Fish oil: What's the difference?

Ultra-purified, pharmaceutical grade, molecularly distilled. Over-the-counter vs. prescription. Gelcap, liquid, emulsion.

There's a mind-boggling variety of choices in fish oil today. A visit to any health food store, or any "big box" store for that matter, will yield at least several, if not dozens, of choices, all with varying and often extravagant claims of purity and potency.

So what's the real story?

Given the analyses conducted over the years, along with my experience with dozens of different preparations, I believe that several conclusions can be reached about fish oil:

Fish oil is free of contamination with mercury, dioxin, PCBs, or furans. To my knowledge, only one fish oil preparation has been found to have a slight excess of PCBs. (This is different from cod liver oil that has been found by one source to have a slight excess of PCBs.)

Oxidative breakdown products differ among the various brands. Consumer Lab (http://www.consumerlab.org/), for instance, has found that several widely available brands of fish oil contained excessive oxidative breakdown products (TOTOX). You can perform you own simple test of oxidative breakdown products: Sniff it. Your fish oil should pass the "sniff test." High quality fish oil should smell non-fishy to lightly fishy. Rancid fish oil with excessive quantities of oxidative breakdown products will smell nasty fishy.

FDA approval does not necessarily mean greater potency, purity, or effectiveness. It just means that somebody assembled the hundreds of millions of dollars to obtain FDA approval, followed by lots of marketing savvy to squash the competition.

This means that there are a number of excellent fish oil products available. My favorites are the liquid fish oils from Pharmax, Nordic Naturals, and Barleans. Capsules from Carlson, PharmaNutrients, and Fisol have also performed consistently. The "big box" capsules from Sam's Club and Costco have also performed well and are wonderfully affordable.

Wheat-free pie crust

I've been working on wheat-free yet healthy recipes these past two months.

You can buy wheat-free, gluten-free foods at the store, of course. But the majority of these products are unhealthy because cornstarch, rice starch, potato starch, or tapioca starch are commonly used in place of wheat. Recall that these are among the few foods that increase blood glucose higher than even wheat.

Here's a simple recipe for wheat-free pie crust that works best for cheesecake, pumpkin pie, and cream pies, but not for berry or other fruit pies like apple.

You will need:
?
1½ cups ground pecans
6 tablespoons melted butter?or melted coconut oil
1 teaspoon vanilla extract?
2 teaspoons cinnamon
1 medium egg
2 tablespoons Truvia™ or ½ teaspoon stevia extract or ½ cup Splenda®

Mix all ingredients thoroughly in bowl. Pour mixture into pie pan and press onto bottom and sides.

Fill pie crust with desired filling. You can fill it with your favorite cheesecake recipe (e.g., Neufchatel or cream cheese, sour cream, eggs, vanilla, and stevia; add pumpkin for pumpkin cheesecake) and bake, usually at 350 degrees F for one hour. 

Yes, the butter provokes insulin and artificial sweeteners can trigger appetite. But, for the holidays, a slice or two of pie made with this crust will not increase blood sugar nor trigger the uncontrolled impulse eating that wheat crust will trigger.

Have a cookie

Here's a great insight dating all the way back to 1966 from one of the early explorations in lipoproteins from the National Institutes of Health lab of Levy, Lees, and Fredrickson:

The nature of pre-beta (very low density) lipoproteins

The subject is a 19 year old female (among the total of 11 in the this small, diet-controlled study) who was first fed a low-carbohydrate (50 grams per day), low-cholesterol diet; followed by a high-carbohydrate (500 grams per day), low-fat (5 grams per day) diet.






To B or not to B

Apoprotein B (apo B) is the principle protein that resides in LDL particles along with other proteins, phospholipids, triglycerides, and, of course, cholesterol.

There's a curious thing about apo B. Just like one child per family in China or one television per household in 1950s America, there is only one apo B for every LDL particle.

So measuring apo B, in effect, provides a virtual count of LDL particles. (Actually, VLDL particles, the first lipoprotein to emerge from the liver, also have one apo B per particle but LDL particles far outnumber VLDL particles.) While apo B structure can show limited structural variation from individual to individual, the effect on measured apo B is negligible.

One apo B per LDL particle . . . no more, no less. What about the other components of LDL particles?

The other components of LDL particles are a different story. Cholesterol and triglycerides in LDL particles vary substantially. Diet has profound effects on cholesterol and triglyceride content of LDL particles. A diet rich in carbohydrates, for instance, increases triglycerides in LDL particles while reducing cholesterol. This means that measuring cholesterol in the LDL fraction will be misleading, since cholesterol will be falsely low. LDL cholesterol is therefore a flawed means to assess the behavior and composition of LDL particles. In particular, when LDL particles become enriched in triglycerides, they go through a process that transforms them into small LDL particles, the variety most likely to cause atherosclerosis.

In other words, when the worst situation of all--an abnormal abundance of small LDL particles develops--it is usually not signalled by high LDL cholesterol.

Because apo B is not sensitive to the composition of LDL particles--high cholesterol, low cholesterol, high triglycerides, etc.--it is a superior method to characterize LDL particles. While apo B doesn't tell you whether LDL particles are big, small, or in between, it provides a count of particles that is far more helpful than measuring this deeply flawed thing called "LDL cholesterol."

(Even better: Count LDL particles and measure LDL size, since size gives us insight into sensitivity to oxidation, glycation, adhesiveness, ability to trigger inflammatory pathways via monocyte chemoattractant protein, various interleukins, tunor necrosis factor and others. This is why cholesterol panels should go the way of tie dye shirts and 8-track tapes: They are hopelessly, miserably, and irretrievably inaccurate. Cholesterol panels should be replaced by either apoprotein B or lipoprotein measures.)

Put lipstick on a dwarf

Today, virtually all wheat products are produced from the Triticum aestivum dwarf mutant.

You might call it "multi-grain bread,""oat bread," or "flaxseed bread." You could call it "organic," "pesticide-free," "non-GMO," or "no preservatives." It might be shaped into a ciabatta, bruschetta, focaccia, or panini. It might be sourdough, unleavened, or sprouted. It could be brown, black, Pumpernickel, or white. It could be shaped into a roll, bun, bagel, pizza, loaf, pretzel, cracker, pancake, brioche, baguette, or pita. It could be matzah, challah, naan, or Communion wafers.

No matter what you call it, it's all the same. It's all from the dwarf mutant Triticum aestivum plant, the 18-inch tall product of hybridizations, backcrossings, and introgressions that emerged from genetics research during the 1960s and 70s.

According to Dr. Allan Fritz, Professor of Wheat Breeding at Kansas State University, and Dr. Gary Vocke at the USDA, over 99% of all wheat grown today is the dwarf variant of Triticum aestivum. (For you genetics types, Triticum aestivum is the hexaploid, i.e., 3 combined genomes, product of extensive hybridizations, while ancestral einkorn is a diploid, i.e., a single genome, grass. Hexaploid Triticum aestivum contains the especially hazardous "D" genome, the set of genes most commonly the recipient of genetic manipulations to modify the characteristics of flour, such as gluten content. Einkorn contains only the original "A" genome.)

No matter what you call it, add to it, how you shape it, etc., it's all the same. It's all the dwarf mutant product of tens of thousands of hybridizations.

You can put lipstick on a pig, but it's still a pig. By the way, lipstick may contain wheat.

What the Institute of Medicine SHOULD have said

The news is full of comments, along with many attention-grabbing headlines, about the announcement from the Institute of Medicine that the new Recommended Daily Allowance (RDA) for vitamin D should be 600 units per day for adults.

