussing once again.

What happens when you lose weight?

The process of weight loss is characterized by multiple shifts in metabolic patterns that can be confusing. To the uninitiated eye, weight loss can look like a disastrous distortion in metabolism. The naive doctor on seeing your lab values, for instance, might insist you take a statin drug, a fibrate like Tricor (to reduce triglycerides or increase HDL), or simply berate you for your bad health habits--when it's actually a good thing you've accomplished.

So when you lose weight, say, 30 pounds in 3 months, what have you accomplished?

Energy stored as fat, especially from visceral fat stores, is mobilized into the bloodstream. It floods the bloodstream as fatty acids and triglycerides. These fatty acids and triglycerides don't occur in isolation, but interact with other particles and metabolic patterns. The resulting blood patterns include:

--Increased triglycerides--An increase in triglycerides, for instance, from 90 mg/dl to 200 mg/dl in the midst of weight loss is common.

--Reduced HDL--The flood of triglycerides leads to increased degradation of HDL, thus a drop. A drop in HDL from, say, 40 mg/dl to 27 mg/dl--very frightening to people--is exceptionally common.

--Increased blood sugar--The flood of fatty acids and triglycerides results in insulin resistance, leading to higher blood sugars. It is not uncommon for someone with pre-diabetes to develop diabetic-range blood sugars, or a non-diabetic to show pre-diabetic blood sugars.

--Increased small LDL particles--Though small LDL is highly variable during weight loss. When it does happen, it's probably from the interaction of VLDL (triglycerides) with LDL particles and the reaction that overloads LDL particles with triglycerides and conversion to small LDL particles.

So why don't doctors often recognize these patterns when a patient loses weight? Because they rarely see it. Most of my colleagues are accustomed to having patients come back with weight gain, getting heavier and heavier each time. Lose weight? Impossible! So they just don't recognize weight loss effects when they see it. As followers of The Heart Scan Blog know, a frequent conversation around here is "Am I too skinny?" or "How do I stop losing weight?"

The solution: Be patient. Be patient and wait about two months after a weight plateau has been achieved. That's when the numbers "settle down" and you see marked drops in triglycerides, increases in HDL, drops in blood sugar, reductions in small LDL.

As with many things, it's all about timing.

Why small LDL particles are the #1 cause of heart disease in the US

Ask your doctor: What is the #1 cause of heart disease in the US?

Let's put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol

Too much saturated fat

Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.

I'd tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

--Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

--In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here's a 2006 review.

--Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to "cut fat and eat more healthy whole grains." Conventional diet advice has therefore triggered an expllosion in small LDL particles.

--When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either "pattern B," meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus "pattern A," meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called "pattern A."

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with "pattern B" small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat ("wheat belly") to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

Even moore from Jimmy Moore

The ubiquitous and irrepressible Jimmy Moore posted even more commentary about the Wheat Belly phenomenon here, what he calls "The Wheat Belly Bonanza."

Is low-carb really, at its core, little more than elimination of wheat? Sure, corn, rice, and sugar exert deleterious effects. But the dominant effect--by far--is the elimination of wheat. So is the low-carb movement really, at its core, a wheat-elimination movement?

Food (non-wheat-containing, of course) for thought.

Triglyceride and chylomicron "stacking"

Continuing the comments started in Grazing is for cattle, here's an interesting study from the Oxford Center for Diabetes, Endocrinology and Metabolism.

Volunteers were fed a test meal breakfast of Rice Krispies, a banana, and a chocolate milkshake (76.4 grams carbohydrates, 51.9 grams fat, 12.2 grams protein). Lunch was served 5 hours later and consisted of a cheese sandwich and a second chocolate milkshake 43.4 grams carbohydrates, 49.6 grams fat, 24.0 grams protein). Frequent blood samples were then assessed over the day. (Don't try this at home: These are obviously very dangerous foods!)

Here's the pattern of triglycerides that was observed (1st dotted vertical line = breakfast, 2nd dotted vertical line = lunch):



Note that triglycerides only begin to decline 3-4 hours after breakfast, only to peak higher after lunch.


Here's the pattern observed for chylomicrons, the "granddaddy" of lipoproteins that derives from intestinal absorption of fatty acids:



Both graphs from Heath RB et al Am J Phyiol Endocrinol Metab 2006.


