Statin stupid

19. March 2010 William Davis (0)
If we followed the lead of the pharmaceutical industry and my cardiology colleagues, we would all subscribe to the "statins for all" philosophy. There is now $2 billion of clinical "research" to back up this "evidence-based" practice.

I do not endorse this "statins for all" philosophy. I believe it is a product of the raw profiteering of the pharmaceutical industry, who are adept at recruiting physicians to their cause.

But lost in the confusion of tainted studies and over-the-top media saturation is the fact that there are small groups of people who likely do obtain benefit from statin drugs. They would certainly benefit from better informed scrutiny of their lipoprotein and metabolic abnormalities. But treatment may involve statins.

This is entirely distinct from the "statins for all" argument, the simpleminded rule that primary care physicians and cardiologist are told to follow.

Groups who may indeed benefit from statin therapy include:

Homozygous or heterozygous familial hypercholesterolemia--Lacking a receptor for LDL particles, LDL piles up to very high levels in these people. LDLs of 300+ are common and lead to heart disease and stroke at relatively young ages.

Combined mixed hyperlipidemia--Among the one or more genetic defects underlying this condition involves excessive production of apoprotein B and VLDL particles. This leads to high risk for heart disease.

People unable to follow a diet to correct their lipid disorder--I have 80+-year old patients, for instance, who say, "I've eaten this way for 82 years. I'm not going to change now!" In the absence of diet and other efforts (e.g., omega-3 fatty acids from fish oil), drugs may be the answer.

In other words, of the $27 billion annual bill for statin drugs, perhaps a tiny fraction is truly necessary. The majority of people taking statin drugs would not really need them if they had the real answers. But don't let that confuse us: There are some people who do indeed benefit.

Butter and insulin

19. March 2010 William Davis (83)
In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008


From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Vitamin D as a cardiovascular risk factor gains ground

18. March 2010 William Davis (0)
If you were reading The Heart Scan Blog back in 2007, or read my Life Extension article on vitamin D deficiency as a cardiovascular risk factor, you already knew that vitamin D deficiency is rampant and adds to cardiovascular risk.

Results of a study from the Intermountain Medical Center Heart Institute in Utah bolster the concept that vitamin D deficiency is a cardiovascular risk factor, vitamin D normalization/supplementation reduces cardiovascular risk.

Science Daily reported:

For the first study, researchers followed two groups of patients for an average of one year each. In the first study group, over 9,400 patients, mostly female, reported low initial vitamin D levels, and had at least one follow up exam during that time period. Researchers found that 47 percent of the patients who increased their levels of vitamin D between the two visits showed a reduced risk for cardiovascular disease.


In the second study, researchers placed over 31,000 patients into three categories based on their levels of vitamin D. The patients in each category who increased their vitamin D levels to 43 nanograms per milliliter of blood or higher had lower rates of death, diabetes, cardiovascular disease, myocardial infarction, heart failure, high blood pressure, depression, and kidney failure. Currently, a level of 30 nanograms per milliliter is considered "normal."


Over the past 4 years, people in our program have been enjoying the extravagant benefits of vitamin D restoration. Cardiovascular benefits are becoming better documented and the bone health, cancer-preventing, insulin-normalizing, mood-adjusting, and anti-inflammatory effects likewise.

Atkins Diet: Common errors

18. March 2010 William Davis (74)
No doubt: The diet approach advocated by the late Dr. Robert Atkins was a heck of a lot closer to an ideal diet than the knuckleheaded advice emitting from the USDA, American Heart Association, American Diabetes Association, and the Surgeon General's office.

But having just spent a week with Atkins low-carbers, here are some common errors that I see many make, errors that I believe have long-term health consequences, including impairment of weight loss.

Excessive consumption of animal products--Non-restriction of fat often leads to over-reliance on animal products. Higher intakes of red meats (heme proteins?) have been strongly associated with increased risk for colon and other gastrointestinal tract cancers. It is not a fat issue; it is an animal product issue. We should consume less meat, more vegetables and other plant-sourced foods.

Consumption of cured meats--Cured, processed meats, such as sausage, hot dogs, salami, bologna, and bacon, have a color fixative called sodium nitrite, an additive that has been confidently linked to gastrointestinal cancers. Risk is likely dose-dependent: The more you ingest, the greater the long-term risk.