What surprised me was the certainty with which some of the more outspoken committee members expressed with their view that 1) the desirable serum 25-hydroxy vitamin D level was only 20 ng/ml, and 2) that most Americans already obtain a sufficient quantity of vitamin D.

Here's what I believe the Institute of Medicine SHOULD have said:

Multiple lines of evidence suggest that there is a plausible biological basis for vitamin D's effects on cancer, inflammatory responses, bone health, and metabolic responses including insulin responsiveness and blood glucose. However, the full extent and magnitude of these responses has not yet been fully characterized.

Given the substantial observations reported in several large epidemiologic studies that show an inverse correlation between 25-hydroxy vitamin D levels and mortality, there is without question an association between vitamin D and mortality from cancer, cardiovascular disease, and all cause mortality. However, it has not been established that there are cause-effect relationships, as this cannot be established by epidemiologic study.

While the adverse health effects of 25-hydroxy vitamin D levels of less than 30 ng/ml have been established, the evidence supporting achieving higher 25-hydroxy vitamin D levels remains insufficient, limited to epidemiologic observations on cancer incidence. However, should 25-hydroxy vitamin D levels of greater than 30 ng/ml be shown to be desirable for ideal health, then vitamin D deficiency has potential to be the most widespread deficiency of the modern age.

Given the potential for vitamin D's impact on multiple facets of health, as suggested by preliminary epidemiologic and basic science data, we suggest that future research efforts be focused on establishing 1) the ideal level of 25-hydroxy vitamin D levels to achieve cancer-preventing, bone health-preserving or reversing, and cardiovascular health preventive benefits, 2) the racial and genetic (vitamin D receptor, VDR) variants that may account for varying effects in different populations, 3) whether vitamin D restoration has potential to exert not just health-preserving effects, but also treatment effects, specifically as adjunct to conventional cancer and osteoporosis therapies, and 4) how such vitamin D restoration is best achieved.

Until the above crucial issues are clarified, we advise Americans that vitamin D is a necessary and important nutrient for multiple facets of health but, given current evidence, are unable to specify a level of vitamin D intake that is likely to be safe, effective, and fully beneficial for all Americans.


Instead of a careful, science-minded conclusion that meets the painfully conservative demands of crafting broad public policy, the committee instead chose to dogmatically pull the discussion back to the 1990s, ignoring the flood of compelling evidence that suggests that vitamin D is among the most important public health issues of the age.

Believe it or not, this new, though anemic, RDA represents progress: It's a (small) step farther down the road towards broader recognition and acceptance that higher intakes (or skin exposures) to achieve higher vitamin D levels are good for health.

My view: Vitamin D remains among the most substantial, life-changing health issues of our age. Having restored 25-hydroxy vitamin D levels in over 1000 people, I have no doubt whatsoever that vitamin D achieves substantial benefits in health with virtually no downside, provided 25-hydroxy vitamin D levels are monitored.

Coronary calcium: Cause or effect?

Here's an interesting observation made by a British research group.

We all know that coronary calcium, as measured by CT heart scans, are a surrogate measure of atherosclerotic plaque "burden," i.e., an indirect yardstick for coronary plaque. The greater the quantity of coronary calcium, the higher the heart scan "score," the greater the risk for heart attack and other unstable coronary syndromes that lead to stents, bypass, etc.

But can calcium also cause plaque to form or trigger processes that lead to plaque formation and/or instability?

Nadra et al show, in an in vitro preparation, that calcium phosphate crystals are actively incorporated into inflammatory macrophages, which then trigger a constellation of inflammatory cytokine release (tumor necrosis factor-alpha, interleukins), fundamental processes underlying atherosclerotic plaque formation and inflammation.

Here's the abstract of the study:
Proinflammatory Activation of Macrophages by Basic Calcium Phosphate Crystals via Protein Kinase C and MAP Kinase Pathways:

A Vicious Cycle of Inflammation and Arterial Calcification?


Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophagescolocalize with BCP deposits in developing atherosclerotic lesionsand in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages.BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNF{alpha}, IL-1ß and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme.

The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.



This observation adds support to the notion that increasing coronary calcium scores, i.e., increasing accumulation of calcium within plaque, suggests active plaque. As I say in Track Your Plaque, "growing plaque is active plaque." Active plaque means plaque that is actively growing, inflamed and infiltrated by inflammatory cells like macrophages, eroding its structural components, and prone to "rupture," i.e., cause heart attack. Someone whose first heart scan score is, say, 100, followed by another heart scan score two years later of 200 is exposed to sharply increasing risk for cardiovascular events which may, in part, be due to the plaque-stimulating effects of calcium.

Conversely, reducing coronary calcium scores removes a component of plaque that would otherwise fuel its growth. So, people like our Freddie, who reduced his heart scan score by 75%, can be expected to enjoy a dramatic reduction of risk for cardiovascular events.

Less calcium, less plaque to rupture, less risk.

Wheat one-liners

If you're having difficulty convincing a loved one or someone else that wheat should be eliminated from the human diet, here are some useful one-liners to use:

Wheat makes your boobs big.
(This is true. Priceless for women to use on their husbands.)

Wheat causes dementia.
(And confirmed on examination of brain tissue at autopsy. Yes, autopsy.)

Wheat makes you look pregnant.
(The visceral fat of a wheat belly does a darn good imitation of a near-term infant.)

The first sign of wheat intolerance can be wetting your pants.
(Cerebellar ataxia, i.e., destruction and atrophy of the cerebellum, caused by wheat leads to loss of coordination and bladder control. Average age of onset: 53 years old.)

White flour bad, whole grain better; just as Marlboros are bad, Salems are better.
(The flawed syllogism that led to the "eat more healthy whole grain" colossal blunder.)

Wheat is the only food with its very own mortality rate.
(Celiac disease, osteoporotic hip fractures, and the neurologic diseases triggered by wheat can be fatal.)

"Wheat" is no longer wheat; it's the dwarf mutant that came from genetics research in the 1960s.
(Over 99% of all wheat today comes from the 18-inch tall dwarf mutant.)

Wheat increases blood sugar higher than nearly all other foods.
(Higher than Milky Way bars, higher than Snickers bars, higher than table sugar.)


There you have it: A full arsenal of one-liners to shoot at your husband, wife, or friend when they roll their eyes at your refusal to consume this thing called "wheat."

The happy homeotherm

If you were a "cold blooded" poikilotherm unable to regulate internal body temperature, you would have to sun yourself on rocks to raise your body temperature, just like turtles and snakes. When it got cold, your metabolic rate would slow and you might burrow into the mud to hide.

You and I, however, are homeotherms, terrestrial animals able to regulate our own internal body temperature. Principal responsibility for keeping your body temperature regulated falls with the thyroid gland, your very own thermoregulatory "thermostat."

But internal body temperature, even in a homeotherm, varies with circadian rhythm: Highest temperature occurs in the early evening around 8 p.m.; the low temperature nadir occurs at around 4 a.m.

The notion that normal human temperature is 98.6 degrees Fahrenheit is a widely-held fiction, a legacy of the extraordinary experience of 19th century German physician, Carl Reinhold August Wunderlich, who claims to have measured temperatures of one million people using his crude, uncalibrated thermometer to obtain axillary (armpit) body temperatures.

Dr. Broda Barnes was a 20th century American proponent of using the nadir body temperature to gauge thyroid function. Like Wunderlich, Barnes also used axillary temperatures.