With chylomicrons, note a similar pattern to triglycerides: Chylomicrons begin to decline at 3-4 hours, only to peak higher after lunch.

This is the first study to examine the effect of sequential meals on such postprandial (after-eating) patterns. But it makes the graphic point that, if insufficient time is permitted between meals, both triglycerides and chylomicrons will "stack" themselves higher and higher. (Chylomicrons are subjected to processing by the enzyme, lipoprotein lipase, to form highly atherogenic, or plaque-causing, chylomicron remnants.)

While not examined in this study, my bet is that "grazing," i.e., eating small meals or snacks frequently, is an extreme instance of triglyceride, chylomicron, and chylomicron remnant stacking. That can only lead to one thing: accelerated heart and vascular plaque.

What is a healthy vitamin D blood level?

When measuring blood levels of vitamin D (as 25-hydroxy vitamin D), what constitutes a desirable level?

There's no study that directly examines this question, no study that enrolled thousands of people and assigned a placebo group and groups receiving escalating doses of vitamin D and/or achieved higher levels of vitamin D, then observed for development of cancer, diabetes, depression, heart disease, multiple sclerosis, osteoporosis, osteoarthritis, etc. Such a study would requires many thousands of participants (particularly to observe cancer and multiple sclerosis incidence), many years of observation, and many tens of millions of dollars. Nope, only a drug company could afford such costs.

So we have to piece together various observations and extrapolate what we believe to be the ideal level of vitamin D. Epidemiologic observations in several cancers (breast, colon, prostate, and bladder) suggest that a 25-hydroxy vitamin D level of 30 ng/ml or higher is desirable (with less cancer incidence above this level). Other data suggest a level of 52 ng/ml or greater is desirable. Unfortunately, much cancer research looked at intake of vitamin D from food and supplement sources, rather than actual blood levels. We also have to factor in the great individual variation in vitamin D metabolism, with a single dose yielding variable blood levels (as much as a 10-fold difference). There's also the variation introduced by vitamin D-receptor variation (genetic polymorphisms).

A new study using vitamin D administration helps chart the desirable levels of vitamin D.

Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.

In this New Zealand study, 42 women (23 to 68 years old) were given 4000 units vitamin D, 39 women given placebo. Median 25-hydroxy vitamin D levels increased from 21 nmol/L (8.4 ng/ml) to 75 nmol/L (30 ng/ml). Both HOMA (a measure of insulin sensitivity) and fasting insulin levels improved, with greatest improvement seen at 25-hydroxy vitamin D levels of 80-119 nmol/L (32-47.6 ng/ml) or greater.

We also know that a vacation on a Caribbean beach in a bathing suit will increase vitamin D blood levels to the 80-110 ng/ml range without ill-effect (at least in young people who maintain the capacity to activate vitamin D in the skin, a phenomenon that declines as we age).

So do we really know the truly ideal level of vitamin D to achieve? I believe that, given the above observations, it is reasonable to extrapolate that the ideal vitamin D blood level likely lies somewhere above 50 ng/ml. We also know that vitamin D toxicity (i.e., hypercalcemia) is virtually unheard of until vitamin D blood levels approach 150 ng/ml, and even then is inconsistent. The health benefits of vitamin D supplementation are so tremendous, that I am not willing to wait for the prospective data to explore this question fully. For now, I aim for a blood level of vitamin D of 60-70 ng/ml (150-175 nmol/L).

Grazing is for cattle

Many dietitians and nutritionists advise many people today to "graze," i.e., to eat small snacks every couple of hours. They argue that it blocks the drop in insulin and blood sugar that can trigger greater appetite and claim it can facilitate weight loss.



This is an absurd notion. Humans are not meant to graze. Humans are meant to find a wild boar or other animal, kill it, gorge on the meat, organs, and fat, then revert to berries, roots, leaves, and other foraged foods until the next kill. A human living in the wild does not have a cupboard or refrigerator full of ready-to-eat snacks to graze on.

The several hours after a meal is the most dangerous for creating coronary atherosclerotic plaque, i.e., the post-prandial period. In other words, eat dinner and, for the next 6-12 hours, your intestinal tract degrades the food; food byproducts are absorbed into the blood or lymph system. The blood is literally flooded with the byproducts of your meal.

