High blood pressure vanquished

Heart Scan Blog reader, Eric, related his blood pressure success story to me:

I'm 34 and have been battling chronic hypertension (systolic 150-200, depending on my anxiety levels) even with multiple prescriptions for over a decade now. I've seen four different cardiologists, all stumped as to what is causing my hypertension. First, they suspected coarctation of my aorta [a constriction in the aorta], but an angiogram determined blood pressure readings were the same on both sides of the narrowing.

The second angiogram performed last year to determine if my coarct had worsened determined that it had not, but that my aorta had calcium build up. The cardiologist was stumped because he told me he hasn't seen calcium in a patient so young. Needless to say, this scared me to death, with my wife being pregnant with our first child. I asked if it could be reversed and he didn't know so he sent me to get a Berkeley lab.

The Berkeley came back with LDL 91, HDL 41, Triglycerides 73, CRP 4.1, vit D 26. The doctors weren't very knowledgeable about explaining to me what these meant and how I could correct the low vit D and high CRP. They told me to follow the low-fat diet recommended by Berkeley. Well I've already tried the DASH diet and didn't like how I felt or my energy levels, so I didn't transition.

I was at a loss until I encountered your blog and it was truly a gift. It was a refreshing feeling to meet a knowledgeable Dr. who knew what I was going through and seems to truly care about reversing calcium in the heart (something I never got from my any of my cardiologists). With your blog I have an appointment to get a heart scan here in CO and take that number along with my Berkeley results and join Track Your Plaque.

For the past 2 weeks I've been following your advice by taking a D3+K2 supplement with Omega3 Fish oil and avoiding all grain, wheat, sugar and I'm already down 4lbs to 223.5lbs at 6'5" tall and my blood pressure readings have been 128/54 and 129/60 the past 2 days! With your help I may not have the dark future my father had: dead at 48 with a massive heart attack.

Stay on the look out because I look forward to telling you how I'm one of your top calcium losers!

Eric, Colorado


Conventional medical care fails at so many levels for so many people. While Eric's doctors were busy contemplating the next angiogram, they were neglecting several crucial aspects of his health.

It's really not that tough. But it can mean doing the opposite of what conventional "wisdom" tell us.

DHEA and Lp(a)

DHEA supplementation is among my favorite ways to deal with the often-difficult lipoprotein(a), Lp(a).

DHEA is a testosterone-like adrenal hormone that declines with age, such that a typical 70-year old has blood levels around 10% that of a youthful person. DHEA is responsible for physical vigor, strength, libido, and stamina. It also keeps a lid on Lp(a).

While the effect is modest, DHEA is among the most consistent for obtaining reductions in Lp(a). A typical response would be a drop in Lp(a) from 200 nmol/L to 180 nmol/L, or 50 mg/dl to 42 mg/dl--not big responses, but very consistent responses. While there are plenty of non-responders to, say, testosterone (males), DHEA somehow escapes this inconsistency.

Rarely will DHEA be sufficient as a sole treatment for increased Lp(a), however. It is more helpful as an adjunct, e.g., to high-dose fish oil (now our number one strategy for Lp(a) control in the Track Your Plaque program), or niacin.

Because the "usual" 50 mg dose makes a lot of people bossy and aggressive, I now advise people to start with 10 mg. We then increase gradually over time to higher doses, provided the edginess and bossiness don't creep out.

The data documenting the Lp(a)-reducing effect of DHEA are limited, such as this University of Pennsylvania study, but in my real life experience in over 300 people with Lp(a), I can tell you it works.

And don't be scared by the horror stories of 10+ years ago when DHEA was thought to be a "fountain of youth," prompting some to take megadose DHEA of 1000-3000 mg per day. Like any hormone taken in supraphysiologic doses, weird stuff happens. In the case of DHEA, people become hyperaggressive, women grow mustaches and develop deep voices. DHEA doses used for Lp(a) are physiologic doses within the range ordinarily experienced by youthful humans.

No more cookies

Jeanne enjoyed her Christmas holidays. She especially liked sharing the cookies she made for her grandchildren, sneaking 2 or 3 every day over a couple of weeks. On top of this, she enjoyed the Christmas candy, egg nog, leftover stuffing and cranberry sauce, topped off with a night of nutritional debauchery on New Year's Eve.

Lipid panel in October:

Total cholesterol 146 mg/dl
LDL cholesterol 72 mg/dl
HDL cholesterol 64 mg/dl
Triglycerides 49 mg/dl

Lipid panel in early January:

Total cholesterol 229 mg/dl
LDL cholesterol 141 mg/dl
HDL cholesterol 59 mg/dl
Triglycerides 147 mg/dl


I call the holidays The Annual Wheat and Sugar Frenzy. It's the carbohydrates, especially those from products made of wheat and sucrose, that caused the marked shifts in Jeanne's lipid patterns. Let's take each parameter apart:

--Triglycerides go up due to de novo lipogenesis, liver conversion of carbohydrates into triglycerides. Triglycerides enter the bloodstream as VLDL particles which, in turn, interact with LDL and HDL.