Modern temperature assessments have employed radiotransmitting thermistors that are swallowed, with temperatures tracked as the thermistor travels through the stomach, duodenum, small intestine, large intestine, rectum, then peek-a-boos back out. Such internal "core temperature" assessments have shown that:

--Axillary temperatures do not track with internal core temperatures very well, often veering off course due to external factors.
--Axillary temperatures are subject to ambient temperatures, such as room temperature, and are affected by clothing.
--Axillary temperatures are more susceptible to physical activity, e.g., increased with exercise or physical work.

Even right vs. left axillary temperatures have been shown to vary up to 2 degrees Fahrenheit.

Studies such as this demonstrate that normal oral temperature upon arising is around 97.2-97.3 degrees Fahrenheit. While we lack data correlating thyroid function with circadian temperature variation, the a.m. nadir does indeed, as Dr. Barnes originally suggested, seem to track thyroid status quite well: lower with hypothyroidism, higher with normal or hyperthyroidism.

I have been using 97.3 degrees F orally as the cutoff for confirming or uncovering thyroid dysfunction, particularly when symptoms or blood tests (TSH, free T3, free T4) are equivocal, a value that has held up well in the majority of cases. I find it helpful when, for instance, someone complains of cold hands and feet and has normal TSH (1.5 mIU/L or less in my view) but low free T3. An a.m. oral temperature of, say, 95.7 degrees F, suggests that there will be a favorable response to T3 supplementation. And it nearly always plays out that way.

Wouldn't it be interesting to know if there was insight into thyroid status provided by also examining the circadian behavior of temperature (e.g., height or timing of the peak)?

Statin buster?

Merck recently reported preliminary results with its drug-in-development, anacetrapib.

After six months of treatment, participants showed:

LDL cholesterol was reduced from 81 mg/dl to 45 mg/dl in those taking anacetrapib, and from 82 mg/dl to 77 mg/dl in the placebo group.

HDL increased from 41 mg/dl to 101 mg/dl in the drug group, from 40 mg/dl to 46 mg/dl in those on placebo.

As you'd expect, the usual line-up of my colleagues gushed over the prospects of the drug, salivating over new speaking opportunities, handsomely-paid clinical "research" trials, and plenty of nice trips to exotic locales.

Anacetrapib is a cholesteryl-ester transfer protein inhibitor, or CETP inhibitor, much like its scrapped predecessor, torcetrapib . . . you know, the one that went down in flames in 2006 after 60% excess mortality occurred in people taking the drug compared to placebo. The hopes of many investors and Pfizer executives were dashed with torcetrapib's demise. The data on torcetrapib's lipid effects were as impressive as Merck's anacetrapib.

These drugs block the effects of the CETP enzyme, an enzyme with complex effects. Among CETP's effects: mediating the "heteroexchange" of triglycerides from triglyceride-rich VLDL particles that first emerge from the liver for cholesterol from LDL particles. This CETP-mediated process enriches LDL particles with triglycerides, which then make LDL a target for action by another enzyme, hepatic lipase, that removes triglycerides. This yields a several nanometer smaller LDL particle, now the number one most common cause of heart disease in the U.S., thanks to conventional advice to cut fat intake and increase consumption of "healthy whole grains."

With effects like this, anacetrapib, should it hold up under the scrutiny of FDA-required trials and not show the same mortality-increasing effects of torcetrapib, will be a huge blockbuster for Merck if release goes as scheduled in 2015. It will likely match or exceed sales of any statin drug. Statin drugs have achieved $27 billion annual sales, some of it deserved. Anacetrapib will likely handily match or exceed Lipitor's $12 billion annual revenue.

More than increasing HDL, CETP inhibition is really a strategy to reduce small LDL particles.

As with many drugs, there are natural means to achieve similar effects with none of the side-effects. In this case, similar effects to CETP inhibition, though with no risk of heightened mortality, is . . . elimination of wheat, in addition to an overall limitation of carbohydrate consumption. Not just low-carb, mind you, but wheat elimination on the background of low-carb. For instance, eliminate wheat products and limit daily carbohydrate intake to 50-100 grams per day, depending on your individual carbohydrate sensitivity, and small LDL drops 50-75%. HDL, too, will increase over time, not as vigorously as with a CETP inhibitor, but a healthy 20-30% increase, more with restoration of vitamin D.

Eliminating wheat and adjusting diet to ratchet down carbs is, of course, cheap, non-prescription, and can be self-administerd, criteria that leave the medical world indifferent. But it's a form of "CETP inhibition" that you can employ today with none of the worries of a new drug, especially one that might share effects with an agent with a dangerous track record.

Protecting the right to use bio-identical hormones in your heart disease prevention program

If you've been following the Track Your Plaque program, you know that we are advocates of "bio-identical hormones", i.e., hormone replacement using forms that are identical to the naturally-occuring human form.

In other words, we find it criminal that pharmaceutical manufacturers continue to promote use of non-identical hormones despite a probable increased side-effect and complication profile (a la Premarin). This unhappy situation persists because bio-identical hormones cannot be patent protected, meaning profits cannot be protected. Synthetic hormones can be patented and profits protected, thus their popularity among drug companies.

If that's not bad enough, Wyeth Pharmaceuticals--maker of synthetic hormone preparations, Premarin and Prempro--has filed an FDA petition to disallow the use of bio-identical hormones as prepared and dispensed by "compounding pharmacies". These are specialty pharmacies that mix and dispense hormones like estrogens (human estradiol, estriol, and estrione) and testosterone. They do so only with a doctor's prescription. Most are members of the Professional Compounding Centers of America (www.pccarx.com), a professional organization devoted to promoting quality-control over compounding practices.

Compounding pharmacies are occasionally guilty of compounding some suspect preparations. Witness the Fentanyl lollipops of 2002 in which the pain medication, Fentanyl, was put into lollipops for patients with chronic pain. This posed obvious dangers to any children who unsuspectingly ate the lollipops.

But the majority of compounding pharmacies are not guilty of such exotic practices. Most are simply pharmacies who might, for instance, mix a specific dermatologic preparation according to the orders of a dermatologist. Likewise with bio-identical hormones.

We have extensive experience with such a pharmacy in Madison, Wisconsin, the Women's International Pharmacy. They have filled hundreds of hormone prescription for us. They are responsible in their dispensing practices, in our experience. In fact, they have been at least as good, if not better, than other pharmacies we've dealt with.

We believe in protecting our rights to prescribe and you to use the choice of hormone preparations you and your doctor desire. This should include bio-identical hormones. The transparent profit motive from Wyeth should raise the hairs on your neck.

If you would like to post your comment to the FDA, there's a little time left. The folks at Womens' International Pharmacy have made it easy by posting links on their website. Go to http://www.womensinternational.com and just follow the instructions.



Here's a sample of some of the objections citizens have raised to Wyeth's petition:


I have been taking bioidentical hormones for two years. Bioidentical Hormones have been a great relief to me without the risk. I consult with my Physician who prescribes bio-identical hormones specifically for me, and my pharmacist prepares them. Without this medication and I would not be able to sleep; I would not be able to work due to the constant hot flashes. Without this medication, I find that I have less tolerance and I am considerably disagreeable. I also have problem with my memory without them. I want the bioidentcial hormones for the health benefits they provide. I urge you to not be swayed by Wyeth's petition. The product Premarin made by Wyeth, is made from pregnant horses not natural sources. Wyeth's hormones have been shown to cause cancer. I would not expect my government and its officials to submit to the highly funded petitioning of a pharmaceutical company who product is threatened by bioidentcial hormones. I do not expect my government to approved Wyeth's petition and leave me no choice of bioidentcial hormones and only the choice of Wyeth's cancer causing drugs Preamrin and Prempro. I ask that the FDA reject Wyeth's petition Docket #2005P-0411.