Postprandial abnormalities are emerging to be a potent, and much underappreciated, means of causing heart disease and atherosclerosis in other vascular territories (especially carotid arteries and thoracic aorta).

Not eating--i.e., the fasting state--for extended periods is good for you. Encouraging people to graze amplifies atherosclerotic risk, since it creates an abnormal prolonged postprandial state.

The disastrous results of a low-fat diet

Rob was never that committed to following the program in the first place.

I met Rob because of a modest heart scan score and consultation for a cholesterol abnormality. Rob had been cycled through all the statin agents by his primary care physician, all of which resulted in terrible muscle aches that he found intolerable.

I started out, as usual, characterizing his cholesterol abnormality with lipoprotein testing (NMR):

LDL particle number 1489 nmol/L
LDL cholesterol (Friedewald calculation) 143 mg/dl
Small LDL 52% of total LDL
HDL 50 mg/dl
Triglycerides 82 mg/dl

(LDL particle number is the emerging gold standard for LDL quantification, superior to calculated or Friedewald LDL cholesterol for prediction of cardiovascular events.)

Rob is a busy guy. After only a couple of brief visits, life and work got in the way and Rob let his attentions drift away from heart health. Since the information I provided made little impact on his thinking, he reverted to the low-fat diet his primary care doctor had originally prescribed and that he read about in magazines and food packages. He also ran out of the basic supplements I had advised, including fish oil and vitamin D, and just never restarted them.

A couple of years passed and Rob decided that just poking around on his own might not cut it. So he came back to the office. We repeated his NMR lipoprotein analysis:

LDL particle number 2699 nmol/L
LDL cholesterol (Friedewald calculation) 229 mg/dl
Small LDL 81% of total LDL
HDL 53 mg/dl
Triglycerides 78 mg/dl


Two years of a low-fat diet had caused Rob's LDL particle number to skyrocket by 81%, nearly all due to an explosion of small LDL. Recall that small LDL is more susceptible to oxidation, more inflammation-provoking, more adhesive--the form of LDL particles most likely to cause heart disease.

Also, note that, despite the enormous increase in small LDL, HDL and triglycerides remained favorable. This counters the popular rule-of-thumb offered by some that small LDL is not present when HDL is "normal."

Low-fat diets as commonly practiced are enormously destructive. In Rob's case, a low-fat diet caused both calculated Friedewald LDL as well as LDL particle number to increase dramatically. In many other people, low-fat diets increase calculated Friedewald LDL modestly or not at all, but cause the more accurate LDL particle number to increase significantly, all due to small LDL.

I'm happy to say that, once Rob witnessed how far wrong he could go on the wrong program, he's back on Track. (Sorry, pun intended.) He has resumed his supplements and eliminated the food triggers of small LDL--wheat, cornstarch, and sugars.

Dr. David Grimes reminds us of vitamin D

In response to the Heart Scan Blog post, Fish oil makes you happy: Psychological distress and omega-3 index, Dr. David Grimes offered the following argument.

Dr. Grimes is a physician in northwest England at the Blackburn Royal Infirmary, Lancashire. He is author of the wonderfully cheeky 2006 Lancet editorial, Are statins analogues of vitamin D?, questioning whether the benefits of statin drugs simply work by way of increased vitamin D blood levels.


There is a fashionable interest in Omega-3 fatty acids, and these become equated with fish oil.

But fish oil is much more. Plankton synthesise the related squalene (shark oil) which, in turn, is converted into 7-dehydrocholesterol (7-DHC). The sun now comes into play and it converts 7-DHC into vitamin D (a physico-chemical process).

Small fish eat plankton, large fish eat small fish, and we eat large fish. So vitamin D passes through the food chain.

This has been a vital source of vitamin D for the the Inuits and also for the Scots and other dwellers of northwest Europe. (Edinburgh is on the same latitude as Hudson Bay and Alaska, further north than anywhere in China). In these locations there is not adequate sunlight energy to guarantee synthesis of adequate amounts of vitamin D, again by the action of sunlight on 7-DHC in the skin.

When the Scots moved from coastal fishing villages to industrial cities such as Glasgow, they became seriously deficient in vitamin D, and so the emergence of rickets. This was followed by a variety of other diseases resulting from vitamin D deficiency: tuberculosis, dental decay, coronary heart disease, and even multiple sclerosis and depression (the Glasgow syndrome).