--LDL goes up because carbohydrate exposure increases VLDL, followed by conversion to LDL. The triglyceride-rich LDL created is converted to small LDL particles. Had we measured small LDL changes in Jeanne, we likely would have measured something like an increase (by NMR) from 800 nmol/L to 1600 nmol/L, a carbohydrate effect.

--The increased VLDL also makes HDL triglyceride-rich, cause more rapid degradation of HDL particles. (It also makes them smaller, like LDL.) Given sufficient time (a few more months), HDL would drop into the 40's.

--Total cholesterol changes reflect the composite of the above numbers. (Total cholesterol = LDL cholesterol + HDL cholesterol + Trig/5) (Note that, as HDL drops, so will total cholesterol; that's why this value is worthless and should be ignored.)

So don't be surprised by the above distortions after a period of carbohydrate indulgence. Although your unwitting primary care doc will see such changes as opportunity for Lipitor, it is nothing more than the cascade of effects from a carbohydrate-driven distortion of lipoproteins.

How to become diabetic in 5 easy steps

If you would like to become diabetic in as short a time as possible, or if you have someone you don't like--ex-spouse, nasty neighbor, cranky mother-in-law--whose health you'd like to booby trap, then here's an easy-to-follow 5-step plan to make you or your target diabetic.


1) Cut your fat and eat healthy, whole grains--Yes, reduce satiety-inducing foods and replace the calories with appetite-increasing foods, such as whole grain bread, that skyrocket blood sugar higher than a candy bar.

2) Consume one or more servings of juice or soda per day--The fructose from the sucrose or high-fructose corn syrup will grow visceral fat and cultivate resistance to insulin.

3) Follow the Institute of Medicine's advice on vitamin D--Take no more than 600 units vitamin D per day. This will allow abnormal levels of insulin resistance to persist, driving up blood sugar, grow visceral fat, and allow abnormal inflammatory phenomena to persist.

4) Have a bowl of oatmeal or oat cereal every morning--Because oat products skyrocket blood sugar, the repeated high sugars will damage the pancreatic beta cells ("glucose toxicity"), eventually impairing pancreatic insulin production. (Entice your target even further: "Would you like a little honey with your oatmeal?") To make your diabetes-creating breakfast concoction even more effective, make the oatmeal using bottled water. Many popular bottled waters, like Coca Cola's Dasani or Pepsi's Aquafina, are filtered waters. This means they are devoid of magnesium, a mineral important for regulating insulin responses.

5) Take a diuretic (like hydrochlorothiazide, or HCTZ) or beta blocker (like metoprolol or atenolol) for blood pressure--Likelihood of diabetes increases 30% with these common blood pressure agents.

There you have it! Perhaps we should assemble a convenient do-it-yourself-at-home diabetes kit to help, complete with several servings of whole grain bread, a big bottle of cranberry juice, some 600 unit vitamin D tablets, a container of Irish oatmeal, and some nice bottled water.

Restaurant eating: A fructose landmine

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

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?

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

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

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?

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.
All posts by william-davis

Weight loss and blood pressure

Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise.

Blood pressure also shows a curious pattern that is largely dependent on age.

Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most.

How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop.

Why the age-dependent difference?

It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop.

But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.

"I lost 30 lbs and my triglycerides went . . . up?"

Brad needed to lose weight.

At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly.

He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise).

Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats.

Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years.

His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"

Yes, I had said that. But I was oversimplifying.

The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.

So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's.

Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.

In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.

I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it.

I call these changes "transitional" changes in lipids.

Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.

Divorce court for the doctor-patient relationship?

The doctor-patient relationship has gone sour.

This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:

Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.

Exploitation of trust, my observation that the enormous gap in heart disease prevention between the woefully ignorant (by necessity) level of sophistication of the primary care physician and the procedure-obsessed cardiologist leads to an exploitation of humans-for-heart-procedures because of the failure to institute genuine preventive efforts.

Bait and switch , a description of how a minor test or symptom can reap a bonanza of medical testing; a $20 "screening" test yields $10's of thousands in hospital procedures. If it were entirely due to the imprecision of medical testing and detection of disease, that might be forgivable. But it often is not: It has become utterly distorted by the profit model.



Lest you think that I am a kook ranting off in some backwoods corner (Milwaukee), here are the comments of New York Times' Health Editor Tara Parker-Pope in a series called Doctor and Patient, Now at Odds:

Lately I've been hearing a lot from patients who are frustrated, angry, and distrustful of doctors. Their feelings speak to a growing disconnect between doctors and patients and worries that drug companies, insurance rules, and hospital cost-cutting are influencing the care and advice that doctors provide.

Research shows that even among patients who like their personal physicians, there is a simmering distrust of the medical system and the doctors who work inside it.


(There's also a series of candid video interviews with people who echo these sentiments.)