Another petitioner writes:

As a woman I take exception to Wyeth accusing the Compounding Pharmacy industry of unsafe practices. As a citizen of the United States I expect the FDA to stand up for my rights and the rights of all women who have found or in the future may seek consistent, safe and effective treatment with bioidentical hormones. Eliminating options by bowing to a large pharmaceutical company like Wyeth is not in the public interest and would deprive hundreds of thousands of American women from access to bioidentical hormones. Synthetic hormone replacement has been proven unequivocally unsafe in a government sponsored study and should not be forced as the sole treatment option for women. I hereby request the FDA rule against Wyeth's request. The FDA should not close down the bioidentical option of healthcare. I welcome studies of bioidentical hormones even though they are already FDA-approved and have been working effectively for decades. We already have the proof - hundreds of thousands of women, who over the past two decades have chosen bioidentical hormones based on their physicians' assessments. They are living proof that bioidentical hormones are safer and more effective and reliable than synthetic hormone drugs.

A physician and user of bio-identical hormones writes:

Wyeth, the filer of this complaint, is trying to prevent women from being able to choose less expensive compounded options for hormone replacement. There is medical evidence that in modifying the structure of their drugs (such as Premarin and Prempro) so that they could be patented, they may have introduced factors that cause the health risks identified in the Women's Health Initiative. This complaint appears to be filed for commercial purposes because of the market share that has shifted from Wyeth's products to bio-identical products from compounding pharmacies. If the complaint were upheld, patients and their doctors would not have a choice in hormone treatments. Wythe's commercial strategy of trying to eliminate the 'competition' from compounding pharmacies is against the public interest and in the interest of its own corporate profits. Women and their doctors should be able to choose between patented formulations such as those offered by Wyeth, bioidentical formulas available from compounding pharmacies, and no hormone treatment. I have been taking bio-identical hormones for several years and have had excellent results in improving my symptoms. I have been unable to take other synthetic hormones in the past, and am very concerned that my best treatment option will be taken away.

If you get a 64-slice CT coronary angiogram

With new 64-slice CT scanners popping up everywhere nowadays, be sure to get your heart scan with it.

The new scanners do indeed provide wonderful images of the coronary arteries. But, say you have a 20% blockage in one artery by a coronary angiogram generated on one of these devices. What will you do in 1, 2, or 3 years when you want to know if you have progressed? Should you have the CT angiogram repeated?

Well, if you did you'll be exposed to a large dose of radiation--appropriate for a diagnostic test, but not for a screening test. The radiation exposure is not that different from undergoing a full conventional cardiac catheterization, or up to 100 chest x-rays.

"20% blockage" is also, contrary to popular opinion, not a quantitative measure. It is just an estimate of the diameter reduction at one spot. That number says nothing about the lengthwise extent of plaque. It also says nothing about the potential for "remodeling", the phenomenon of artery enlargement that occurs as plaque grows. In other words, if you had another CT coronary angiogram a year later and was told that your blockag was still 20%, in reality you could have had substantial plaque growth but it would not be reflected in that value.

People will come to me after having a CT angiogram for an opinion. Unfortunately, I send them back to their scan center to get a simple coronary calcium score. That measure is easy, quantitative, precise, and can be repeated yearly if necessary to track progression. (Track Your Plaque--I hope most of you get this by now.) Some physicians poke fun at the heart scan, or calcium, score--it's old, boring, only a measure of hard plaque. None of that's true. The coronary calcium score is a measure of total plaque (hard and soft). And when you are empowered to learn how to control and reduce your score, then it's the most exciting number in your entire health program!

Don't fall for the hype. If you go to a scan center and they insist on a 64-slice CT scanner, or if your doctor orders one, you should insist on getting a calcium score out of the test. Just ask. If they refuse, go somewhere else. Centers that refuse to generate a score have one thing on their mind: identifying people with severe blockages sufficient to obtain the downstream financial bonanza--angioplasty, stents, and bypass surgery.

If you have hypertension, think Lp(a)

Clair has coronary disease.

Clair first came to attention at age 57 when she suffered a large heart attack involving the front of her heart (the "anterior wall") two years ago. Her cardiologist implanted a drug-coated stent. Her doctors advised her to "cut the fat" in her diet, exercise, and take Lipitor.

One year later, she required a stent to another artery (circumflex). At this point, Clair was thoroughly demoralized and terrified for her future. Her first heart attack left her heart muscle with only 50% of normal strength.

She came to my office for another opinion. Of course, one of the first things we did was to identify all causes of her heart disease. No surprise, Clair had 7 new causes not previously identified, including low HDL (37 mg/dl), a severe small LDL particle pattern (75% of all particles were small), and Lp(a).

Her blood pressure was also 190/88, despite her relatively slender build and 3 medications that reduced blood pressure. That's a Lp(a) effect: Exagerrated coronary risk along with unexpected hypertension that often seems inappropriate.

In fact, I saw several patients just this week with lipoprotein(a), Lp(a), and exagerrated high blood pressure (hypertension). It's not that uncommon.

Though it has not been described in the medical literature, our experience is that hypertension is a prominent part of the entire Lp(a) "syndrome".

Lp(a) is responsible for much-increased potential for coronary disease (coronary plaque). It increases in importance as estrogen recedes in a woman (pre-menopause and menopause) and testosterone in a man, since both hormones powerful suppress Lp(a) expression (though why and how nobody knows).

I believe that Lp(a) is also responsible for hypertension that most commonly develops in a persons mid-50s and onwards, often with a vengeance. 3 or 4 anti-hypertensive medications and still not controlled.



Role of l-arginine

L-arginine may be more helpful in this situation than others. L-arginine, recall, is the supply for your body's nitric oxide, a powerful dilator of the body's arteries and thereby reduces blood pressure. We use 6000 mg twice a day, a large dose that requires use of powder preparations rather than capsules.

More reading about l-arginine and nitric oxide is available through Nobel laureate, Dr. Louis Ignarro's book, NO More Heart Disease : How Nitric Oxide Can Prevent--Even Reverse--Heart Disease and Stroke, available at Amazon.com ( http://www.amazon.com/gp/product/0312335814/104-1247258-6443909?v=glance&n=283155).




Will l-arginine truly reverse heart disease on its own? No, I don't believe so. Contrary to Dr. Ignarro's extravagant claims, I find l-arginine a facilitator of plaque regression, i.e, it helps other strategies achieve regression, but it does not achieve regression or reversal by itself. (Note that Dr. Ignarro is a lab researcher who studies rats and has never treated a human being.)

But l-arginine may have special application in the person with lp(a), particularly if hypertension is part of the syndrome.


Note: As always, please note that I talk frankly about l-arginine and other supplements and medications but have no hidden agenda: I am not selling anything, nor am I affiliated with any source/website/store etc. that sells these products. If I advocate something, I do so because I truly believe it, not because I'm trying to sell something. I make this point because so much nonsense is propagated in the media because of profit-motive. That's not true here.

Dr. Ornish: Get with the program!


In the era up until the 1980s, most Americans indulged in excessive quantities of saturated fats: fried chickem, spare ribs, French fries, gravy, bacon, Crisco, butter, etc.

Along came people like Nathan Pritikin and Dr. Dean Ornish, both of whom were vocal advocates of a low-fat nutritional approach. In their programs, fat composed no more than 10% of calories. This represented a dramatic improvement--at the time.


