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.
All posts by william-davis

Jogging does NOT cause heart disease


Periodically, I'll come across a knuckleheaded report like this one from Minneapolis:

Marathon Man’s Heart Damaged by Running?


Of course, the obligatory story about how a cardiologist came to the rescue and "saved his life" with a stent follows. In other words, a stent purportedly saved the life of this vigorous man with no symptoms and high capacity for exercise.

Does vigorous exercise, whether it's marathon running, long-distance biking, or triathlons, cause coronary disease? Should all vigorous athletes run to their doctor to see if they, too, need their lives to be "saved."

Let me tell you what's really going on here. People with the genetic pattern lipoprotein(a), or Lp(a), tend to be slender, intelligent and athletic. For genetic reasons, these people gravitate towards endurance sports like long-distance running. Lp(a) is a high-risk factor for coronary disease. It is the abnormality present in the majority of slender, healthy people who are shocked when they receive a high heart scan score or have a heart attack or receive a stent. (I call Lp(a) "the most aggressive known coronary risk factor that nobody's heard about.")

The association between endurance exercise and heart disease is just that: an association. It does not mean that exercise is causal. Having seen coronary plaque detected with heart scans in many runners, virtually all of whom demonstrated increased Lp(a), I believe that Lp(a) is causal.

Unfortunately, the man in the Minneapolis story, now that his life is "saved," will likely be advised to take a statin drug and follow a low-fat diet . . . you know, the diet that increases Lp(a).

Warning: Your pharmacist may be hazardous to your health

Pharmacists can be very helpful resources when it comes to questions about prescription drugs.

The operant word here is drugs.

What they are most definitely not expert on are nutritional supplements. In fact, a day doesn't pass by without having to dispell one falsehood or another conveyed to a patient about a nutritional supplement by a pharmacist.

Among the more common falsehoods told to patients by pharmacists:

"You have to take Niaspan. Sloniacin doesn't work."

Patent nonsense. A few years back, I was the largest prescriber of Niaspan in Wisconsin. Although I am embarassed to admit it, I also spoke for the company, educating fellow physicians on the value of niacin for correction of lipid disorders.

Then I shifted to Sloniacin due to cost--it costs 1/20th the cost of prescription Niaspan. I examined the pharmacokinetic data (pattern of release in the body), the published literature (e.g., the famous HATS Trial), and have used Sloniacin over 1000 times in patients. In my experience, there is no difference: no difference in efficacy, no difference in safety, no difference in side-effects. There is a BIG difference in price.

Unfortunately, most pharmacists get their information on niacin from the Niaspan representative.


"You shouldn't be taking vitamin D supplements. I have prescription vitamin D here."

What the pharmacist means is that you should replace your vitamin D3, or cholecalciferol--the form recognized as vitamin D by the human body--with the plant form of vitamin D, vitamin D2 or ergocalciferol.

Since when is a plant form of a hormone (vitamin D is a potent hormone, not a vitamin; it was misnamed) better than the human form?

I've previously talked about this issue in a blog post called Vitamin D for the pharmaceutically challenged.

The notion that D2 is somehow superior to the real thing, D3, is absurd. I use D3 only in my practice and have checked blood levels thousands of times. As long as the D3 comes as a gelcap, drops, or powder in a capsule, it works great, yielding predictable and substantial increases in blood levels of 25-hydroxy vitamin D. If it comes as prescription D2 (or over-the-counter D2), I have seen many failures: no increase in blood levels of vitamin D or meager increases.

Prescription status is no guarantee of effectiveness.


"Why do you need iodine? You already get enough from food."

The NHANES data over the last 25 years argue otherwise: Iodine deficiency is growing, particularly as people are avoiding iodized salt and the iodine content of processed foods is diminishing. The explosion in goiters in my office also suggest this is no longer a settled issue.

On the positive side, it is exceptionally easy to remedy with an inexpensive iodine supplement. That is, until the pharmacist intervenes and injects his bit of nutritional mis-information.


I'm not bashing pharmacists. In fact, Track Your Plaque's own Dr. BG has a pharmacy background, and she is an absolute genius with nutritonal supplements. But she is a rare exception to the rule: Most pharmacists know virtually nothing about nutritional supplements. You might as well ask your hairdresser.

"Healthy" people are the most iodine deficient

Ironically, the healthiest people are the most likely to be deficient in iodine.

Why?

Healthy people tend to:

--Avoid iodized salt because of public health advice to limit sodium
--Use sea salt to obtain minerals like magnesium--but sea salt contains little iodine
--Limit meat--Carnivores obtain more iodine than vegetarians or vegans. In one study, up to 80% of vegans were iodine-deficient (Krajcovicova-Kudlackova M et al 2003).
--Exercise--Substantial amounts of iodine are lost through sweating. In a study of high school soccer players, 38.5% were severely iodine deficient, compared to 2% of sedentary students (Mao IF et al 2001).


That is indeed what I am seeing in my office, as well: The healthiest, most attentive to healthy eating, and most physically active are the ones showing up with small goiters (enlarged thyroid glands) and increased TSH and low free T4 levels.

Why am I checking thyroid and talking about iodine? Because even the smallest degree of thyroid dysfunction can double, triple, or quadruple your risk for cardiovascular events. See the posts Is normal TSH too high? and Thyroid perspective update.

What kind of iodine do you take?

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

204 respondents answered the question:


Do you take an iodine supplement?

The responses:

Yes, I take Iodoral, Lugol's, or SSKI
26 (12%)

Yes, I take potassium or sodium iodide
19 (9%)

Yes, I take kelp tablets or powder
64 (31%)

No, I rely on generous use of iodized salt
23 (11%)

No, I don't supplement iodine at all
66 (32%)

Isn't iodine something you put on cuts and scratches?
6 (2%)


I am heartened by the number of respondents taking iodine in some form. After all, iodine is an essential trace mineral. Without it and health suffers, often dramatically.

However, I am concerned by the percentage of people who don't supplement iodine at all: 32%. Interestingly, this is approximately the proportion of people who come to my office who also do not supplement iodine who are now showing goiters, or enlarged thyroid glands due to iodine deficiency. Goiters lead to hypothyroidism (low thyroid hormone levels), followed by hyperactive nodules, not to mention undesirable effects like weight gain, fatigue, hair loss, constipation, intolerance to cold, higher LDL cholesterol and triglycerides, and heart disease.

11% of respondents report using lots of iodized salt. This may or may not be sufficient to provide enough iodine to prevent goiter and allow normal thyroid function. The success of this strategy depends to a great extent on how often salt is purchased. Salt that sits on the shelf for more than a month is devoid of iodine, given iodine's volatility.