There are a number of reasons for this increasing "disconnect," some of them articulated by Ms. Parker-Pope, others detailed in my blog posts.

The solutions, however, will not be found by advancing technology: the newest robotic surgery, a better defibrillator, a new statin drug, the next best chemotherapeutic agent. It will not be found by adding a new wing to the hospital. It will not be found by the reorganization of healthcare delivery achieved by converting primary care and specialty practice into an arm of hospital care. It will not be improved by employing "hospitalists." It will not emerge from legislation controlling insurance company practices. It certainly will not come from increasing marketing dollars spent by drug companies (who make $4 for every $1 spent on direct-to-consumer marketing).

The solutions will come from shifting the idea of care from a paternalistic, "I'm the doctor and I'll tell you what to do" approach, to the doctor-as-advocate-and-supporter of the patient. The physician should act as someone with a particular sort of expertise that can advise a patient.

But a caveat: The patient MUST be informed.

Proper information will not originate with the doctor. It will originate with internet-based information portals and tools that help you understand the issues, often with far greater depth than your doctor could ever provide. The physician needs to accept this role, one of advocate, adviser, but not of being in charge, not of viewing the patient as profit-center, not as an opponent in a power struggle.

Sadly, the last few years in online information portals has been dominated by the drug company-dominated websites like WebMD, nothing more than a deliverer of the conventional wisdom with nothing whatsoever aimed towards empowering patients in a self-directed healthcare model.

Some people call the emerging new empowered and information-armed patient Medicine 2.0. Unfortunately, Medicine 2.0 will first benefit the intellectual upper crust of Americans, the web-savvy and motivated to engage in health issues. But, give it 10 years, and we will witness the effects on an unprecedented broad scale. Part of the Information Age is acceleration of information dissemination. Imagine your children, facile with a computer mouse, posting comments on FaceBook, doing homework with Google and Wikipedia, now turning their attentions to health.

It will be a startling change.

In the meantime, be wary. Be empowered. Think increasingly about self-direction in your health.


In a comment to the Bait and switch post, Jennytoo offered an insightful response:

You are getting to the essence of the problem, and it's not just cardiology that is rife with what is, at bottom, malpractice.

There is little incentive for the profession as a whole to know anything about or promote prevention, and many incentives from hospitals, drug and insurance companies to stick with the status quo or to change it in their corporate favor. The formulaic, conventional statements purporting to be guidelines for prevention that are put out by various interest groups and in such publications as hospital-sponsored newsletters ("eat a 'balanced diet', avoid stress, etc.") are useless sops to the concept of prevention.

It is, and I fear is going to remain, up to motivated individuals, both physicians and patients, to reshape the system, and it's going to be a long frustrating struggle.

It's my personal conviction that if just 4 things were promoted to the public, and people actually practiced them, we could change the health profiles of the majority of people in this country for the better within two years or less. They are:

(1) education on and promotion of a true low-carbohydrate, whole foods, diet,
(2) measurement and supplementation of Vitamin D3,
(3) supplementation with DHA/EPA (found in Fish Oils), and
(4) measurement and supplementation of intracellular magnesium.

I am not a health professional, and others may want to add to this list, but I don't think any strong case can be made against any of the items. The wonderful and hopeful thing is that each of us can implement them ON OUR OWN, and thereby take charge of our own well-being. (The Life Extension Foundation is one organization which provides access to lab tests you can request on your own.)

If you have a physician who is willing and capable of being your partner, you are richly blessed, and that is the ideal we all should hope for. But in the more likely event that you do not have such a physician, and if your physician demonstrates little potential for becoming one, think about firing the one you have and finding another.

Sometimes we are forced by circumstances, particularly urgent ones, to deal with physicians who are not ideal, but the main impetus for change will come from us, the patients, and the expectations we communicate to our individual doctors. In the meantime, we can be self-reliant in our own prevention practices.


Wow. A woman after my own heart.

How much fish oil is enough?


This post just furthers this line of thinking out loud: How much fish oil is "enough"?

Observations over the last 30 years followed this path: If a little bit of omega-3 fatty acids from fish are beneficial in reducing cardiovascular events, and a moderate intake is even better, is even more better? When have we reached a plateau? When do adverse effects outweigh the benefits?

Some insight can be gained through studies that examined blood levels of omega-3s. Let's take a look at some data from 2002, a comparison of men dying from heart disease vs. controls in the Physicians' Health Study, Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death.

This is a table that shows the blood levels of various fatty acids Group with sudden death vs Control Group:




Several observations jump out:

--The total omega-3 blood content differed significantly, 4.82 vs 5.24% ("Total long-chain n-3 polyunsaturated")
--Total omega-6 content did not differ
--Arachidonic acid (AA) content did not differ
--Linolenic acid content did not differ (i.e., plant sourced omega-3)

The fact that neither omega-6 nor arachidonic acid content differed counters the argument that Simopoulos has made that the omega-6 to omega-3 ratio (intake, not blood levels) is what counts. It also argues against the EPA to AA ratio (and similar manipulations) that some have argued is important. In this study, only the omega-3 level itself made a difference; no ratio was necessary to distinguish sudden death victims vs controls.