In 2006, a low-fat diet is a perversion of health. It means over-reliance on breads, breakfast cereals, pasta, crackers, cookies, pretzels, etc., the foods that pack supermarket shelves and that now constitute 70-80% of most Americans' diet.

Dr. Ornish still carries great name recognition. As a result, his outdated concepts still gain media attention. The June, 2006 issue of Reader's Digest, in their RDHealth column, carried an interview with Dr. Ornish in which he reiterates his fat-phobia.

However, on this occasion he takes a different tack. This time he rails against the "dangers" of fish oil and omega-3 fatty acids. "I've recently learned that omega-3s are a double-edged sword...In some cases, omega-3s could be fatal."

He goes on to say that, while he believes that fish oil may prevent heart attacks, it has fatal effect if you already have heart disease.

Does this make sense to you?

He's basing his views on a single, obscure study published in 2003 conducted in rural England that showed an increase in death and heart attack on fish oil. Most authorities have not taken these findings seriously, since they are wildly contrary to all other observations and because the study had some design flaws.

Despite the fact that this isolated study runs counter to all other, better-conducted studies seems not to matter to Dr. Ornish.

Clinging to the low-fat concept is like hoping 8-track tapes will make a comeback. It's not going to happen. We enjoyed the benefits while they lasted, appropriate for the era. But now, they're woefully outdated.

The overwhelming evidence is that fish oil provides tremendous benefits with little or no downside. In the Track Your Plaque program, fish oil remains a crucial supplement to gain control over your coronary plaque and stop or reduce your heart scan score. Ignore the doomsday preachings of Dr. Ornish.

(Watch for an article I wrote updating the benefits of fish oil for Life Extension magazine.)

The cholesterol fallacy

Evan spotted the kiosk set up in the middle of the local mall. "Free cholesterol screenings. Know your heart health!" the sign declared.

It was a free cholesterol screening being offered by a local hospital.

The friendly nurse behind the kiosk had Evan fill out a form, then pricked his finger. Five minutes later, she reported to him with a smile, "Sir, your cholesterol is 177--your heart's fine! We get concerned when cholesterol is over 200. So you're in a safe range."

What the nurse failed to recognize is that Evan's HDL was 30 mg, a low value that actually places him at high risk for heart disease. Low HDL also signifies high likelihood of the small LDL particle pattern, a marked predisposition towards pre-diabetes and diabetes, a probable over-reliance on processed carbohydrates in his diet, a dramatically increased probability of hidden inflammation (e.g., elevated C-reactive protein), increased tendency for high blood pressure. . .

In other words, Evan's "favorable" total cholesterol is, in truth, nonsense. It's misleading, falsely reassuring, and provided none of the insight that a real effort might have yielded. Like hippies, tie-dye, other relics of the 1960s, total cholesterol needs to be put to rest. It has served many people poorly and been responsible for countless deaths.

When you see a kiosk or other service like this, even if it's free, run the other way.

"Heart disease a growth business"





So announced a Boston newspaper recently, featuring a story about new heart program at a local hospital.

They were announcing how a hospital had entered the cardiovasculare procedure game and how it would boost their bottom line. The article discussed how the hospital administration was anticipating "a surge in patients from the baby boom generation."

To justify this new program, the article quoted an administrator from another hospital: "Cardiovascular issues is [sic] the number one cause people sought treatment at our hospital."

The hospital featured in the story had spent $13.5 million dollars to develop their program.

Do you think they'll make it back?

You bet they will--many times over. Hospitals are businesses, complete with a bottom line, an expectation of profit and an eye towards growth.

The hospitals in the city where I live (Milwaukee, Wisconsin) are, as in Boston and elsewhere, very aggressive--expanding into new territories, hiring new "salesmen" (physicians), all to capture more marketshare and produce more "product" (your coronary angioplasty, stent, bypass surgery, defibrillator, etc.).

The equation for hospital profits is tried and true. Ignore your heart disese risk and you can help your local hospital grow its business. Neglect to get your heart scan and you can help your hospital pay down its debt. Get a heart scan, then do nothing about it, and you may even justify a pay raise for the hospital administrators for record revenue growth and profit.

Hospitals are a growth business because of the failure of most people and their doctors to 1) identify hidden coronary disease (CT heart scan to obtain your heart scan score), then 2) seize control over it (the Track Your Plaque program or, at least, your doctor's guidance along with your efforts at prevention).

Unless you do so, you are highly likely to help your hospital boost its annual goal for procedures.

The myth of small LDL

Annie's doctor was puzzled.

Despite an HDL cholesterol of 76 mg (spectacular!) and LDL of 82 mg, her CT heart scan showed a score of 135. At age 51, this placed her in the 90th percentile.

Not as bad, perhaps, as her Dad might have had, since he died at age 54 of a heart attack.

So we submitted blood for lipoprotein testing. Surprise! over 90% of all her LDL particles were small. (By NMR, they're called "small". By gel electropheresis, or the Berkeley Lab test, or VAP (Atherotech) technique, they're called "HDL3".)

What gives? Traditional teaching in the lipid world is that if HDL equals or exceeds 40 mg/dl, then small LDL will simply not be present.

Well, as you can see from Annie's experience, this is plain wrong. Yes, there is a graded, population-based effect--the lower your HDL, the greater the likelihood of small LDL. But small LDL is remarkably persistent and prevalent--regardless of your HDL.

We've seen small LDL even with HDLs in the 90's! I call small LDL the "cockroach" of lipids. If you think you have it, you probably do. Getting rid of small LDL requires a specific bug killer. (Track Your Plaque Members: Read Dr. Tara Dall's interview on small LDL.)

Don't let anybody blow off your request for lipoprotein testing just because your HDL is high. That's just not acceptable. Loads can be wrong even with a favorable HDL.

My stress test was normal. I don't need a heart scan!

Katy had undergone a stress test while being seen in an emergency room, where she'd gone one weekend because of a dull pain on the right side of her chest. After her stress test proved normal, she was diagnosed (I believe correctly) with esophageal reflux, or regurgitation of stomach acid up the esophagus. She was prescrbed an acid-suppressing medication with complete relief.

But Katy also had coronary plaque. Three years ago, her CT heart scan score was 157. She'd made efforts to correct the multiple causes, though she still struggled with keeping weight down to gain full control over her small LDL particle pattern.

I felt it was time for a reassessment: another heart scan. After three years, without any preventive efforts, Katy's score would be expected to have reached 345! (That's 30% per year plaque growth.) It's a good idea to get feedback on just how much slowing you've accomplished.

But Katy declared, "But I didn't think another heart scan was necessary. My stress test was normal!"

What Katy was struggling to understand was that even at the time of her first scan, a stress test would have been normal. Plaque can be present with a normal stress test.

Plaque can even show explosive growth all while stress tests remain normal. Just ask former President, Bill Clinton, how much he should have relied on stress tests. (Mr. Clinton underwent annual stress nuclear tests. All were normal and he had no symptoms--all the way up 'til the time he needed urgent bypass surgery!)

Of course, at some point even a crude stress test will reveal abnormal results. But that's years into your disease and a lot closer to needing procedures and experiencing heart attack.

So, yes, Katy would benefit from another heart scan despite her normal stress test.

The message: Don't rely on stress tests to gauge whether or not plaque has grown, stabilized, or reversed. Stress tests can be used to gauge the safety of exercise, blood pressure response, and the potential for abnormal heart rhythms. Stress tests can be used as a method to determine whether blood flow in your coronary arteries is normal through an area with plaque.