Overconsumption of dairy products--Dairy products, especially milk, yogurt, cottage cheese, and butter, are potent insulinotropic foods, i.e., foods that trigger insulin release. There can be up to a tripling of insulin (area-under-the-curve) levels. This is not good in a world populated with tired, overworked pancreases, exhausted from a lifetime of high-carbohydrate eating.

Too many calories--While I agree that "a calorie is a calorie" and "calories in, calories out" are faulty concepts, I have anecdotally observed that long-time low-carbers often trend towards unlimited consumption of food, a phenomenon that seems to result in weight gain, especially in the sedentary. I wonder if this is a reflection of the insulinotropic action of dairy products and other proteins, compounded by the poor insulin responsiveness that develops with lack of physical activity. Factor into this conversation that lower calorie intake extends life, probably substantially (Sirt-2 activation and related phenomena, a la resveratrol). If lower calorie intake extends life, unlimited calorie intake likely shortens life.

Please don't hear this as low-carb bashing--it is not. It is a call to improve diets and not stumble into common traps that can impair heart health, weight loss, and longevity.

Fat Head: Tom Naughton's manifesto for low-carb eating

12. March 2010 William Davis (16)
I just got back from Jimmy Moore's low-carb cruise to the Bahamas.

Among the many interesting people I met on the cruise was the creator of the documentary film, Fat Head, Tom Naughton.

Tom brings both creative insights into low-carbohydrate eating as well as humor. Low-carb eating can be a pretty contentious issue, but Tom made it fun. He will make you laugh about many of the odd notions we have about diet.

Among the best parts of Fat Head is Tom's portrayal of the effects of carbohydrates on insulin and fat metabolism:






Fat Head joins the ranks of films like Food, Inc, that make nutrition information entertaining. For anyone interested in a unvarnished look at diet, weight loss, along with a few laughs along the way, Tom Naughton's Fat Head is worth viewing.

Oatmeal: Good or bad?

11. March 2010 William Davis (67)

You've heard it before: oatmeal reduces cholesterol. Oatmeal producers have obtained permission from the FDA to use a cholesterol-reducing claim. The American Heart Association provides a (paid) endorsement of Quaker Oats.

I've lost count of the times I've asked someone whether they ate a healthy breakfast and the answer was "Sure. I had oatmeal."

Is this true? Is oatmeal heart healthy because it reduces LDL cholesterol?

I don't think so. Try this: Have a serving of slow-cooked (e.g., steel-cut, Irish, etc.) oatmeal. Most people will consume oatmeal with skim or 1% milk and some dried or fresh fruit. Wait an hour, then check your blood sugar.

If you are not diabetic and have a fasting blood sugar in the "normal" range (<100 mg/dl), you will typically have a 1-hour blood glucose of 150-180 mg/dl--very high. If you have mildly increased fasting blood sugars between 100 and 126 mg/dl, postprandial (after-eating) blood sugars will easily exceed 180 mg/dl. If you have diabetes, hold onto your hat because, even if you take medications, blood sugar one hour after oatmeal will usually be between 200 and 300 mg/dl.

This is because oatmeal is converted rapidly to sugar, and a lot of it. Even if you were to repeat the experiment with no dried or fresh fruit, you will still witness high blood sugars in these ranges. Do like some people and pile on the raisins, dried cranberries, or brown sugar, and you will see blood sugars go even higher.

Blood sugars this high, experienced repetitively, will damage the delicate insulin-producing beta cells of your pancreas (glucose toxicity). It also glycates proteins of the eyes and vascular walls. The blood glucose effects of oatmeal really don't differ much from a large Snickers bar or bowl of jelly beans.

If you are like most people, you too will show high blood sugars after oatmeal. It's easy to find out . . . check your postprandial blood sugar.

In past, I recommended oat products, specifically oat bran, to reduce LDL, especially small LDL. I've changed my mind: I now no longer recommend any oat product due to its blood sugar-increasing effects.

Better choices: eggs, ground flaxseed as a hot cereal, cheese (the one dairy product that does not excessively trigger insulin), raw nuts, salads, leftovers from last evening's dinner.