Further, quartiles of omega-3 blood levels showed graded reductions of risk:




An omega-3 blood level of 6.87% conferred greatest risk reduction. Depending on the model of statistical analysis, risk reductions of up to 81-90% were observed. Wow.

Taken at face value, this study would argue that:

--An omega-3 fatty acid blood level of 6.87% (or greater?) is ideal
--The omega-3 fatty acid blood level stands alone as a predictor without resorting to any further manipulation of numbers, such as relating EPA and/or DHA to AA levels.

Of course, this is just one study, though an important one. It is also not a study based on any intervention, just an observational effort. But it does add to our understanding.


We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.

Omega-6 / omega-3 ratio

Most of us already know that the intake of omega-6 fatty acids in the American diet has gone overboard, much at the expense of the omega-3 fraction. This occurred as a result of the misguided advice of the 1970s and 1980s to eat polyunsaturated oils like corn, sunflower, and safflower, because of their presumed cholesterol-reducing properties compared to saturated fats. However, more recent examinations of this advice have suggested that the omega-6 fraction of oils present in polyunsaturated oils may amplify arachidonic acid and other inflammatory patterns despite the reduction in cholesterol (total and LDL).

Dr. Artemis Simopoulos of the Center for Genetics, Nutrition and Health in Washington, D.C. has written extensively on the role of omega-6 and omega-3 fatty acids in diet.

In a review entitled The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cadiovacular Disease and Other Chronic Disease , Dr. Simopoulos collects the following comparison of omega-6 to omega-3 ratios from various populations:


Paleolithic humans 0.79
Greece (prior to 1960) 1.00-2.00
Current Japan 4.00
Current India, rural 5-6.1
Current United Kindom and northern Europe 15.00
Current United States 16.74
Current India, urban 38-50

(The numbers refer to the ratio of omega-6 to omega-3 intake.)


If we believe the observations of Dr. Loren Cordain and others, while paleolithic man died of trauma and infectious diseases, they did not die of heart disease. Paleolithic human intake of omega-3 exceeded that of omega-6.

Likewise, the traditionally low cardiac event regions of the world like Japan and Greece have less omega-3 intake than Paleolithic man, but still many times more than the U.S. and U.K.

Worst of all with an enormous preponderance of omega-6 over omega-3 are urban Indians, who experience among the highest rates of heart disease in the world.

Just for perspective, let's assume you eat an 1800 calorie per day diet, of which 30% of calories come from fat. This would amount to 540 calories per day from fat. With 9 calories per gram of fat, this means that there are 60 grams, or 60,000 mg, of fat in your diet per day.

Paleolithic man has been found to have existed on a diet consisting of 21% of calories from fats. Again assuming an 1800 calorie per day diet, that comes to 42 grams of fat per day (42,000 mg).

If we were to try to recreate the Paleolithic fat composition of diet, we would ingest 21,000 mg of omega-3 fatty acids (EPA, DHA, linolenic acid) per day. Even recreating a Japanese experience with a 4:1 ratio, it would mean 8400 mg of omega-3 per day. (Curiously, this does not agree with all estimates of Japanese intake of omega-3s.)

No matter how you look at it, cultures with lower rates of cardiovascular disease take in greater--much greater--quantities of omega-3 fatty acids.

So don't complain about your six fish oil capsules (usually containing 6000 mg of total oil, 1800 mg omega-3s)!

Dr. Bernadine Healy on heart scans


A Heart Scan Blog reader brought the following tidbit to my attention.

Cardiologist and now writer for U.S. News and World Report, Dr. Bernadine Healy, wrote this editorial, a glowing endorsement of heart scans:

The approach is beautifully simple. Calcium accumulates in advanced plaques, so calcium visible in the heart's arteries indicates atherosclerosis. An exploding number of studies in the past few years have unequivocally shown that the calcium score predicts both heart attack and sudden death. As a generalization, patients with scores between 100 and 400 face three to four times the risk of a heart attack or death compared with others at the same age with a zero score. Over 400, that elevated risk more than doubles.

Most doctors rely instead on the Framingham calculator, which estimates a symptom-free person's risk of a heart attack in the next 10 years based on smoking history, blood pressure, cholesterol levels, sex, and age. It's available free online from the National Institutes of Health. Most people taking the test will have minimal or no coronary disease, though risk estimates over 9 percent should inspire vigorous preventive efforts. For some, however, coronary heart disease is sneaky, and Framingham will underestimate what lies ahead. Roughly half of those who suffer a major heart attack or sudden coronary death are symptom free. Calcium scores are additive to Framingham; they pick up the individual surprises by using X-ray vision to look inside the heart. No wonder insurance companies are scrambling to use coronary calcium scores—life insurers, that is.