But a stress test cannot be used to gauge whether plaque has grown. It's as simple as that. Gauging plaque growth requires a heart scan.

Patient-napping: Yet another reason to stay clear of hospitals!

When I started practicing medicine around 20 years ago, it was common practice to alert a physician when their patient was seen in an emergency room.

If John Smith, for example, went to the emergency room with chest pain, the physician who had an established relationship with the patient--knew their history, had managed their health and illnesses, etc.--was notified, even if the hospital ER had no relationship with the physician. It was not uncommon for the patient to then be transferred to the hospital where their own doctor practiced.

Though cumbersome at times, it preserved the relationship of the patient with their doctor.

Over the past few years, this practice has crumbled. Nowadays, hospitals and their employed physicians (and other unscrupulous physicians acting in the name of profit) "fail" to notify the physician with an established relationship.

Guess what happens? The patient all too often ends up being put through the gamut of testing and procedures.

Why? For hospital profit, of course. If failure to notify a doctor who's had a 10-year long relationship with the patient is "overlooked" or, even more commonly, it's "unsafe" to transfer the patient because the patient is too "unstable" to be transferred, then this patient becomes ripe for picking--heart catheterization, stents, bypass surgery, etc. Ten's, if not hundreds, of thousands of dollars can be reaped by this deception. I call it "patient-napping".

I see this at least several times every month. As hospitals are becoming increasingly competitive, and as they put pressure on their physicians to churn patients for revenues, you're going to see more and more of this.

As always, what is your protection from this expanding influence of hospitals and the doctors too meek to stand up to them? Education and information. Arm yourself with an understanding of what is accomplished in hospitals, when you truly need them, and when you don't.

Take it one step further. At least from a heart disease standpoint--the #1 profit-maker for hospitals--aim to 1)identify your coronary plaque, then 2) seize control over your coronary plaque and reduce your risk for heart attack and heart procedures as much as humanly possible. That's the goal of the Track Your Plaque program.

Don't believe the negative press on fish oil



A British Medical Journal study released in March, 2006 has prompted a media flurry of reports on the worthlessness of fish oil. (Hooper L, Thompson RL, Harrison RA et al. Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: a systematic review. BMJ March,2006)

Don't believe it for a second.

First of all, the study was a re-analysis of the existing published scientific literature. It was not a new study. It included a wild conglomeration of different clinical observations, as the studies examining fish oil over the years have been extraordinarily heterogeneous--in populations examined, omega-3 supplement (e.g., fish vs. capsule), period of observation, endpoints measured.

The results were skewed by inclusion of a moderate-sized British study by Burr et al in men with angina. In this study, no benefit was demonstrated and, in fact, a negative effect--more heart attack and death--was observed with fish oil. This was not news, since the study was published in 2003. It's results have been a mystery to everyone, since its unexpected negative result for fish oil was so starkly different from virtually every other study that preceded it (suggesting a study flaw or statistical fluke).

Nonetheless, the Burr study served to throw off the overall analysis. It diluted the dramatic and persuasive outcome of the GISSI-Prevenzione Study of 11,000 people in which a 28% reduction in heart attack and 45% reduction in cardiovascular death was observed. Note that the substantial numbers of the GISSI make the study's outcome nearly unassailable.

Another important fact: fish oil is among the most powerful tools available to correct elevated triglycerides. Drops of 50% are common. Recall that triglycerides are a necessary ingredient to create the nasty LDL, as well as VLDL, Intermediate-density lipoprotein, and an undesirable shift from large to ineffective small HDL. Reducing triglycerides is therefore crucial for your plaque control program.

This re-analysis serves to prove nothing. Such analyses can only pose questions for further study in a real study like GISSI: a randomized (random participant assignment), controlled (treatment vs. placebo or other treatment) study.

The weight of evidence remains heavily in favor of fish oil, not only as helpful, but fabulously beneficial, particularly for anyone aiming to reduce coronary plaque.
Treat the patient, not the test

Treat the patient, not the test

"Treat the patient, not the test."

That is a common "pearl" of medical wisdom often passed on during medical training.

It refers to the fact that we should always view any laboratory or imaging test in the context of the live, human patient and not just treat any unexpected value that doesn't seem to make sense.

I raise this issue because it recently came up on a discussion on the Track Your Plaque Forum. A Member with a high heart scan score of around 1100 was advised by his doctor that it should be ignored, because he'd prefer to treat the patient, not the test. The patient is apparently slender, physically active, and entirely without symptoms, with favorable cholesterol values as well. The high heart scan score didn't seem to jive with the appearance of the patient, as viewed by this doctor.

This common phrase is meant to impart wisdom. It is a reminder that we treat real people, not just a jumble of laboratory values.

But the unspoken part of the equation is that judgment needs to be applied. A well looking person who shows an unexpected rise in white blood cell count could just have a screwy result, or could have leukemia. Liver tests (AST, ALT) that top 400 could represent a fluke, or dehydration incurred during a long workout, or hepatitis from a long ago blood transfusion.

Yes, treat the patient. But don't be an idiot and entirely dismiss the signficance of an unexpected laboratory or imaging test. A heart scan score of 1100 should be as readily dismissed as discovering a white blood cell count of 90,000 (normal is less than 12,000), or a 5 cm mass in the lung. The absence of symptoms or the failure of conventional risk factors to suggest causation is insufficient reason to dismiss the concrete findings of a test.

In this particular person, dismissing the significance of the heart scan finding by suggesting that the doctor should treat the patient, not the test, is tantamount to:

--Colossal ignorance
--Malpractice
--A certain sentencing of the hapless patient to future major heart procedures, heart attack or death (20-25% likelihood every year, or a virtual certainty over the next 5 years).

There is an ounce of wisdom in this old medical pearl. But there's also plenty of room for a knuckleheaded doctor to misconstrue and abuse its meaning for the sake of covering up his/her ignorance, laziness, or lack of caring.
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All posts by william-davis

The costs of doing drug business?

Here's a telling situation.

Liz had been on prescription niacin, Niaspan, 1500 mg per day (3 x 500 mg tablets) for several years to treat her severe small LDL pattern and familial hypertriglyceridemia (triglycerides 500-1000 mg/dl). Because her health insurance had been paying for the "drug," she insisted on taking the prescription form.

A change in insurance, however, meant that the Niaspan was no longer covered. Her pharmacy wanted to charge $227 per month.

Liz came to the office in tears, worried that she was going to have to choke up $227 per month. I reminded her that, as I had told her several years ago, she could easily replace the Niaspan with over-the-counter Sloniacin or Enduracin. Both release niacin over approximately 6 hours, just like Niaspan.

Here are the prices I've seen with Sloniacin, 100 tablets of 500 mg:

Walgreens: $15.99
Walmart: $12.99
Costco: $8.99

So the most expensive source, Walgreens, would cost Liz just under $15.99 per month to take 1500 mg per day.

$15.99 versus $227.00 per month for preparations that are highly similar. Hmmmmmm.

I wonder what the $211.01 extra per month goes towards? Admittedly, Abbott Labs, the current company selling Niaspan (after Abbott acquired Kos), has invested in a few clinical trials, such as ARBITER-HALTS6. But does supporting research justify this much difference, a difference that amounts to $2532 over a year? If just 100,000 patients are prescribed Niaspan at this dose (a typical dose), this generates $253 million.

Is the cost of developing and marketing a supplement-turned-drug that great? Is this justifiable? Is it any wonder that our health insurance premiums continue to balloon?

I use Sloniacin and Enduracin almost exclusively.