Mustard: Super health food?

6. March 2010 William Davis (32)
Could mustard--yes, the yellow condiment you smear on hot dogs--be a super heart healthy food in disguise?

Consider that mustard contains:

Vinegar

Turmeric

No appreciable sugar


The vinegar slows gastric emptying, resulting in slower absorption of any carbohydrates and a reduced glucose area-under-the-curve. Of the little fats contained (about 3 grams per 1/4 cup), most are desirable monounsaturates. Mustards are relatively rich in selenium, with 20 mcg per 1/4 cup, helpful for protection against cancer and thyroid disease, and magnesium, 31 mg per 1/4 cup.

Turmeric is added to most mustards. One of the constituents of turmeric, curcumin, the substance that confers the bright yellow color, has been a focus of interest for its anti-inflammatory effects. Curcumin has been documented to reduce activity of the inflammatory enzymes cyclooxygenase-2 (COX-2), lipoxygenase, and reduce activity of inflammatory signal molecules, tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1,2,6,8, and 12, and monocyte chemoattractant protein (MCP). Curcumin also has been shown to reduce LDL oxidation, a potentially important step in atherosclerotic plaque formation. Turmeric is used as a tea by Okinawans. (Hmmmm . . . )

Turmeric content of mustard can vary, of course. Likewise, sugar content. Look for mustards that are not sweetened, so avoid honey mustard in particular. Look for hot, brown, horseradish, Dijon, etc. If there is a downside to mustard, it's sodium content, though the 709 mg per 1/4 cup should only be a problem for those who are sodium-sensitive (African Americans, in particular).

So perhaps mustard isn't exactly a super health food. But it may have some bona fide health effects and should be used generously especially if you are concerned about blood sugar and inflammatory phenomena.

Exercise and blood sugar

5. March 2010 William Davis (30)
There is no doubt that exercise yields benefits across a spectrum of health: reduced blood pressure,  reduced inflammation, reduced blood coagulation, better weight control, stronger bones, less depression, reduced risk for heart attack.

Exercise also influences blood sugar. Diabetics understand this best: Exercise reduces blood sugar 20, 30, 50 or more milligrams. A starting blood sugar, for instance, of 160 mg/dl can be reduced to 80 mg/dl by jogging or riding a bicycle. (I recently had brunch at an Indian restaurant with my family. Blood sugar one-hour postprandial: 134 mg/dl. I was sleepy and foggy. I got on my stationary bike and pedalled at a moderate clip for 60 minutes. Blood sugar: 90 mg/dl.)

Could the reduction of blood sugar with exercise be THE reason that exercise and physical activity provide such substantial benefits?

Think about it. Reduced blood sugar:

1) Reduces risk for future cardiovascular events.
2) Reduces glycation of proteins, i.e., reduced glucose binding to proteins like the ones in artery walls and the lenses of your eyes.
3) Reduces blood coagulation
4) Reduces endothelial dysfunction (abnormal artery constriction that leads to atherosclerosis)

This might explain why it doesn't require high levels of aerobic activity to derive benefit from exercise, since even modest efforts (e.g., a 15-minute walk after eating) reduce blood sugar substantially.

The incredible 33-year, 18,000-participant Whitehall study tells us that a postprandial (after-eating) blood sugar of an impossibly-difficult 83 mg/dl is required to erase the excess cardiovascular risk of blood sugar. Could this simply be telling us that physical activity or exercise is required to suppress blood sugars to these low levels?

It makes me wonder if an index of the adequacy of exercise is your post-exercise blood glucose.

Restaurant eating: A fructose landmine

13. January 2011 William Davis (25)
There is no remaining question that fructose is among the worst possible things humans can consume.

Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.

Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.

Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.

Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.

Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.

A glycation rock and a hard place

12. January 2011 William Davis (15)
Advanced Glycation End-products, or AGEs, the stuff of aging that mucks up brains, kidneys, and arteries, develop via two different routes: endogenous (from within the body) and exogenous (from outside the body).