I am also favorably impressed by the number of people who take "serious" iodine supplements like Lugol's solution, Iodoral, or SSKI. Of course, people who read The Heart Scan Blog tend to be an unusually informed, healthy population. The 12% of people in the poll who take these forms of iodine does clearly not mean that 12% of the general population also takes them. But 12% is more than I would have predicted.

On the Track Your Plaque website, we are awaiting an interview with iodine expert, Dr. Lyn Patrick. I'm hoping for some juicy insights.

And you thought gasoline was expensive

In 1995, the Palmaz coronary stent was introduced, the brainchild of Drs. Julio Palmaz and Richard Schatz. Medical device manufacturer, Johnson & Johnson, priced the device at $2500 per stent.

Let's put this into perspective: At just 0.05 grams per 15 millimeter stent, that put the price of the common stainless steel used to manufacture the stent at $22,650,000 per pound.

Only after several competing stents finally made it to market did J&J reduce its price to its bargain price of $1200, or $10,872,000 per pound. And to think that most of us were shocked to find out that the U.S. military paid $200 for a hammer.

Since 1995, a competitive market for stents has developed, pushing prices down. Now, you can purchase a brand-new coronary stent for as little as $4,000,000 per pound.

Medical device manufacturers have been guilty of a degree of greed that would make many Wall Street bankers blush. That's why I call medical devices "the industry of infinite markups."

"Hey buddy, wanna buy some exorphins?"

Dr. Christine Zioudrou and colleagues at the National Institutes of Mental Health got this conversation going back in 1979 with their paper, Opioid peptides derived from food proteins: The exorphins.

Exorphins are exogenously-derived peptides (i.e., short amino acid sequences obtained from outside the body) that exert morphine-like properties. Mimicking the digestive process that occurs in the gastrointestinal tract using the gastric enzyme, pepsin, and hydrochloric acid (stomach acid), Zioudrou et al isolated peptides from wheat gluten with morphine-like activity. They followed this research path because of the apparent association of wheat and mental illness.

In the bioassays used, wheat-derived exorphins competed successfully with the endogenous opiate, met-enkephalin. Interestingly, casein-derived (i.e., casein milk protein) exorphins were also identified that also displayed opiate-binding activity, though less powerfully. The morphine-like activity was also blocked by the drug, naloxone (the same stuff given to people exposed to morphine overdose).

Among the many devastating effects of celiac disease , the immune disease that develops from wheat gluten exposure, are mental and emotional effects, such as anxiety, fatigue, mental "fog," depression, bipolar illness, and schizophrenia, that disappear with removal of gluten. Many parents of autistic children also advocate wheat-free diets for similar reasons.

Among the many wonderful comments posted on the last Heart Scan Blog post, "I can't do it," was Anne's:

I am not the Anne in your post, but I was addicted to wheat. It was my favorite food. I lived on and for breads. Then I discovered I was gluten sensitive and I did go through a withdrawal of about 4 days. After 4 days I noticed my health problems were disappearing. Depression, brain fog and joint pain are 3 of the many symptoms that disappeared. That was 6 yrs ago.

Tell Anne that I had dreams about bread in the beginning - they will pass. Now the donuts, breads, cookies and cakes in the stores and at work don't even look good. In fact, I don't like the smell of bread anymore. It takes time, but the cravings do pass.



Combine wheat"s exorphin-driven addictive potential with its flagrant blood sugar-increasing properties, and you have a formula that:

1) makes you fat
2) increases likelihood of diabetes, and
3) makes you want to keep on doing it.

Reminds me of nicotine.

My personal view: I have absolutely no remaining doubt that wheat products have no place in the human diet. Not only does the research provide a plausible basis for its adverse health effects, but having asked hundreds of people to remove it from their habits has yielded consistent and remarkable health benefits. Just read the reader comments here and here.

"I can't do it"

Anne sat across from me, bent over and sobbing.

"I can't do it. I just can't do it! I cut out the breads and pasta for two days, then I start dreaming about it!

"And my husband is no help. He knows I'm trying to get off the wheat. But then he brings home a bunch of Danish or something. He knows I can't help myself!"

Having asked hundreds of people to completely remove wheat from their diet, I witness 30% of them go through such emotional and physical turmoil, not uncommonly to the point of tears. For about 10-20% of people who try, it is as hard as quitting cigarettes.

Make no mistake about it: For many people, wheat is addictive. It meets all the criteria for an addictive product: People crave it, consuming it creates a desire for more, lacking it triggers a withdrawal phenomenon. If wheat were illegal, there would surely be an active underground trafficking illicit bagels and pretzels.

Withdrawal consists of fatigue and mental fogginess that usually lasts 5-7 days. Just like quitting smoking, wheat withdrawal is harmless but no less profound in severity.

People who lack an addictive relationship with wheat usually have no idea what I'm talking about. To them, wheat is simply a grain, no different than oats.

But wheat addicts immediately know who they are. They are the ones who can't resist the warm dinner rolls served at the Italian restaurant, need to include something made of wheat at every meal, and crave it every 2 hours (matching the cycle of blood sugar peaks and valleys, the "valley" triggering the craving). When they stop the flow of immediately-released glucose that comes from wheat (with blood sugar peaks that occur higher and faster than table sugar), irresistible cravings kick in. Then watch out: They'll bite your hand off if you reach for that roll before they do.

Break the cycle and the body is confused: Where's the sugar? The body is accustomed to receiving a constant flow of easily-digested sugars.

Once the constant influx of sugars ceases, it takes 5-7 days for metabolism to shift towards fat mobilization as a source of energy. But along with fat mobilization comes a shrinking tummy, reducing the characteristic wheat belly.

If you try to quit smoking, you've got "crutches" like nicotine patches and gum, Zyban, Chantix, hypnosis, and group therapy sessions. If you try and quit wheat, what have you got? Nothing, to my knowledge. Nothing but sheer will power to divorce yourself from this enormously destructive, diabetes-causing, small LDL-increasing, inflammation-provoking, and addictive substance.

Spontaneous combustion, vampires, and goitrogens

What do the following have in common:

Lima beans
Flaxseed
Broccoli
Cabbage
Kale
Soy
Millet
Sorghum?

They are all classified as goitrogens, or foods that have been shown to trigger goiter, or thyroid gland enlargement. Most of them do this either by blocking iodine uptake in the thyroid gland or by blocking the enzyme, thyroid peroxidase. This effect can lead to reduction in thyroid hormone output by the thyroid gland, which then triggers increased thyroid stimulating hormone (TSH) by the pituitary; increased TSH acts as a growth factor on the thyroid, thus goiter.