Measurement

A crucial component of self-empowerment in healthcare is to be able to measure various health parameters. More and more measurement tools are entering the direct-to-consumer arena.

Quantification of various phenomena is important in managing many aspects of health. Imagine a carpenter trying to build a house without the use of a tape measure, level, or other measuring tools. In health, as in building a house, measurement, adjustment, and correction are critical.

Among the most helpful health measurement tools:

Blood glucose meters--Blood glucose meters aren't just for diabetics. They are among the most powerful weight loss tools available.

Blood pressure cuffs--There's no better way to assess blood pressure than to assess it under all the varied conditions of life: When you're tired, when you're excited, when you're upset, when you're happy, hungry, stomach full, morning, night. This is a lot better than the one isolated measure in the doctor's office.

Digital thermometers--Your first a.m. oral temperature is a great way to assess thyroid status. We aim to maintain first a.m. oral temperature around 97.3 degrees F, the normal human temperature upon arising that reflects normal thyroid function. (No, Dr. Broda Barnes fans, axillary temperatures should NOT be used due to flagrant variation from right armpit to left armpit, modifying effects of clothing and ambient temperature, etc. Oral temperature tracks internal, "core," temperature fluctuations reliably, including circadian variation, far better than axillary temperatures.)

Fingerstick blood tests--An incredible number of blood tests are now available just by performing a simple fingerstick in your kitchen or bathroom. You can get 25-hydroxy vitamin D, lipids, thyroid measures (TSH, free T3, free T4), hormones (DHEA, testosterone, estrogens). And the list is growing rapidly. Salivary tests are also growing in number for many of the same measures.

A variation on fingerstick blood tests are devices like CardioChek that allow you to do a fingerstick, but also run the test on your own device at home. (The CardioChek device tests total cholesterol, triglycerides, and HDL.)

Urine pH--You can dipstick your own urine to assess the relative acidity or alkalinity of your lifestyle. Acid pH (7 or below) suggests that diet is weighed too heavily in favor of animal products and grains. An alkaline pH (above 7) suggests plentiful vegetables and fruits, not counteracted by animal products and grains.

There are many more, including the ZEO device to monitor sleep quality, RESPeRATE for reduction of blood pressure, HeartMath to manage stress and augment the parasympathatic (relaxation) response. We've come a long way compared to the health monitoring devices of just 25-30 years ago.

Anyway, that's a partial list. Given the rapid advances in technology that allow such home tests, I anticipate a much longer list in the coming few years.

For some perspective on how far these devices have come, here's a great graphic of an early sphygmomanometer, or blood pressure gauge.


Courtesy Wellcome Library, London

I lost 37 lbs with a fingerstick

Jack needed to lose weight.

At 5 ft 7 inches, he weighed in at 273 lbs, putting his BMI at a sobering 42.8. (A BMI of 30 or above is classified as "obese.") In addition to lipoprotein(a), Jack had an extravagant quantity of small LDL (the evil "partner" of lipoprotein(a)), high triglycerides, and blood sugars in the diabetic range. With a heart scan score of 1670, Jack had little room for compromises.

Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.

So I taught Jack how to check his blood sugars using a fingerstick device, what I call the most important weight loss tool available. I asked Jack to check his pre-meal blood glucose and his one-hour after-meal blood glucose and not allow the after-meal blood glucose to rise any higher than the pre-meal. For example, if blood glucose pre-meal was 115 mg/dl, after-meal blood glucose should be no higher than 115 mg/dl.

If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 mg/dl, reduce or eliminate the mashed potatoes. If slow-cooked, stone ground oatmeal causes blood glucose to increase from 115 mg/dl to 185 mg/dl (a typical response to oatmeal), then eliminate it.

Having immediate feedback on the effects of various foods finally did it for Jack: It identified foods that were triggering excessive blood sugar rises (and thereby insulin) and foods that did not.

What Jack did not do is limit or restrict calories. In fact, I asked him to eat portion sizes that left him comfortable. There was no need to reduce calories, push the plate away, etc. Just don't allow blood sugars to rise.

Six months later, Jack came back 37 lbs lighter. And he got there without calorie-counting, without regulating portion sizes, without hunger.

The two kinds of small LDL

You won't find this in any publication nor description (at least ones that I've come across) about the ubiquitous small LDL particles. It's an observation I've made having obtained thousands of advanced lipoprotein panels of the sort that break lipoproteins down by size. I've discussed this issue previously here. But small LDL is so ubiquitous, not addressed by conventional strategies like statin drugs or fat restriction (it is made worse, in fact, by reducing fat in the diet), that it is worth keeping at the top of everyone's consciousness.

(Because most of the lipoprotein analyses performed in my office are done via NMR, I will discuss in terms relevant to NMR. This does not necessarily mean that similar observations cannot be made with centrifugation, i.e, VAP from Atherotech, or gel electropheresis from Berkeley, Boston Heart Lab, Spectracell, and others).

There are two basic varieties of small LDL particles:

1) Genetically-programmed--e.g., via cholesteryl-ester transfer protein (CETP) activity
2) Acquired--via carbohydrate consumption


It means that people with acquired small LDL from carbohydrate consumption can reduce small LDL to zero with reduction of carbohydrates, especially the most small LDL-provoking foods of all: wheat, cornstarch, and sucrose.

It also means that people who have small LDL for genetically-determined reasons can only minimize, not eliminate, small LDL. By NMR, we struggle to keep small LDL in the 300-600 nmol/L range when genetically-determined. (People typically start with 1400-3000 nmol/L small LDL particles prior to diet changes and other efforts.) We can only presumptively identify genetically-determined small LDL when all the appropriate efforts have been made, including reduction in weight to ideal, yet small LDL persists.

Here is where we need better tools: when you've done everything possible, yet small LDL persists.

While we break LDL particles (NOT LDL cholesterol, the crude and misleading way of viewing atherosclerosis causation) down by size, it's really about all the undesirable characteristics that accompany small size:

--Distortion of Apo B conformation--i.e., the primary protein that directs LDL particle fate is distorted, making it less likely to be cleared by the liver but more likely to be taken up by inflammatory (macrophages) in the artery wall, creating plaque. It means that small LDL particles linger for a longer time than larger particles.

--Small LDLs are more oxidation-prone. Oxidized LDL are more avidly taken up by inflammatory macrophages.

--Small LDLs are more glycation-prone.

--Small LDLs are more adherent to structural tissues, e.g., glycosaminoglycans, that reside in the artery wall.

You and I cannot measure such phenomena, so we resort to distinguishing LDL particles by size.

The drug industry believes it may have a solution to small LDL in the form of CETP-inhibiting drugs, like anacetrapib. In the way of nutritional solutions beyond carbohydrate reduction, weight loss/exercise, niacin, vitamin D normalization, and omega-3 fatty acid supplementation, there are exciting but very preliminary data surrounding the possibility that anthocyanins may inhibit CETP activity. Having toyed with this concept for the past 6 months, I remain uncertain how meaningful the effect truly is, but it is harmless, since we obtain anthocyanins from foods colored purple or purplish, such as blackberries, blueberries, cherries, red leaf lettuce, red cabbage, etc.

I welcome any unique observations on this issue.

Wheat-free pumpkin bread

Try this recipe for a wheat-free, gluten-free yet healthy "bread." Unlike many gluten-free foods that send blood sugar skyward, this will not.