Dr. Bernadine Healy is no small-time player. In addition to her academic credentials, she is former chief of the National Institutes of Health (the first woman to hold the influential post), former head of the American Red Cross, and former deputy director of the White House Office of Science and Technology Policy under the Reagan administration. An endorsement of CT heart scans, though written under the guise of a probing editorial, will do an enormous amount of good to overcome the hurdles in gaining wider acceptance of heart scans.

Those of us applying heart scans in everyday practice have long appreciated their enormous power to detect and track coronary plaque. Framingham scoring can't even touch the certainty and quantification provided by heart scans in day-to-day life. Hundreds of studies have validated their use, but they still suffer from lying in the shadows of the procedural bullies aiming to boost the number of heart catheterizations, angioplasties, stents, bypass surgeries.

Dr. Healy, a voice with great weight, not just a political figure but also a cardiologist and scientist, has done a great service to broadcast the message of heart scanning.

Mercury and fish oil

As time passes, the dose of fish oil advocated in the Track Your Plaque program is going upward.

While epidemiologic studies, like the Chicago Western Electric Study and the Nurses' Health Study suggest that decreases in mortality from heart disease begin by just eating fish a couple times per month, there are newer data that suggest greater quantities confer greater benefits.

In the last Heart Scan Blog post, I discussed the recently-released ERA JUMP Study that demonstrated a relationship between higher omega-3 fatty acid blood content and reduced quantities of carotid and coronary plaque. The JELIS Study demonstrated a 19% reduction in cardiovascular events when fish-consuming Japanese added 1800 mg of EPA (only).

However, the suggestion that increased quantities of fish oil potentially yield greater protection from heart attack and facilitate coronary plaque regression is also stirring up worries about mercury exposure. So I dug up a Heart Scan Blog post from a year ago that discussed this issue and reprint it here.


I often get questions about the mercury content in fish oil. I've even had patients come to the office saying their primary care doctor told them to stop fish oil to avoid mercury poisoning.

Manufacturers of fish oil also make claims that this product or that ("super-concentrated", "pharmaceutical grade", "purified", etc.) is purer or less contaminated than competitors' products. The manufacturers of the "drug" Omacor [now Lovaza], or prescription fish oil, have added to the confusion by suggesting that their product is the most pure of all, since it is the most concentrated of any fish oil preparation (900 mg EPA+DHA per capsule). They claim that "OMACOR is naturally derived through a unique, patented process that creates a highly concentrated, highly purified prescription medicine. By prescribing OMACOR® (omega-3-acid ethyl esters), a prescription omega-3, your doctor is giving you a concentrated and reliable omega-3. Each OMACOR capsule contains 90% omega-3 acids (84% EPA/DHA*). Nonprescription omega-3 dietary supplements typically contain only 13%-63% EPA/DHA."

How much truth is there in these concerns?

Let's go to the data published by the USDA, FDA, and several independent studies. Let's add to that the independent (and therefore presumably unbiased) analyses provided by Consumer Reports and Consumer Labs (www.consumerlab.com). How much mercury has been found in fish oil supplements?

None.

This is different from the mercury content of whole fish that you eat. Predatory fish that are at the top of the food chain and consume other fish and thereby concentrate organic methyl mercury, the toxic form of mercury. Thus, shark, swordfish, and King mackerel are higher in mercury than sardines, herring, and salmon.

The mercury content of fish oil capsules have little to do with the method of processing and much more with the animal source of oil. Fish oil is generally obtained from sardines, salmon, and cod, all low in mercury. Fish oil capsules are not prepared from swordfish or shark.

Thus, concerns about mercury from fish oil--regardless of brand--are generally unfounded, according to the best information we have. Eating whole fish--now that's another story for another time. But you and I can take our fish oil to reduce triglycerides, VLDL, IDL, small LDL, and heart attack risk without worrying about mercury.



I am not advocating ad libitum eating of fish. Sadly, this may be related to excessive accumulation of contaminants. I am suggesting that greater quantities of omega-3 fatty acids from relatively contaminant- and mercury-free fish oil capsules.

More on this in an upcoming webinar on the Track Your Plaque website: Fish Oil and the Track Your Plaque Program - Is More Better?

ERA JUMP: Omega-3 fatty acids and plaque


The results of the uniquely-constructed ERA JUMP Study were just released, a fascinating study of the relationship of omega-3 fatty acids to coronary and carotid plaque.

The study adds insight into why the Japanese experience only one third of the heart attacks of Americans, and why Japan occupies the bottom of the list for least heart attacks among all developed countries.

The Electron-Beam Tomography, Risk Factor Assessment Among Japanese and U.S. Men in the Post-World War II Birth Cohort Study (ERA JUMP), a collaborative U.S.-Japanese effort, compared three groups of men:

-- 281 Japanese men living in Japan
-- 306 non-Japanese men living in the U.S. (Pittsburgh, Pennsylvania)
-- 303 Japanese Americans (having both parents Japanese without “ethnic admixture”) living in Hawaii.