Add to this list of goitrogens the flavonoid, quercertin, found in abundance in red wine, grapes, apples, capers, tomatoes, cherries, raspberries, teas, and onions. Most of us obtain around 30 mg per day from our diet. Quercetin, often touted as a healthy flavonoid alongside resveratrol (e.g., Yang JY et al 2008), has been shown to be associated with reduced risk for heart disease and cancer. Many people even take quercetin as a nutritional supplement.

Quercetin has also been identified as a goitrogen (Giuliani C et al 2008).

What to make of all this?

Most of these observations have been made in in vitro ("test tube") preparations or in mice. Rabbits who consume a cabbage-only diet can develop goiter.

How about humans? The few trials conducted in humans have shown little or no effect. In most instances, the adverse effects of goitrogens have been eliminated with supplemental iodine. In other words, goitrogens seem to exert their ill thyroid effects when iodine deficiency is present. Restore iodine . . . no more goitrogens (with rare exceptions).

Should we as humans adopt a diet that avoids apples, grapes, tomatoes, red wine, tea, onions, soy etc. on the small chance that we will develop goiter?

I believe that we should avoid these common food-sourced goitrogens with as much enthusiasm as we should be worried about spontaneous combustion of humans or the appearance of vampires on our front porches. We are as likely to suffer low thyroid activity from quercetin or other "goitrogens" as we are to experience the "mitochondrial explosions" that are purported to set innocent people afire.

Magnesium and you-Part II

Blood magnesium levels are a poor barometer for true body (intracellular) magnesium.

Only 1% of the body’s magnesium is in the blood, the remaining 99% stored in various body tissues, particularly bone and muscle. If blood magnesium is low, cellular magnesium levels are indeed low—very low.

If blood magnesium is normal, cellular or tissue levels of magnesium may still be low. Unfortunately, tissue magnesium levels are not easy to obtain in living, breathing humans. In all practicality, a blood magnesium test only helps if it’s low, while normal levels don’t necessarily mean anything and may provide false reassurance.

Short of performing a biopsy to measure tissue magnesium levels, several signs provide a tip-off that magnesium may be low:

• Heart arrhythmias—Having any sort of heart rhythm disorder should cause you to question whether magnesium levels in your body are adequate, since low magnesium levels trigger abnormal heart rhythms. In fact, in the hospital we give intravenous magnesium to quiet down abnormal rhythms.
• Low potassium— Low magnesium commonly accompanies low potassium. Potassium is another electrolyte depleted by diuretic use and is commonly deficient in many conditions (e.g., excessive alcohol use, hypertension, loss from malabsorption or diarrhea). Like magnesium, potassium may not be fully replenished by modern diets.
• Muscle cramps— Magnesium regulates muscle contraction. Leg cramps, or “charlie-horses”, painful vise-like cramps in calves, fingers, or other muscles, are a common symptom of magnesium deficiency. (Leg cramps that occur with physical activity, such as walking, are usually due to atherosclerotic blockages in the leg or abdominal arteries, not low magnesium.)
• Migraine headaches—Reflective of magnesium’s role in regulating blood vessel tone, low magnesium can trigger vascular spasm in the blood vessels of the brain. In some emergency rooms, they will actually administer intravenous magnesium to break a migraine.
• Metabolic syndrome—Magnesium plays a fundamental role in regulating insulin responses. Metabolic syndrome (low HDL, high triglycerides, small LDL, high blood pressure, increased blood sugar, excessive abdominal fat, etc.) is triggered by insulin responses gone awry and is clearly linked to low magnesium levels.

The absence of any of these tell-tale signs does not necessarily mean that tissue levels of magnesium are normal.

Then how do you really know? There really is no easy, available method to gauge body magnesium. As a practical solution, we therefore have aimed for maintaining serum levels of >2.1 mg/dl or RBC magnesium (a surrogate for tissue levels) of >6.0 mg/dl. (Going too high is not good either, so occasional monitoring really helps. However, I've only seen this once in a psychotic woman who drank ungodly amounts of magnesium-containing antacids for no apparent reason; she almost ended up on a respirator due to respiratory suppression by the magnesium level of 11 mg/dl!)

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water, supplemental magnesium is necessary for nearly everyone to ensure healthy levels.

More on magnesium to come.

Lethal Lipids II

I call the combination of low HDL, small LDL, and lipoprotein(a) "lethal lipids," since the trio is an exceptionally potent predictor for heart disease. Uncorrected, the combination is a virtual guarantee of heart disease.

Ed is a perfect example of someone who came to my office recently with this pattern. His starting values:

HDL: 34 mg/dl

Small LDL: 78% of total LDL
NMR: Small LDL 1655 nmol/L; total LDL particle number 2122 nmol/L)

Lipoprotein(a): 205 nmol/L



The atherogenicity, or plaque-causing potential, of this pattern was reflected in Ed's heart scan score of 2133.

You can readily see that, of this combination, only HDL cholesterol would be adequately identified through conventional lipid testing. Small LDL and lipoprotein(a) need to be specifically measured via lipoprotein testing.

And, contrary to the drug industry's "statin drugs for everybody" motto, this pattern, while improved with statin therapy, is not shut off.

Specific correction of each abnormality is required. For instance, niacin addresses all three: increases HDL, reduces small LDL, and (usually) reduces lipoprotein(a). A standard low-fat diet makes this pattern worse by reducing HDL, increasing small LDL, and (usually) increasing lipoprotein(a).
All posts by william-davis

Jogging does NOT cause heart disease


Periodically, I'll come across a knuckleheaded report like this one from Minneapolis:

Marathon Man’s Heart Damaged by Running?


Of course, the obligatory story about how a cardiologist came to the rescue and "saved his life" with a stent follows. In other words, a stent purportedly saved the life of this vigorous man with no symptoms and high capacity for exercise.

Does vigorous exercise, whether it's marathon running, long-distance biking, or triathlons, cause coronary disease? Should all vigorous athletes run to their doctor to see if they, too, need their lives to be "saved."

Let me tell you what's really going on here. People with the genetic pattern lipoprotein(a), or Lp(a), tend to be slender, intelligent and athletic. For genetic reasons, these people gravitate towards endurance sports like long-distance running. Lp(a) is a high-risk factor for coronary disease. It is the abnormality present in the majority of slender, healthy people who are shocked when they receive a high heart scan score or have a heart attack or receive a stent. (I call Lp(a) "the most aggressive known coronary risk factor that nobody's heard about.")