And so it was with the Inuits. When their diet changed from fish for breakfast, fish for lunch, fish for dinner, they became deficient of vitamin D and they developed diseases characteristic of industrial cities, where there is indoor work for long hours, indoor activities, and atmospheric pollution.

It is the vitamin D component of fish and fish oils that is important.

I recently saw an elderly lady from Bangladesh living in northwest England. I would have expected her to have a very low blood level of vitamin D, as her exposure to the sun was minimal. However the blood level was 47ng/ml, not 4 as expected. She eats oily fish from Bangladesh every day, showing its value as a source of vitamin D with subsequent good health. I expect her blood levels of omega-3 fatty acids would also be high.

But it is unfashionable vitamin D that is important, not fashionable omega-3.

David Grimes
www.vitamindandcholesterol.com


Excellent point. The health effects of omega-3 and vitamin D are intimately intertwined when examining populations that consume fish.

In this study of Inuits, it is indeed impossible to dissect out how much psychological distress was due to reduced vitamin D, how much due to reduced omega-3s. My bet is that it's both. Thankfully, we also have data examining the use of pure omega-3 fatty acids in capsule (not intact fish) form, including studies like GISSI Prevenzione.

Nonetheless, Dr. Grimes reminds us that both vitamin D and omega-3 fatty acids from fish oil play crucial roles in mental health and other aspects of health, and that it's the combination that may account for the extravagant health effects previously ascribed only to omega-3s.

Why does fish oil reduce triglycerides?

Beyond its ability to slash risk for cardiovascular events, omega-3 fatty acids from fish oil also reduce triglycerides.

There's no remaining question that omega-3s do this quite effectively. After all, the FDA approved prescription fish oil, Lovaza, to treat a condition called familial hypertriglyceridemia, an inherited condition in which very high triglycerides in the 100s or 1000s of milligrams typically develop.

The omega-3 fraction of fatty acids are unique for their triglyceride-reducing property. No other fraction of fatty acids, such as omega-6 or saturated, can match the triglyceride-reducing effect of omega-3s.

But why does fish oil reduce triglycerides?

First of all, what are triglycerides? As their name suggests, triglycerides consist of three ("tri-") fatty acids lined up along a glycerol (sugar) "backbone." Triglycerides are the form in which most fatty acids occur in the bloodstream, liver, and other organs. (Fatty acids, like omega-3, omega-6, mono- or polyunsaturated, or saturated, rarely occur as free fatty acids unbound to glycerol.) In various lipoproteins in the blood, like LDL, VLDL, and HDL, fatty acids occur as triglycerides.

Of all lipoproteins, chylomicrons (the large particle formed through intestinal absorption of fatty acids and transported to the liver via the lymph system) and VLDL (very low-density lipoprotein, very low-density because they are mostly fat and little protein) particles are richest in triglycerides. Thus, we would expect that omega-3s exert their triglyceride-reducing effect via reductions in either chylomicrons or VLDL.

Indeed, that seems to be the case. The emerging evidence suggests that omega-3 fatty acids from fish oil reduce triglycerides through:

--Reduced VLDL production by the liver (Harris 1989)
--Accelerating chylomicron and VLDL elimination from the blood
--Activation of peroxisome proliferator-activated receptor gamma (PPAR-gamma)--Omega-3s ramp up the cellular equipment used to convert fatty acids to energy (oxidation) (Gani 2008)

Combine omega-3 fatty acids from fish oil with wheat elimination and you have an extremely potent means of reducing triglycerides. Read a previous Heart Scan Blog post here to read how a patient reduced triglycerides 93.5% from 3100 mg/dl to 210 mg/dl in just a few weeks using fish oil and wheat elimination.

Fish oil makes you happy: Psychological distress and omega-3 index

For another perspective on omega-3 blood levels, here's an interesting study in northern Quebec Inuits.

Traditionally, Inuits consumed large quantities of omega-3-rich seal, fish, caribou, and whale, even eating the fat. However, like the rest of the world, modern Inuits have increased consumption of store-bought foods, largely processed carbohydrates. Along with this trend has emerged more heart disease, diabetes, and depression.