The last group represents a group that is genetically similar to the group in Japan, but exposed to an American diet and lifestyle.

Three main measures were compared:

-- Blood levels of omega-3 fatty acids, EPA and DHA)
-- Carotid intimal-medial thickness (CIMT, the thickness of the carotid artery lining that can serve as an index of body-wide atherosclerosis)
-- Coronary calcium (heart scan) scores.

Interestingly, at the start of the study, the Japanese men possessed an overall cardiovascular risk profile worse than the Americans: Though more slender (BMI 23.6), Japanese men were more likely to be smokers, alcohol drinkers, had more high blood pressure, and were less likely to take cholesterol medications. The Americans, conversely, although heavier (BMI 27.9), were less likely to be smokers and drinkers, and had a four-fold greater use of cholesterol medications.

The Japanese Americans were the most likely to be hypertensive, diabetic, with a similar proportion of overweight as the non-Japanese Americans.

Despite the overall greater heart disease risk for profile for Japanese men, compared to non-Japanese Americans they had 10% less CIMT. In addition, only 9.3% of Japanese men had abnormal coronary calcium scores vs. 26.1% of non-Japanese Americans. Japanese-Americans were the worst, however, with nearly 10% more CIMT than non-Japanese Americans and 31.4% with abnormal calcium scores.

The most intriguing finding of all was the fact that, of all the various groups and degrees of atherosclerosis, whether gauged via CIMT or coronary calcium scores, the blood level of omega-3 fatty acids was inversely related, i.e., the greater the omega-3 blood level, the less plaque by either measure was detected.

Japanese men had the highest omega-3 blood levels: twice that of the non-Japanese Americans. The Japanese-Americans had levels only slightly greater than non-Japanese Americans.

While other studies, like the GISSI Prevenzione study, have persuasively demonstrated that omega-3 fatty acids substantially reduce heart attack, a weak link in the omega-3 argument has been a study that links greater omega-3 intake with less atherosclerosis. The unique construction of the ERA JUMP Study, employing two groups with sharply different omega-3 intakes, very powerfully argues for the plaque-inhibiting effects of this fraction of fats.

How much omega-3 fatty acids do Japanese people eat? Estimates vary, depending on part of the country, coastal vs. inland, age, etc., but Japanese tend to ingest anywhere from 5 to 15-times more omega-3 fatty acids than Americans. The actual intake of omega-3 fatty acids (EPA +DHA) in Japanese ranges from 850 to 3100 mg per day.

Mediterranean diet and blood sugar


Data such as that from the Lyon Heart Study have demonstrated that a so-called Mediterranean diet substantially reduces risk for heart attack.

But there are aspects of the Mediterranean diet and lifestyle that are not entirely sorted out.

For instance, what specific component(s) of the diet provide the benefit? Is it olive oil and linolenic acid? Is it red wine? Is it the reduced exposure to processed snack foods that Americans are indundated with? Is it their more slender builds and greater tendency to walk? How about exposure to the Mediterranean sun? What about the inclusion of breads, since in the Track Your Plaque program I advocate elimination of wheat products for many abnormalities?

Anyway, here's a wonderfully thoughtful set of observations from Anna about her experiences traveling Italy, trying to understand the details of the Mediterranean diet while also trying to keep blood sugar under control.


I just returned from a two week stay in Italy, doing a bit of my own "Mediterranean Diet" experiments. When practical, we sought out food sources and places to eat that were typical for the local area, and tried as much as possible/practical to stay away from establishments that mostly catered to tourist tastes. I was really curious to see how the mythical "Mediterranean Diet" we Americans are urged to follow compared to the foods really consumed in Italy.

The first week, we stayed in a rural Tuscan farmhouse apartment (agriturismo), so many, if not most of our meals were prepared by me with ingredients I bought at the local grocery store (Coop) or the outdoor market in Siena. In addition, I purchased really fantastic free-range eggs from the farm where we were staying. (Between some language issues and seasonality, eggs and wine were what we could buy from them - though I was tantalized by the not-quite-ripe figs heavy on many trees). Mostly, our meals consisted of simple and easily prepared fresh fruits and vegetables, rustic cured meats (salami, proscuitto, pancetta, etc.) hand-sliced at the deli down the road, fresh sausages, various Italian cheeses, plus plenty of espresso. It was a bit disappointing to find underripe fruit & tomatoes as well as old green beans in the grocery stores, not to mention too many low fat and highly processed foods, but all over Europe the food supply is becoming more industrialized, more centralized, and homogenous, so I'm not too surprised that it happens even in Italy. But even with the smaller grocery store size, the amount of in-season produce was abundant, yet one still was better off shipping from the perimeter of the store, venturing into the aisles only for spices, olive oil, vinegar, coffee, etc. Without the knowledge of where to go and the language to really talk in depth about food with people, I wasn't able to find truly direct and local sources for as many foods as I would have liked, but still, we ate well enough!