The association between endurance exercise and heart disease is just that: an association. It does not mean that exercise is causal. Having seen coronary plaque detected with heart scans in many runners, virtually all of whom demonstrated increased Lp(a), I believe that Lp(a) is causal.

Unfortunately, the man in the Minneapolis story, now that his life is "saved," will likely be advised to take a statin drug and follow a low-fat diet . . . you know, the diet that increases Lp(a).

Warning: Your pharmacist may be hazardous to your health

Pharmacists can be very helpful resources when it comes to questions about prescription drugs.

The operant word here is drugs.

What they are most definitely not expert on are nutritional supplements. In fact, a day doesn't pass by without having to dispell one falsehood or another conveyed to a patient about a nutritional supplement by a pharmacist.

Among the more common falsehoods told to patients by pharmacists:

"You have to take Niaspan. Sloniacin doesn't work."

Patent nonsense. A few years back, I was the largest prescriber of Niaspan in Wisconsin. Although I am embarassed to admit it, I also spoke for the company, educating fellow physicians on the value of niacin for correction of lipid disorders.

Then I shifted to Sloniacin due to cost--it costs 1/20th the cost of prescription Niaspan. I examined the pharmacokinetic data (pattern of release in the body), the published literature (e.g., the famous HATS Trial), and have used Sloniacin over 1000 times in patients. In my experience, there is no difference: no difference in efficacy, no difference in safety, no difference in side-effects. There is a BIG difference in price.

Unfortunately, most pharmacists get their information on niacin from the Niaspan representative.


"You shouldn't be taking vitamin D supplements. I have prescription vitamin D here."

What the pharmacist means is that you should replace your vitamin D3, or cholecalciferol--the form recognized as vitamin D by the human body--with the plant form of vitamin D, vitamin D2 or ergocalciferol.

Since when is a plant form of a hormone (vitamin D is a potent hormone, not a vitamin; it was misnamed) better than the human form?

I've previously talked about this issue in a blog post called Vitamin D for the pharmaceutically challenged.

The notion that D2 is somehow superior to the real thing, D3, is absurd. I use D3 only in my practice and have checked blood levels thousands of times. As long as the D3 comes as a gelcap, drops, or powder in a capsule, it works great, yielding predictable and substantial increases in blood levels of 25-hydroxy vitamin D. If it comes as prescription D2 (or over-the-counter D2), I have seen many failures: no increase in blood levels of vitamin D or meager increases.

Prescription status is no guarantee of effectiveness.


"Why do you need iodine? You already get enough from food."

The NHANES data over the last 25 years argue otherwise: Iodine deficiency is growing, particularly as people are avoiding iodized salt and the iodine content of processed foods is diminishing. The explosion in goiters in my office also suggest this is no longer a settled issue.

On the positive side, it is exceptionally easy to remedy with an inexpensive iodine supplement. That is, until the pharmacist intervenes and injects his bit of nutritional mis-information.


I'm not bashing pharmacists. In fact, Track Your Plaque's own Dr. BG has a pharmacy background, and she is an absolute genius with nutritonal supplements. But she is a rare exception to the rule: Most pharmacists know virtually nothing about nutritional supplements. You might as well ask your hairdresser.

"Healthy" people are the most iodine deficient

Ironically, the healthiest people are the most likely to be deficient in iodine.

Why?

Healthy people tend to:

--Avoid iodized salt because of public health advice to limit sodium
--Use sea salt to obtain minerals like magnesium--but sea salt contains little iodine
--Limit meat--Carnivores obtain more iodine than vegetarians or vegans. In one study, up to 80% of vegans were iodine-deficient (Krajcovicova-Kudlackova M et al 2003).
--Exercise--Substantial amounts of iodine are lost through sweating. In a study of high school soccer players, 38.5% were severely iodine deficient, compared to 2% of sedentary students (Mao IF et al 2001).


That is indeed what I am seeing in my office, as well: The healthiest, most attentive to healthy eating, and most physically active are the ones showing up with small goiters (enlarged thyroid glands) and increased TSH and low free T4 levels.

Why am I checking thyroid and talking about iodine? Because even the smallest degree of thyroid dysfunction can double, triple, or quadruple your risk for cardiovascular events. See the posts Is normal TSH too high? and Thyroid perspective update.

What kind of iodine do you take?

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

204 respondents answered the question:


Do you take an iodine supplement?

The responses:

Yes, I take Iodoral, Lugol's, or SSKI
26 (12%)

Yes, I take potassium or sodium iodide
19 (9%)

Yes, I take kelp tablets or powder
64 (31%)

No, I rely on generous use of iodized salt
23 (11%)

No, I don't supplement iodine at all
66 (32%)

Isn't iodine something you put on cuts and scratches?
6 (2%)


I am heartened by the number of respondents taking iodine in some form. After all, iodine is an essential trace mineral. Without it and health suffers, often dramatically.

However, I am concerned by the percentage of people who don't supplement iodine at all: 32%. Interestingly, this is approximately the proportion of people who come to my office who also do not supplement iodine who are now showing goiters, or enlarged thyroid glands due to iodine deficiency. Goiters lead to hypothyroidism (low thyroid hormone levels), followed by hyperactive nodules, not to mention undesirable effects like weight gain, fatigue, hair loss, constipation, intolerance to cold, higher LDL cholesterol and triglycerides, and heart disease.

11% of respondents report using lots of iodized salt. This may or may not be sufficient to provide enough iodine to prevent goiter and allow normal thyroid function. The success of this strategy depends to a great extent on how often salt is purchased. Salt that sits on the shelf for more than a month is devoid of iodine, given iodine's volatility.

I am also favorably impressed by the number of people who take "serious" iodine supplements like Lugol's solution, Iodoral, or SSKI. Of course, people who read The Heart Scan Blog tend to be an unusually informed, healthy population. The 12% of people in the poll who take these forms of iodine does clearly not mean that 12% of the general population also takes them. But 12% is more than I would have predicted.

On the Track Your Plaque website, we are awaiting an interview with iodine expert, Dr. Lyn Patrick. I'm hoping for some juicy insights.

And you thought gasoline was expensive

In 1995, the Palmaz coronary stent was introduced, the brainchild of Drs. Julio Palmaz and Richard Schatz. Medical device manufacturer, Johnson & Johnson, priced the device at $2500 per stent.

Let's put this into perspective: At just 0.05 grams per 15 millimeter stent, that put the price of the common stainless steel used to manufacture the stent at $22,650,000 per pound.

Only after several competing stents finally made it to market did J&J reduce its price to its bargain price of $1200, or $10,872,000 per pound. And to think that most of us were shocked to find out that the U.S. military paid $200 for a hammer.