Endogenous AGEs develop via glycation. Glycation of proteins in the body occurs when there are glucose excursions above normal. For instance, a blood glucose of 150 mg/dl after your bowl of stone-ground oatmeal causes glycation of proteins left and right, from the proteins in the lens of your eyes (cataracts), to the proteins in your kidneys (proteinuria and kidney dysfunction), to skin cells (wrinkles), to cartilage (brittle cartilage followed by arthritis), to LDL particles, especially small LDL particles (atherosclerosis).

At what blood sugar level does glycation occur? It occurs even at "normal" glucose levels below 100 mg/dl (with measurable long-term cardiovascular effects as low as 83 mg/dl). In other words, some level of glycation proceeds even at blood glucose levels regarded as normal.

There's nothing we can do about the low-level of glycation that occurs at low blood sugar levels of, say, 90 mg/dl or less. However, we can indeed do a lot to not allow glycation to proceed more rapidly, as it inevitably will at blood sugar levels higher than 90 mg/dl.

How do you keep blood sugars below 90 mg/dl to prevent excessive glycation? Avoid or minimize the foods that cause such rises in blood sugar: carbohydrates.

What food increases blood sugar higher than nearly all other known foods? Wheat.

Is einkorn the answer?

11. January 2011 William Davis (14)
People ask: "What if I would like a piece of bread or other baked product just once in a while? What is safe?"

Eli Rogosa, Director of The Heritage Wheat Conservancy, believes that a return to the wheat of our ancestors in the Fertile Crescent, circa 10,000 years ago, is the answer.

Former science teacher, now organic farmer, farm researcher, and advocate of sustainable agriculture, Eli has been reviving "heritage" crops farmed under organic conditions, some of her research USDA-funded.

In particular, Eli has been cultivating original 14-chromosome ("diploid") einkorn wheat. Although einkorn contains gluten (in lesser quantities despite the higher total protein content), the group of proteins that trigger the immune abnormalities of celiac disease and other immune phenomena, Eli tells me that she has witnessed many people with a variety of wheat intolerances, including celiac disease, tolerate foods made with einkorn wheat. (The variety of glutens in einkorn differ from the glutens of the dwarf mutant that now dominate supermarket shelves.)

Eli travels to Israel every year, returning with "heritage" seeds for wheat and other crops. She formerly worked in the Israel GenBank as Director of the Ancient Wheat Program. She has written a brochure that describes her einkorn wheat.

Eli sent me 2 lb of her einkorn grain that nutritionist, Margaret Pfeiffer, and I ground into bread. Our experience is detailed here. My subsequent blood sugar misadventure, comparing einkorn bread to conventional organic whole wheat bread is detailed here, followed by the odd neurologic effects I experienced here.

Anyone else wishing to try this little ancient wheat experiment with einkorn can also obtain either the unground grain or ground flour through Eli's website, www.growseed.org. Most recently, einkorn pasta is being retailed under the Jovial brand at Whole Foods Market.

If anyone else makes bread or any other food with Eli's einkorn wheat, please let me know:

1) Your blood sugar response (before and 1 hour after consumption)
2) Whether you experienced any evidence of wheat intolerance similar to what you experienced with conventional wheat, e.g., rash, acid reflux, gas and cramping, moodiness, asthma, etc.

But remember: Wheat effects or no, einkorn is still a grain. My belief is that humans do best with little or no grain. The einkorn experience is an effort to identify reasonable compromises so that you and I can have a piece of birthday cake once a year without getting sick.

Genetic incompatibility

10. January 2011 William Davis (29)
Peter has lipoprotein(a), or Lp(a), a genetic pattern shared by 11% of Americans.

It means that Peter inherited a gene that codes for a protein, called apoprotein(a), that attaches to LDL particles, forming the combined particle Lp(a). It also means that his overall pattern responds well to a high-fat, high-protein, low-carbohydrate diet: The small LDL particles that accompany Lp(a) over 90% of the time are reduced, Lp(a) itself is modestly reduced, other abnormalities like high triglycerides (that facilitate Lp(a)'s adverse effects) are corrected. Small LDL particles are, by the way, part of the genetic "package" of Lp(a) in most carriers.