The first week I maintained blood sugar levels very similar to those I get at home, because except for the Italian specialties, we ate much like we always do. A few rare exceptions to my normal BG tests were after indulging in locally made gelato or a evening limoncello cordial, but even then, the BG rise was relatively modest and to me, acceptable under the circumstance. Even with the gelato indulgences, it felt like I might have even lost a few pounds by the end of the first week and my FBG didn't rise much over 100.

The second week we stayed in two cities (Florence & Rome), and I didn't prepare any of my own food because I didn't have a kitchen/fridge. I found it impossible to get eggs anywhere for breakfast, and the tickets our hotels provided for a "continental" breakfast at a nearby café/bar was always for a coffee or hot chocolate drink and some sort of bread or roll (croissant, brioche, danish, etc.). At first I just paid extra for a plate of salami and cheese if that was available - or went to a small grocery store for some plain yogurt, but then I decided to go off low-carb and conduct a short term experiment, though I didn't consume nearly as many carbs as a typical Italian or tourist would.

So I breakfasted with a brioche roll or plain croissant for breakfast with my cappuccino, but unfortunately no additional butter was available. I didn't feel "full" enough with such a breakfast and I was usually starving an hour or two later. Additionally, when I ate the "continental" breakfast, I noticed immediate water retention - my ankles, lower legs, and knees looked like someone else's at the end of a day walking and sightseeing, swollen heavy. Exercising my feet and lower legs while waiting in lines or sitting didn't seem to help.

Food is much more expensive in Europe than in the US, and the declining US$ made everything especially expensive (not to mention the higher cost of dining out rather than cooking at home), so we tried to manage food costs by eating simple lunches at local take-away places, avoiding the corporate fast food chains. I was getting tired of salami/proscuitto & cheese plates, but the typical "quick" option was usually a panini (sandwich). At first I tried to find alternatives to paninis, but the available salads were designed for side dishes, not main meals and rarely had any protein, and the fillings of the expensive sandwiches were too skimpy to just eat without the bread. So I started to eat panini, although I sometimes removed as much as half of the bread (though it was nearly always very excellent quality pan toasted flatbreads or crusty baguette rolls, not sliced America bread). So of course, my post-prandial BGs rose, as did my FBG. I also found my hunger tended to come back much too soon and I think overall I ate more than usual in terms of volume.

Then we deviated from the "Italian" lunch foods and found a better midday meal option (quick, cheaper, and easier to customize for LC) - stopping at one of the numerous kebab shops and ordering a kebab plate with salad, hold the bread (not Italian, but still Mediterranean, I guess). I felt much better fueled on kebab plates (more filling and enough protein) than paninis, though I must say I still appreciated the taste of caprese paninis (slices of fresh mozzerella and tomato, basil leaves, mustard dressing on crusty, pan-toasted flat bread). If I followed my appetite, I could have eaten two caprese paninis.

We had some great evening dinners, at places also frequented by locals. This often was a fixed price dinner of several courses ("we feed you what we want you to eat"). Multi-course meals included house wine, and invariably consisted of antipasta (usually LC, such as a cold meat and cheese plate), pasta course (much smaller servings than typical US pasta dishes), main course plus some side vegetables, and dessert/coffee. These were often the best meals we experienced, full of local flavor and tradition (sometimes with a grandmotherly type doing the cooking), and definitely of very good quality, though we noticed the saltiness overall tended to be on the high side. I ate from every course, including some of the excellent bread (dipped in plenty of olive oil) and usually about half of the pasta served (2 oz dry?), plus about half of the dessert. After these meals I always ran BGs higher than usual, varying from moderately high (120-160 - at home I would consider this very high for me) to very high (over 180). By late in the week, my FBG was into the 115 range every morning (usually I can keep it 90-100 on LC food). Nearly everything that week was delicious, well-prepared food, but the high carb items definitely were not good for my BG control in the long run.

And most days I was doing plenty of walking, sprinting for the Metro subway trains, stair climbing (4th and 5/6th floor hotel rooms!), etc. but since I didn't have my usual housework to do, it probably wasn't too different from my usual exertion level.

So it was very interesting to experience the "Mediterranean Diet" first hand. Meats and cheeses were plentiful, fruits and vegetables played a much more minor role (main courses didn't come with vegetables other than what was in the sauce, but had to be ordered as additional items), but the overall carbs were decidedly too many. As I expected, it wasn't nearly as pasta-heavy as is portrayed in the US media/health press, but it is still full of too much grain and sugar, IMO. Low fat has become the norm in many dairy products, sadly, and if the grocery stores are any indication, modern families are gravitating towards highly processed, industrial foods. Sugar seems to be in everything (I quickly learned to order my caffe freddo con panno or latte sensa zuccero - iced coffee with cream or milk without sugar) after realizing that adding lots of sugar was the norm).