Since 1995, a competitive market for stents has developed, pushing prices down. Now, you can purchase a brand-new coronary stent for as little as $4,000,000 per pound.

Medical device manufacturers have been guilty of a degree of greed that would make many Wall Street bankers blush. That's why I call medical devices "the industry of infinite markups."

"Hey buddy, wanna buy some exorphins?"

Dr. Christine Zioudrou and colleagues at the National Institutes of Mental Health got this conversation going back in 1979 with their paper, Opioid peptides derived from food proteins: The exorphins.

Exorphins are exogenously-derived peptides (i.e., short amino acid sequences obtained from outside the body) that exert morphine-like properties. Mimicking the digestive process that occurs in the gastrointestinal tract using the gastric enzyme, pepsin, and hydrochloric acid (stomach acid), Zioudrou et al isolated peptides from wheat gluten with morphine-like activity. They followed this research path because of the apparent association of wheat and mental illness.

In the bioassays used, wheat-derived exorphins competed successfully with the endogenous opiate, met-enkephalin. Interestingly, casein-derived (i.e., casein milk protein) exorphins were also identified that also displayed opiate-binding activity, though less powerfully. The morphine-like activity was also blocked by the drug, naloxone (the same stuff given to people exposed to morphine overdose).

Among the many devastating effects of celiac disease , the immune disease that develops from wheat gluten exposure, are mental and emotional effects, such as anxiety, fatigue, mental "fog," depression, bipolar illness, and schizophrenia, that disappear with removal of gluten. Many parents of autistic children also advocate wheat-free diets for similar reasons.

Among the many wonderful comments posted on the last Heart Scan Blog post, "I can't do it," was Anne's:

I am not the Anne in your post, but I was addicted to wheat. It was my favorite food. I lived on and for breads. Then I discovered I was gluten sensitive and I did go through a withdrawal of about 4 days. After 4 days I noticed my health problems were disappearing. Depression, brain fog and joint pain are 3 of the many symptoms that disappeared. That was 6 yrs ago.

Tell Anne that I had dreams about bread in the beginning - they will pass. Now the donuts, breads, cookies and cakes in the stores and at work don't even look good. In fact, I don't like the smell of bread anymore. It takes time, but the cravings do pass.



Combine wheat"s exorphin-driven addictive potential with its flagrant blood sugar-increasing properties, and you have a formula that:

1) makes you fat
2) increases likelihood of diabetes, and
3) makes you want to keep on doing it.

Reminds me of nicotine.

My personal view: I have absolutely no remaining doubt that wheat products have no place in the human diet. Not only does the research provide a plausible basis for its adverse health effects, but having asked hundreds of people to remove it from their habits has yielded consistent and remarkable health benefits. Just read the reader comments here and here.

"I can't do it"

Anne sat across from me, bent over and sobbing.

"I can't do it. I just can't do it! I cut out the breads and pasta for two days, then I start dreaming about it!

"And my husband is no help. He knows I'm trying to get off the wheat. But then he brings home a bunch of Danish or something. He knows I can't help myself!"

Having asked hundreds of people to completely remove wheat from their diet, I witness 30% of them go through such emotional and physical turmoil, not uncommonly to the point of tears. For about 10-20% of people who try, it is as hard as quitting cigarettes.

Make no mistake about it: For many people, wheat is addictive. It meets all the criteria for an addictive product: People crave it, consuming it creates a desire for more, lacking it triggers a withdrawal phenomenon. If wheat were illegal, there would surely be an active underground trafficking illicit bagels and pretzels.

Withdrawal consists of fatigue and mental fogginess that usually lasts 5-7 days. Just like quitting smoking, wheat withdrawal is harmless but no less profound in severity.

People who lack an addictive relationship with wheat usually have no idea what I'm talking about. To them, wheat is simply a grain, no different than oats.

But wheat addicts immediately know who they are. They are the ones who can't resist the warm dinner rolls served at the Italian restaurant, need to include something made of wheat at every meal, and crave it every 2 hours (matching the cycle of blood sugar peaks and valleys, the "valley" triggering the craving). When they stop the flow of immediately-released glucose that comes from wheat (with blood sugar peaks that occur higher and faster than table sugar), irresistible cravings kick in. Then watch out: They'll bite your hand off if you reach for that roll before they do.

Break the cycle and the body is confused: Where's the sugar? The body is accustomed to receiving a constant flow of easily-digested sugars.

Once the constant influx of sugars ceases, it takes 5-7 days for metabolism to shift towards fat mobilization as a source of energy. But along with fat mobilization comes a shrinking tummy, reducing the characteristic wheat belly.

If you try to quit smoking, you've got "crutches" like nicotine patches and gum, Zyban, Chantix, hypnosis, and group therapy sessions. If you try and quit wheat, what have you got? Nothing, to my knowledge. Nothing but sheer will power to divorce yourself from this enormously destructive, diabetes-causing, small LDL-increasing, inflammation-provoking, and addictive substance.

Spontaneous combustion, vampires, and goitrogens

What do the following have in common:

Lima beans
Flaxseed
Broccoli
Cabbage
Kale
Soy
Millet
Sorghum?

They are all classified as goitrogens, or foods that have been shown to trigger goiter, or thyroid gland enlargement. Most of them do this either by blocking iodine uptake in the thyroid gland or by blocking the enzyme, thyroid peroxidase. This effect can lead to reduction in thyroid hormone output by the thyroid gland, which then triggers increased thyroid stimulating hormone (TSH) by the pituitary; increased TSH acts as a growth factor on the thyroid, thus goiter.

Add to this list of goitrogens the flavonoid, quercertin, found in abundance in red wine, grapes, apples, capers, tomatoes, cherries, raspberries, teas, and onions. Most of us obtain around 30 mg per day from our diet. Quercetin, often touted as a healthy flavonoid alongside resveratrol (e.g., Yang JY et al 2008), has been shown to be associated with reduced risk for heart disease and cancer. Many people even take quercetin as a nutritional supplement.

Quercetin has also been identified as a goitrogen (Giuliani C et al 2008).

What to make of all this?

Most of these observations have been made in in vitro ("test tube") preparations or in mice. Rabbits who consume a cabbage-only diet can develop goiter.

How about humans? The few trials conducted in humans have shown little or no effect. In most instances, the adverse effects of goitrogens have been eliminated with supplemental iodine. In other words, goitrogens seem to exert their ill thyroid effects when iodine deficiency is present. Restore iodine . . . no more goitrogens (with rare exceptions).

Should we as humans adopt a diet that avoids apples, grapes, tomatoes, red wine, tea, onions, soy etc. on the small chance that we will develop goiter?