Ingredients:
2 cups ground almond meal (Buy it from Trader Joe's--70% cheaper than other grocery stores.)
1/2 cup ground flaxseed
1/2 cup sour cream (full-fat, of course)
15 oz canned pumpkin (Trader Joe's is bisphenol A-free)
2 medium to large eggs
1/2 cup chopped walnuts or pecans
4 tablespoons butter, melted
2 teaspoons baking powder
2 teaspoons cinnamon
1 teaspoon nutmeg or allspice
Dash of salt
Choice of non-nutritive sweetener (I used 3 teaspoons Trader Joe's stevia extract powder, the one mixed with lactose. Two tablespoons of Truvia, 1/2 teaspoon of the more concentrated stevia extract, or 1/2 cup Splenda are other choices. You can taste the mixed batter to gauge sweetness if in doubt.)

Preheat oven to 350 degrees F. Grease baking pan (e.g., 10 x 6 inch). The pan should be big enough so that the mix will not be more than 2 inches deep, else it will require much longer to bake. (If you have only smaller pans, you will need to cook longer while the pan is covered with aluminum foil.)

Mix all ingredients thoroughly in large bowl. Pour mix into greased baking pan.

Cover with aluminum foil and bake for 30 minutes. Remove foil and bake for additional 30 minutes or until inserted toothpick or knife comes out dry.

Serve with cream cheese or as is.

(I'd have some pictures, but the kids and I ate it up before I thought to take any photographs.)

Vitamin D: Deficiency vs optimum level

Dr. James Dowd of the Vitamin D Cure posted his insightful comments regarding the Institute of Medicine's inane evaluation of vitamin D.

Dr. Dowd hits a bullseye with this remark:

The IOM is focusing on deficiency when it should be focusing on optimal health values for vitamin D. The scientific community continues to argue about the lower limit of normal when we now have definitive pathologic data showing that an optimal vitamin D level is at or above 30 ng/mL. Moreover, if no credible toxicity has been reported for vitamin D levels below 200 ng/mL, why are we obsessing over whether our vitamin D level should be 20 ng/mL or 30 ng/mL?

Yes, indeed. Have no doubts: Vitamin D deficiency is among the greatest public health problems of our age; correction of vitamin D (using the human form of vitamin D, i.e., D3 or cholecalciferol, not the invertebrate or plant form, D2 or ergocalciferol) is among the most powerful health solutions.

I have seen everything from relief from winter "blues," to reversal of arthritis, to stopping the progression of aortic valve disease, to partial reversal of dementia by achieving 25-hydroxy vitamin D levels of 50 ng/ml or greater. (I aim for 60-70 ng/ml.)

The IOM's definition of vitamin D adequacy rests on what level of 25-hydroxy vitamin D reverses hyperparathyroidism (high PTH levels) and rickets. Surely there is more to health than that.

Dr. Dowd and vocal vitamin D advocate, Dr. John Cannell, continue to champion the vitamin D cause that, like many health issues, conradicts the "wisdom" of official organizations like the IOM.

Large LDL counts, too

Chad is a 43-year old father of five kids.

Earlier this year, he developed chest pain that got worse and worse. He ended up with a total of five stents in all three coronary arteries. After a devastating experience with Lipitor that resulted from a ruptured tendon, he came to me for an option.

Chad's lipoproteins:

Slow Burn works

I have been impressed with the results I've been obtaining with Fred Hahn's Slow Burn strength training technique.

Because I have limited time to hang around the gym, any technique that provides outsized results in a limited amount of time, I have to admit, appeals to me. In past, I'd be lucky to squeeze in one or two strength training sessions per week, devoting the rest of the time to biking outdoors, biking on a sedentary bike (while playing XBox), jogging, or doing strenuous yard work like digging trenches and planting shrubs.

Over the years, I've gradually lost muscle, since the strength training effort suffered with my time limitations.

So Fred's time-efficient Slow Burn idea struck a chord. Having now done it with some regularity, usually 1-2 times per week since mid-September, I have gradually added back visible muscle. My Slow Burn workouts, involving 8-10 different movements, seem to have restored the muscle I've lost, with a very modest time effort.

It took a little getting used to. After Fred showed me how to do the movements--slow motion movement in both the "positive" and "negative" directions, with smooth, non-jerking transitions, one set per muscle group, each taken to muscle exhaustion--it left me unusually tired and sore the next day. This surprised me, given the limited time involved. Breathing is also very important; the usual exhale-during-the-positive, inhale-during-the-negative pattern is replaced by breathing freely during the entire set. I didn't get this at first and ended up with headaches that got worse with each set. Breathing freely relieved me from the effect.

I have strength trained since I was around 15 years old. Back in the early 1970s, I had about 2000 lbs of barbells and dumbbells in my garage in New Jersey, while also driving back and forth to the Morristown, NJ, YMCA to train with friends. The Slow Burn movements forced me to break habits established over nearly 40 years of conventional strength training.

I've also played around with mixing conventional movements with Slow Burn movements to keep it fresh. This also seems to work.

If you're interested in giving it a try, here's an animation that demonstrates what Slow Burn movements look like. Fred has also produced an excellent 3-DVD set of videos that more fully describe the practice.

Do your part to save on healthcare costs

While many of the factors that drive the relentless increase in health care costs are beyond individual control, you are still able to exert personal influence over costs. Just as in political elections, your one vote alone may not count; it's the collective effort of many people who share similar opinions that results in real change.

I just got the new monthly premium for my high-deductible health insurance: Up $300 per month, putting my family's total premium over $2000 per month---for four healthy people. (My son fractured his wrist playing high school hockey earlier this year; that may explain at least some of the increase.)

I'm going to shop around for a better deal. However, shopping is likely to only stall the process. It will not address the systemic problems with healthcare that continue to drive premiums up and up and up.

So what can you do to help keep costs down? Here are a few thoughts:

Never accept a prescription for fish oil, i.e., Lovaza. Just buy far less costly over-the-counter fish oil. I treat complex hyperlipidemias, including familial hypertriglyceridemia, ever day. I NEVER use prescription fish oil. A typical 4 capsule per day Lovaza prescription adds around $280 to $520 per month to overall health costs (though your direct out-of-pocket costs may be less, since you shove the costs onto others in your plan).

Never accept a prescription for vitamin D. Prescription vitamin D is the mushroom or invertebrate form anyway. Just buy the human (cholecalciferol, D3) form from your health food store or "big box" store. They yield consistent increases in 25-hydroxy vitamin D levels, superior to the prescription form. And they're wonderfully inexpensive.

Eliminate wheat from your diet. If there is a dietary strategy that yields unexpected and outsized benefits across a wide spectrum of health, it's elimination of this thing we're sold called "wheat," you know, the genetically-transformed, high-yield dwarf mutant that now represents 99% of all wheat sold. Blood sugar drops, pre-diabetics become non-prediabetics, diabetics reduce need for medication or become non-diabetic, cholesterol values plummet, arthritis improves, acid reflux and irritable bowel symptoms improve or disappear, just to mention a few. Wheat elimination alone, I believe, would result in incalculable savings in both healthcare costs and lives saved.

Be sure to obtain iodine. In the fuss to cut salt use, everyone forgot about iodine. Lack of iodine leads to thyroid disease, usually hypothyroidism, that, in turn, causes cholesterol values to increase, weight to increase, and heart disease risk to double, triple, or quadruple. Iodine supplementation is easy and wonderfully inexpensive.

Over time, I hope that all of us can help develop the effort to self-direct more and more of our own health. Our Track Your Plaque program has shown me that, not only can people take the initiative to direct aspects of their own health, they can do it better than 99% of doctors.  

I'm sure there are many, many other ways to help reduce costs. Any suggestions?