A group from Laval University and University of Guelph, both in Canada, examined the relationship of plasma EPA + DHA levels and measures of psychological distress. This group had previously shown that Inuits older than 50 years had twice the plasma omega-3 levels (11.5%) compared to those younger than 50 years (6.5%), reflecting the shift away from the traditional diet.

Psychological distress was measured with The Psychological Distress Index Santé-Québec Survey (PDISQS-14): the higher the score, the greater the psychological distress. (In the graphs, tertile 1 is least distressed; tertile 5 is most distressed. Sorry about the small chart graphic--click on the graphic to make it bigger.)


From Lucas M et al 2009 (http://www.nutrasource.ca/NDI/Assets/Articles/Plasma%20omega-3%20and%20psychological%20distress%20among%20Nunavik%20Inuit.pdf)

"Our main finding was that women in the second and third tertiles of EPA+DHA concentrations in plasma PLs [phospholipids] had a 3 times lower risk of having a high-level PD [psychological distress] score than women in the lowest tertile."

While the relationship is stronger for women, you can see that, the higher the EPA + DHA plasma level, the lower the likelihood of psychological distress. Interestingly, the tertile with the greatest distress and lowest EPA + DHA levels had a plasma level of 7.0-7.5%--far higher than average Americans.

(Plasma levels of EPA + DHA were used in this study, which tend to reflect more recent omega-3 intake than the more stable and slower-to-change RBC Omega-3 Index that we use. Plasma levels also tend to run about 10-20% lower than RBC levels.)

Of course, there's more to psychological distress than omega-3 blood levels. After all, eating fish or taking fish oil capsules won't make money worries go away or heal an unhappy marriage. But it is one variable that can be easily and safely remedied.

Hospitals are a hell of a place to get sick

I answered a page from a hospital nurse recently one evening while having dinner with the family.

RN: "This is Lonnie. I'm a nurse at _____ Hospital. I've got one of your patients here, Mrs. Carole Simpson. She's here for a knee replacement with Dr. Johnson. She says she's taking 12,000 units of vitamin D every day. That can't be right! So I'm calling to verify."

WD: "That's right. We gauge patients' vitamin D needs by blood levels of vitamin D. Carole has had perfect levels of vitamin D on that dose."

RN: "The pharmacist says he can replace it with a 50,000 unit tablet."

WD: "Well, go ahead while Carole's in the hospital. I'll just put her back on the real stuff when she leaves."

RN: "But the pharmacist says this is better and she won't have to take so many capsules. She takes six 2,000 unit capsules a day."

WD: "The 50,000 units you and the pharmacist are talking about is vitamin D2, or ergocalciferol, a non-human form. Carole is taking vitamin D3, or cholecalciferol, the human form. The last time I checked, Carole was human."

RN: (Long pause.) Can we just give her the 50,000 unit tablet?

WD: "Yes, you can. But you actually don't need to. In fact, it probably won't hurt anything to just hold the vitamin D altogether for the 3 days she's in the hospital, since the half-life of vitamin D is about 8 weeks. Her blood level will barely change by just holding it for 3 days, then resuming when she's discharged."

RN: (Another long pause.) Uh, okay. Can we just give her the 50,000 units?"

WD: "Yes, you can. No harm will be done. It's simply a less effective form. To be honest, once Carole leaves the hospital, I will just put her back on the vitamin D that she was taking."

RN: "Dr. Johnson was worried that it might make her bleed during surgery. Shouldn't we just stop it?"

WD: "No. Vitamin D has no effect on blood coagulation. So there's no concern about perioperative bleeding."

RN: "The pharmacist said the 50,000 unit tablet was better, also, because it's the prescription form, not an over-the-counter form."

WD: "I can only tell you that Carole has had perfect blood levels on the over-the-counter preparation she was taking. It works just fine."

RN: "Okay. I guess we''ll just give her the 50,000 unit tablet."


From the alarm it raises trying to administer nutritional supplements in a hospital, you'd think that Osama Bin Laden had been spotted on the premises.

I laugh about this every time it happens: A patient gets hospitalized for whatever reason and the hospital staff see the supplement list with vitamin D, fish oil at high doses, iodine, etc. and they panic. They tell the patient about bleeding, cancer, and death, issue stern warnings about how unreliable and dangerous nutritional supplements can be.