I believe that we should avoid these common food-sourced goitrogens with as much enthusiasm as we should be worried about spontaneous combustion of humans or the appearance of vampires on our front porches. We are as likely to suffer low thyroid activity from quercetin or other "goitrogens" as we are to experience the "mitochondrial explosions" that are purported to set innocent people afire.

Magnesium and you-Part II

Blood magnesium levels are a poor barometer for true body (intracellular) magnesium.

Only 1% of the body’s magnesium is in the blood, the remaining 99% stored in various body tissues, particularly bone and muscle. If blood magnesium is low, cellular magnesium levels are indeed low—very low.

If blood magnesium is normal, cellular or tissue levels of magnesium may still be low. Unfortunately, tissue magnesium levels are not easy to obtain in living, breathing humans. In all practicality, a blood magnesium test only helps if it’s low, while normal levels don’t necessarily mean anything and may provide false reassurance.

Short of performing a biopsy to measure tissue magnesium levels, several signs provide a tip-off that magnesium may be low:

• Heart arrhythmias—Having any sort of heart rhythm disorder should cause you to question whether magnesium levels in your body are adequate, since low magnesium levels trigger abnormal heart rhythms. In fact, in the hospital we give intravenous magnesium to quiet down abnormal rhythms.
• Low potassium— Low magnesium commonly accompanies low potassium. Potassium is another electrolyte depleted by diuretic use and is commonly deficient in many conditions (e.g., excessive alcohol use, hypertension, loss from malabsorption or diarrhea). Like magnesium, potassium may not be fully replenished by modern diets.
• Muscle cramps— Magnesium regulates muscle contraction. Leg cramps, or “charlie-horses”, painful vise-like cramps in calves, fingers, or other muscles, are a common symptom of magnesium deficiency. (Leg cramps that occur with physical activity, such as walking, are usually due to atherosclerotic blockages in the leg or abdominal arteries, not low magnesium.)
• Migraine headaches—Reflective of magnesium’s role in regulating blood vessel tone, low magnesium can trigger vascular spasm in the blood vessels of the brain. In some emergency rooms, they will actually administer intravenous magnesium to break a migraine.
• Metabolic syndrome—Magnesium plays a fundamental role in regulating insulin responses. Metabolic syndrome (low HDL, high triglycerides, small LDL, high blood pressure, increased blood sugar, excessive abdominal fat, etc.) is triggered by insulin responses gone awry and is clearly linked to low magnesium levels.

The absence of any of these tell-tale signs does not necessarily mean that tissue levels of magnesium are normal.

Then how do you really know? There really is no easy, available method to gauge body magnesium. As a practical solution, we therefore have aimed for maintaining serum levels of >2.1 mg/dl or RBC magnesium (a surrogate for tissue levels) of >6.0 mg/dl. (Going too high is not good either, so occasional monitoring really helps. However, I've only seen this once in a psychotic woman who drank ungodly amounts of magnesium-containing antacids for no apparent reason; she almost ended up on a respirator due to respiratory suppression by the magnesium level of 11 mg/dl!)

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water, supplemental magnesium is necessary for nearly everyone to ensure healthy levels.

More on magnesium to come.

Lethal Lipids II

I call the combination of low HDL, small LDL, and lipoprotein(a) "lethal lipids," since the trio is an exceptionally potent predictor for heart disease. Uncorrected, the combination is a virtual guarantee of heart disease.

Ed is a perfect example of someone who came to my office recently with this pattern. His starting values:

HDL: 34 mg/dl

Small LDL: 78% of total LDL
NMR: Small LDL 1655 nmol/L; total LDL particle number 2122 nmol/L)

Lipoprotein(a): 205 nmol/L



The atherogenicity, or plaque-causing potential, of this pattern was reflected in Ed's heart scan score of 2133.

You can readily see that, of this combination, only HDL cholesterol would be adequately identified through conventional lipid testing. Small LDL and lipoprotein(a) need to be specifically measured via lipoprotein testing.

And, contrary to the drug industry's "statin drugs for everybody" motto, this pattern, while improved with statin therapy, is not shut off.

Specific correction of each abnormality is required. For instance, niacin addresses all three: increases HDL, reduces small LDL, and (usually) reduces lipoprotein(a). A standard low-fat diet makes this pattern worse by reducing HDL, increasing small LDL, and (usually) increasing lipoprotein(a).
All posts by william-davis

What if your lipoproteins are perfect?



Sandy is a 56-year old woman--fit, slender, physically active, with no bad habits. A retired teacher, she has time to devote to her health. She bikes several days per week, mountain bikes, walks, and takes fitness classes. In short, she's the picture of perfect health.

Her heart scan score was not terribly impressive: 41. However, at her age, this modest score placed her in the 77th percentile. This suggested a heart attack risk of around 2-3% per year.

So we measured Sandy's lipoproteins. They were shockingly normal. In fact, Sandy is among the very rare person with absolutely no small LDL particles. All other patterns were just as favorable, including an HDL in the 80s.

This may seem like good news, but I find it disturbing. People are often initially upset by seeing multiple abnormal lipoprotein patterns. But lipoprotein abnormalities are the tools that we use to gain control over coronary plaque.

So what do we do when there are no abnormalities?

There are several issues to consider:

1) Your heart scan score reflects the sum total of your life up until that point. What if you were 20 lbs heavier 10 years earlier and your lipoproteins were abnormal during that period? Or you smoked until age 45 and quit? As helpful as they are, lipoproteins and related patterns are only a snapshot in time, unlike the heart scan score.

2) You have a vitamin D deficiency. This is unusual as a sole cause of coronary plaque. Much more commonly, it is a co-conspirator.

3) The heart scan is wrong--highly unlikely. Heart scans are actually quite easy, straightforward tests. (The only time this tends to happen is when scoring that appears in the circumflex coronary artery is actually in the nearby mitral valve. This really occurs only when there's very minimal calcium in the valve.)

4) There's a yet unidentified source of risk. Probably very rare but conceivable. For instance, there's an emerging sense that phopholipid patterns may prove to be coronary risks. One clinically available measure that we've not found very useful is phospholipase A2, known by the proprietary name "PLAC" test. (See http://www.plactest.com for more information from the manufacturer/distributor of the test.) But there's probably lots of others that may prove useful in future.

How often does it happen that someone fails to show any identifiable source for their coronary plaque? I can count the number of instances on two fingers--very unusual. (Thank goodness!)

Sandy's case is therefore quite unique. How should we approach her coronary plaque? In this unusual circumstance, lacking a cause, we tend to introduce therapies that may regress plaque independent of any measurable lipoprotein parameters. But that's a whole new conversation.