Peter also has another gene for Apo E4, another genetically-determined pattern shared by 19% of Americans. (Another 2% of Americans have two "doses" of Apo E4, i.e., they are homozygotes for E4.) This means that the Apo E protein, normally responsible for liver uptake and disposal of lipoproteins (especially VLDL), is defective. In people with Apo E4, the higher the fat intake, the more LDL particles accumulate. (The explanation for this effect is not entirely clear, but it may represent excessive defective Apo E-enriched VLDL that competes with LDL for liver uptake.) People with Apo E4 therefore drop LDL (and LDL particle number and apoprotein B) with reductions in fat intake.

This is a genetic rock-and-a-hard-place, or what I call a genetic incompatibility. If Peter increases fat and reduces carbohydrates to reduce Lp(a)/small LDL, then LDL measures like LDL particle number, apoprotein B, and LDL cholesterol will increase. Paradoxically, sometimes small LDL particles will even increase in some genetically predisposed people.

If Peter decreases fat and increases carbohydrates, LDL particle number, apoprotein B, and LDL cholesterol will decrease, but the proportion of small LDL will increase and Lp(a) may increase.

Thankfully, such "genetic incompatibilities" are uncommon. In my large practice, for instance, I have about 5 such people.

The message: If you witness paradoxic responses that don't make sense or follow the usual pattern, e.g., reductions in LDL particle number, apoprotein B, and small LDL with reductions in their dietary triggers (i.e., carbohydrates, especially wheat), then consider a competing genetic trait such as Apo E4.

The folly of an RDA for vitamin D

9. January 2011 William Davis (26)
Tom is a 50-year old, 198-lb white male. At the start, his 25-hydroxy vitamin D level was 28.8 ng/ml in July. Tom supplements vitamin D, 2000 units per day, in gelcap form. Six months later in January (winter), Tom's 25-hydroxy vitamin D level: 67.4 ng/ml.

Jerry is another 50-year old white male with similar build and weight. Jerry's starting summer 25-hydroxy vitamin D level: 26.4 ng/ml. Jerry takes 12,000 units vitamin D per day, also in gelcap form. In winter, six months later, Jerry's 25-hydroxy vitamin D level: 63.2 ng/ml.

Two men, similar builds, similar body weight, both Caucasian, similar starting levels of 25-hydroxy vitamin D. Yet they have markedly different needs for vitamin D dose to achieve a similar level of 25-hydroxy vitamin D. Why?

It's unlikely to be due to variation in vitamin D supplement preparations, since I monitor vitamin D levels at least every 6 months and, even with changes in preparations, dose needs remain fairly constant.

The differences in this situation are likely genetically-determined. To my knowledge, however, the precise means by which genetic variation accounts for it has not been worked out.

This highlights the folly of specifying a one-size-fits-all Recommended Daily Allowance (RDA) for vitamin D. The variation in need can be incredible. While needs are partly determined by body size and proportion body fat (the bigger you are, the more you need), I've also seen 105 lb women require 14,000 units and 320-lb men require 1000 units to achieve the same level of 25-hydroxy vitamin D.

An RDA for everyone? Ridiculous. Vitamin D is an individual issue that must be addressed on a person-by-person basis.

Heart scan: Standard of care?

6. January 2011 William Davis (0)
If coronary disease is easy to detect by measuring coronary calcium, shouldn't this represent the standard of care?

In other words, if you've been seeing your doctor and he/she has been monitoring cholesterol levels and, inevitably, talks about statin drugs, then you have a heart attack, unstable angina, or die--yet never knew you had heart disease--isn't this negligence?

Coronary calcium, and thereby coronary atherosclerotic plaque, are markers for the disease itself. Unlike cholesterol, high blood pressure, etc., that represent risk factors for coronary atherosclerotic plaque, coronary calcium is a measure of total plaque: "soft" elements like lipid collections, necrotic tissue, fibrous tissue, as well as "hard" elements like calcium. Because calcium occupies 20% of total atherosclerotic plaque volume, it can be used as an indirect "dipstick" for total plaque.

So why isn't an unexpected heart attack, hospitalization for unstable heart symptions, emergency bypass, etc., not regarded as potential malpractice? These are not benign events, but potentially life-threatening.

The costs of doing drug business?

6. January 2011 William Davis (28)
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

4. January 2011 William Davis (9)
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

30. December 2010 William Davis (34)
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

27. December 2010 William Davis (17)
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.