My view is the exact opposite: Nutritional supplements are a wonderful, incredibly varied, and effective array of substances that, when used properly, can provide all manner of benefits. While there are selected instances in which nutritional supplements do, indeed, have interactions with treatments provided in hospitals (e.g., Valerian root and general anesthesia), the vast majority of supplements have none.

Does fish oil cause blood thinning?

Omega-3 fatty acids from fish oil have the capacity to "thin the blood." In reality, omega-3s exert a mild platelet-blocking effect (platelet activation and "clumping" are part of clot formation), while also inhibiting arachidonic acid formation and thromboxane.

But can fish oil cause excessive bleeding?

This question comes up frequently in the office, particularly when my colleagues see the doses of fish oil we use for cardiovascular protection. "Why so much fish oil? That's too much blood thinning!"

The most recent addition to the conversation comes from a Philadelphia experience reported in the American Journal of Cardiology:

Comparison of bleeding complications with omega-3 fatty acids + aspirin + clopidogrel--versus--aspirin + clopidogrel in patients with cardiovascular disease.(Watson et al; Am J Cardiol 2009 Oct 15;104(8):1052-4).

All 364 subjects in the study took aspirin and Plavix (a platelet-inhibiting drug), mostly for coronary disease. Mean dose aspirin = 161 mg/day; mean dose Plavix = 75 mg/day. 182 of the subjects were also taking fish oil, mean dose 3000 mg with unspecified omega-3 content.

During nearly 3 years of observation, there was no excess of bleeding events in the group taking fish oil. (In fact, the group not taking fish oil had more bleeding events, though the difference fell short of achieving statistical significance.) Thus, 3000 mg per day of fish oil appeared to exert no observable increase in risk for bleeding. This is consistent with several other studies, including that including Coumadin (warfarin), with no increased bleeding risk when fish oil is added.

Rather than causing blood thinning, I prefer to think that omega-3 fatty acids from fish oil restore protection from abnormal clotting. Taking omega-3 fatty acids from fish oil simply restores a normal level of omega-3 fatty acids in the blood sufficient to strike a healthy balance between blood "thinning" and healthy blood clotting.

Heart Scan Blog readers take impressive doses of omega-3s

Here are the results from the latest Heart Scan Blog poll:

What is your dose of omega-3 fatty acids, EPA + DHA, from fish oil? (Add up the total content of EPA + DHA per capsules; multiply times number of capsules.)

The 479 respondents answered:

Less than 1000 mg per day
65 (13%)

1000-1999 mg per day
145 (30%)

2000-2999 mg per day
98 (20%)

3000-3999 mg per day
79 (16%)

4000-4999 mg per day
33 (6%)

5000-5999 mg per day
14 (2%)

6000 mg per day or more
45 (9%)


The poll did not discriminate between who has heart disease, who does not; who is taking omega-3 fatty acids for high triglycerides or for reduction of lipoprotein(a) (which requires high doses), or other indications. So variation is to be expected.

We can say that nearly all respondents are likely receiving sufficient omega-3s to impact cardiovascular risk, since the benefits begin just by consuming fish twice per month. I am especially impressed at the proportion of respondents (53%) who take at least 2000 mg per day of EPA + DHA. It's clear that people are really embracing the notion that omega-3 fatty acids pack a real wallop of health benefits.

Because different people in different situations and lipid/lipoprotein patterns have different omega-3 needs, there is really no "right" or "wrong" dose of omega-3 fatty acids.

However, there are several factors that enter into knowing your ideal omega-3 intake:

--Higher triglycerides require higher doses
--Lipoprotein(a) can respond to higher doses
--Having coronary or carotid plaque means you desire a "therapeutic" dose of omega-3s, not just a "preventive" dose

Time is a factor, also: The longer you take omega-3s, the higher your blood levels go. You can accelerate the replacement of non-omega-3s with higher doses of omega-3s.

But too much is not good either. Some participants in Track Your Plaque, for instance, have experimented with very high doses of EPA + DHA in the 9000-10,000 per day range and witnessed dramatic increases in LDL.

Much of the uncertainty about dosing will also be cleared up as we get more experience with the Omega-3 RBC Index, i.e, the proportion of fatty acids in red blood cells that are omega-3s. We are currently aiming for an Omega-3 Index of 10%, given the heart attack reductions observed at this level.