Fly to India for a bypass operation?


In the June 19, 2006 issue of People Magazine, there's an article called "The Doctor is in . . .INDIA". The report talks about how, with health care costs in the U.S. spiralling out of control, more and more Americans are leaving the country to have their procedure performed.

They tell the story of Mr. Carlo Gislimberti of New Mexico and cite these numbers:

Heart Surgery
Cost in U.S.: $200,000

Cost in India: $10,000


Mr. Gislimberti opted to have his coronary bypass operation in India for cost reasons.

But the People magazine report left out one other option: The Track Your Plaque program: $39.00

Do your part to save ballooning health care costs: Engage in a truly powerful program of heart disease prevention like the Track Your Plaque program. The cost difference is laughably huge. And you won't require a 12-inch chest incision.

Follow conventional guidelines and guess what? You're going to have a heart attack. Follow the American Heart Association diet and you'll have heart disease.

Cut to the chase. The only program that is able to detect, track, and control coronary plaque better than any other process I know of is this program.

Note: I am not proposing that a heart disease prevention program like Track Your Plaque can replace a procedure like coronary bypass when a dangerous situation has developed. The Track Your Plaque program is designed to be implemented in the years before heart surgery is required. That's when you have the greatest control over your fate.

Surprise: Heart scan score reversal

Gene is a jovial, fun-loving railroad worker who didn't take anything too seriously--including his heart scan score of 767.

This score placed Gene solidly in the 99th percentile (in the worst 1%). It came as no surprise to Gene. After all, his father died at age 36 of a heart attack and Gene's brother died at 60 of a heart attack. So Gene took life as it came and long ago decided not to fret about his fate.

But Gene's wife prodded him and prodded him to get the heart scan. That's when I met him.

Of course, Gene had been prescribed Lipitor by his doctor for a somewhat high LDL cholesterol. Our assessment uncovered several additional patterns including lipoprotein (a), small LDL, a pre-diabetic tendency, and a severe deficiency of vitamin D.

At 224 lb and 5 ft 6 inches in height, I felt that Gene was at least 40 lbs overweight.

One year later and with reasonable correction of all his patterns except weight loss and Gene's heart scan score was 590--a reduction of 23%!

Gene was thrilled, as was I. But, frankly, I was also surprised. Dramatic regression of coronary plaque tends to not occur so readily as long as pre-diabetic patterns persist and weight is not controlled.

The lesson: Often the only way to tell if you've achieved control or regression of coronary plaque is to have another heart scan. The tremendous variation in human responses never ceases to amaze me.

Call me when you're having chest pain


I met a patient, Anna, yesterday. She was quite frustrated and frightened.

At age 50, Anna suffered a heart attack and received a stent to her left anterior descending coronary artery. What she found upsetting is that, because several members of her family had suffered heart attacks in their 40s (Dad--heart attack at age 45, paternal uncle--heart attack age 40, and even another uncle with heart attack in his late 20s), she had repeatedly asked her doctor whether she was okay.

She received the usual array of false assurances: "You're feeling fine, right? Then don't worry about it." "Look. Your cholesterol is in the normal range. Even your cholesterol/HDL ratio is fine." "Women don't get heart disease until later in life."

All proved absolutely false. As we talked, Anna exclaimed, "I think what I've been told all along is that we'll take you seriously when you finally have a heart attack!"

She's exactly right. The vast majority of times, heart disease is discovered by accident, usually because of an "event" like heart attack. This is like changing the oil in your car when it finally breaks down--it's too late.

CT heart scan, followed by lipoprotein testing and associated values, then correction of your specific causes. It's that simple.

Self-empowerment is coming!

I've discussed this before: The coming wave of self-empowerment in health. Health that is driven by you, not a hospital, not a doctor, not by procedures, but by information and access to tools that are powerful and effective.

The seeds are being planted right now and won't take full root for many years or decades. But it's going to happen.

I previously cited several broad trends that are examples of this emerging wave:

--The nutritional supplement movement. Contrary to the media's ill-informed bashing, nutritional supplements are getting better: improved quality, better substantiation of when/how to use them, new agents that appear rapidly, since introduction is not slowed by the molasses of the FDA.

--Medications moving to over-the-counter status. Health insurers are driving this one. OTC means not paid for by insurance. That also means access to you.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The mind-boggling rapidity and depth of information available on the Internet today is fueling the self-empowerment movement by providing sophisticated information to health care consumers. Information here is uneven at present. But, as consumer sophistication increases and the system of checks and balances evolves, internet-driven information will be often superior to what you get from a doctor or other health professional.

--High-deductible health insurance plans. If health care consumers bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention and minimize long-term costs.

This trend does not mean treating your own infection, taking out your own gall bladder, repairing your own broken leg. It means that conventional routes of health delivery will recede into providing only catastrophic care.

It means that you and your family will take a larger role in learning how to eat and exercise properly, use foods to maintain and promote health (the "designer food" and "nutraceutical" movement), take supplements that have real benefits, use medications for treatment of many everyday ailments.

It also means seizing control of diseases that previously were only treated in hospitals, like coronary heart disease. This, of course, is where our program, Track Your Plaque, is an example of how you can have a powerful and effective role in your heart health. Track Your Plaque goes so far beyond the "eat low-fat, exercise, and know your numbers" media mantra that it's like comparing a brand-new Mercedes to a rusted, run-down '87 Ford Escort. There truly is no comparison. (Sorry if you're an Escort driver!) But you get the idea.

Another option for lipoprotein testing


For those of you who have been frustrated in trying to get your lipoprotein analysis performed, here's another option.

The Life Extension Foundation at www.lef.org provides access to the VAP test, or Vertical Auto Profiler. This is the lipoprotein test run by the Atherotech company in Birmingham, Alabama. The name refers to the method used, a form of centrifugation, or high-speed spinning of your blood (plasma) to separate the various components by density.

This is a fine technique that works well. Though our preferred method is NMR (www.Lipoprofile.com, Liposcience Inc.), the Atherotech VAP is a reasonable alternative.

If you go through the Life Extension process, they will direct you to blood draw sites in your area. They charge $185 for Life Extension members, $247 for non-members. (Membership in Life Extension costs $75.) Drawback: No billing for health insurance reimbursement.

A full description of the significance of lipoproteins can also be found in my article posted on-line at the www.lef.org website at http://www.lef.org/magazine/mag2006/may2006_report_heart_01.htm

Weight and lipoproteins

Tom, an accountant, came into the office eager to know what his 2nd heart scan score showed.

A year ago, Tom's view of himself as a healthy, middle-aged man was shattered when he found out his heart scan score: 1236. Tom had severe coronary plaque with a heart attack risk of 25% per year (without intensive preventive action).

In the way of lipoprotein abnormalities, he had several: low HDL, deficient large HDL, small LDL, high triglycerides, IDL (the after-eating inability to clear dietary fats), and a high blood sugar in the pre-diabetic range. In addition, Tom was hypertensive, with blood pressure so high it even landed him in the emergency room last winter.

In addition to our approach to correct all these patterns, Tom was urged to lose a significant quantity of weight. Starting at 225 lb., at 5 ft 7 inches, Tom was clearly at least 40 lbs over his ideal weight.

I stressed to Tom that the entire spectrum of causes of coronary plaque were weight-related. I likened his patterns to throwing gasoline on a fire: As weight increased, his lipoprotein and other abnormalties flared dramatically.

But each time Tom came back to the office over the ensuing year, he'd gained another 3 to 6 lbs. And each time he had an explanation. "My daughter just got married. I couldn't turn down wedding cake, now could I?" Or, I just survived another tax season. I was working day and night--no time for exercise!" "It's getting too hot to walk anymore."

Well, despite multiple treatments, Tom's repeat heart scan showed a score of 1677, a 35% increase. That's a dangerous rate of growth that virtually guarantees that plaque is building up momentum to "rupture", which results in heart attack.

I therefore stressed to Tom that weight loss was crucial. Control of coronary plaque was simply not going to occur without weight loss to our target. Alternatively, we could add several new prescription medicines and hope that they could achieve the same effect, though at a price (side-effects, expense).

I tell Tom's story to highlight again just how important weight loss can be for a number of lipoprotein abnormalities.

What measures specifically are sensitive to weight? They are:

--HDL cholesterol
--Triglycerides
--Small LDL
--VLDL
--Blood pressure
--Blood sugar and insulin
--C-reactive protein
--LDL

Weight exerts profound influence on these patterns. In Tom and people like him, weight can be a "make it or break it" issue.

If you, like Tom, have any of the above patterns, consider weight loss as a potent tool you can use to gain control of coronary plaque.

Variation in vitamin D requirements


For Track Your Plaque followers, you know we are very concerned about vitamin D blood levels. My prediction is that, in 10 years, vitamin D will be regarded as an important item on the list of coronary artery disease risk factors.

In our experience of trying to stop or reverse heart scan scores, restoration of vitamin D to a blood level of 50 ng/ml appears to have increased our success rate dramatically.

As we've talked about before, on the bell curve of vitamin D dosing in a northern climate, the majority of women require 2000 units per day, men require 3000 units per day to achieve a level of 50 ng. However, there are "outliers" on this bell curve, i.e., people who require much more or much less.

This week, I saw two people who were very instructive cases of extreme requirements on the high end of vitamin D dosing. Both started with unmeasurable blood levels, i.e., essentially zero ng/ml. On 5000 units of vitamin D per day, both raised their blood levels to around 17-18 ng/ml--in the range of severe deficiency (defined as <20 ng/ml). I advised both to increase their oral dose of vitamin D to 8000 units per day.

Notably, both people avoided sunlight and lived in Wisconsin, a terribly sun-deprived locale 10 months a year. Both were also substantially overweight (around 300 lbs each).

The vitamin D issue continues to be endlessly fascinating in all its nuances and twists.

Heart attacks in your own backyard

Two men from my community just died of heart attacks. Both were in their 40s.

What bothers me most about these all too frequent stories is that it is so preventable. You can bet that both had little or no symptoms prior to their deaths. You can also bet that they've had cholesterol panels taken by their doctors.

Followers of the Track Your Plaque program know that these are sure-fire paths to failure. The absence of heart disease symptoms should provide no reassurance whatsoever. High cholesterol, in-between cholesterol, low cholesterol--none are confident indicators in a specific individual.

Stress test? How about the patient I saw today who, until I met him, had been undergoing stress test after stress test, every year--all while the quantity of coronary plaque tripled. False reassurances provided by his cardiologist led him to believe that all was well--while this stack of oily rags was just waiting for the spark to ignite.

Too little time, too much money, too far away--there's a hundred excuses for not getting a heart scan. Or, you've had a heart scan and no one can tell you what to do about it. If you're reading this, however, you've found the most intensive source of information available on how your heart scan can serve as the start of a program of heart attack prevention for a life free of dangers.

It's not that tough. But it won't just go away on its own. I just have to look around me in my own community, watch the local news, talk to friends, and I'll heart about all the people just in my neighborhood who should be learning these lessons. I rant and rave about this but some people need to hear it from a friend, colleague, neighbor, rather than some crazy doctor bucking the standard line.

You, too, should be telling anyone who will listen about how heart disease can be identified and controlled.

Pilot lands safely after heart attack, then dies

That was the disturbing headline on a report from MSNBC, also reported nationally on all the major news networks.

The story goes on:

"A pilot suffering a heart attack made an emergency landing on a highway, saving his three passengers shortly before he died...He landed the single-engine Cessna 185 on Utah 30 near Park Valley and was taken to Bear River Hospital in Tremonton, where he died."

We track these sorts of stories and it's frightening just how common they are. A school bus driver recently had a heart attack while driving 30 children; the bus crashed but no one was hurt. A 52-year old commercial bus driver suffered a heart attack while transporting 49 conference attendees; the bus plunged 400 feet down a ravine. Remarkably, 17 passengers suffered only minor injuries and there were no deaths.

There have even been incidents where the pilot of a jet liner suffered a heart attack in-flight. In 2000, the 53-year old pilot of a Northwest Airlines DC-10 died while in-flight from a heart attack while landing in Minneapolis. The 290 passengers were landed safely by co-pilot.

Most incidents where the driver or pilot has been incapacitated or died resulted in the deaths of only a handful of people. No major catastrophe has yet occured. But--mark my words--it will. These incidents just happen too frequently.

Virtually all of these and similar incidents could have been prevented. If the FAA, for instance, would insist that all pilots have a simple CT heart scan, it would become immediately obvious which pilots should be grounded and who should fly. Similar requirements could easily be applied to persons in charge of the welfare of many people, most notably school bus drivers.

It's not that tough! The FAA currently requires stress testing and cholesterol testing. Well, guess what? Followers of the Track Your Plaque program know that these tests do not effectively identify the person at risk for heart attack in the majority of individuals. Just ask former President Bill Clinton how helpful his stress tests (five in a row!) were. Or how valuable his cholesterol monitoring was--all prior to his emergency bypass surgery.