And, after several days of breakfasting at the café near our Rome hotel (where carbs were the only option in the morning), I learned that our very buff, muscular, very flat-stomached, café owner doesn't eat pasta (said as he proudly patted his 6 pack abs). I probably could have stuck closer to the carb intake I know works better for my BG control, but I figured if I was going to go off my LC way of eating and experiment, this was the time and place.

And yes, there were far fewer really obese people than in the US and lots of very slender people, but I could still see there were *plenty* of overweight, probably pre-diabetic and diabetic Italians (very visible problems with lower extremities, ranging from what looked like diabetic skin issues, walking problems, acanthosis nigricans, etc.). Older people do seem to be generally more fit than in the US (fit from everyday life, not exercise regimes), but there were plenty of "wheat bellies" on men old and young, even more young women with "muffin tops", and simply too many overweight children (very worrisome trend). So it may well be more the relaxed Italian way of living life (or a combination of other factors such as less air conditioning, strong family bonds, lots of sun, etc?) that keeps Italian CVD rates lower than the American rates, more than the mythical "Mediterranean diet".

Who is your doctor?


Primary care physicians are the initial entry point for healthcare for the majority of Americans.

Develop pneumonia; go to your family or internal medicine physician (internist) to be prescribed an antibiotic. Need your blood pressure or cholesterol checked? Develop a sore knee or swelling in your leg? Once again, go to your primary care physician.

Image courtesy Dedde'


Primary care physicians are a patient’s guide to a bewildering array of technology and specialists. If you require a specific diagnostic test or consultation with a specialist, your primary care physician will help you navigate through the maze, choosing the path that is best for you. He or she will order a chest x-ray for a cough and fever, provide vaccines to prevent flu or pneumococcal pneumonia, perform an annual physical. If you require hospitalization, your primary care physician will admit you. He or she will order diagnostic tests like MRI’s, ultrasounds, x-rays, and blood testing, usually performed in the hospital or a hospital-owned facility. If you require the services of a gastroenterologist, orthopedist, general surgeon, or neurologist, your primary care physician will refer you to the appropriate specialist.

That’s how it’s supposed to work, at least in principle. In fact, during the first eight decades of the 20th century, it did work that work way for the most part. Your primary care physician acted not just as a provider of healthcare, but as your advocate, someone who knew you and worked to protect your welfare. Your family doctor often knew your parents, maybe even delivered you at birth, and cared for your children. His children often went to the same schools as your children. He and his family lived in the same town and sometimes went to the same church.

That hardly happens any more. It’s more likely you got the name of your primary care physician from a doctor referral service provided by a hospital. Or you picked a name off a list provided by your health insurer. It’s also common to see one doctor, only to see another a year later. Two, three, or more different primary care physicians over a five-year period are common. Doctors come and go, since physician turnover in clinics and practices has been on the increase for years. Insurance companies frequently force policyholders to change doctors, requiring you to choose from a list.

The end result of this shuffling of primary care is increasing impersonality of the relationship. You probably don’t know your primary care physician outside of the 10-minute interaction you had six months ago. She probably never met your mother and will likely not care for your children. Two years from now, she will likely not be your doctor any more, replaced by someone else who obtains the details of your health from a chart. Your chart is more likely to be electronic, with the details of your health history listed in a checklist. There’s little room to detail the idiosyncrasies and quirks of your unique personality or health profile. Throw into this impersonal equation the fact that many doctors have become scared of patients because of potential for lawsuits, often over the most trivial of issues, or because of an error of oversight or misdiagnosis.

This flawed and impersonal system, though emotionally unsatisfying, can still work if each doctor who assumes a patient’s care maintains the ethic of putting health and welfare above all.

But what if your primary care physician is not just an advocate for your welfare, but is a representative of the hospital? What if there are hidden, unspoken financial incentives paid to your doctor to direct you to the hospital for diagnostic testing, hospitalization, and referral to specialists? If a headache becomes a $4800 MRI, or chest pain becomes a $4200 nuclear stress test, then a $14,000 heart catheterization, your primary care physician becomes the purveyor of far greater financial opportunity for the hospital. The entire interaction, founded on the proposition that your doctor actually cares about you, collapses in a heap of financially motivated testing and procedures. It appears to work, and you and your family can still obtain access to healthcare. The problem is that you’re likely to get too much of it.

This message has not been lost on the shrewd administrators at hospitals. Take a look at the ranks of primary care physicians who refer patients to some of your local hospitals. It is typical that a hospital system maintains several hundred primary care physicians on their payroll, all of whom are expected to refer patients to the hospital, cardiologists, and other proceduralists. Why so many?

Most primary care physicians today have signed contracts with a hospital. In other words, they are employees of the hospital. This practice is not unusual: the American Medical Association reported that 4 of 5 primary care physicians are now bound by such employment arrangements across the U.S. In effect, 80% of primary care physicians are legally bound by contract to direct patients to cardiologists who work at hospitals.

On top of contractual obligations, there are financial incentives for the volume of procedures that are generated as a result of referrals. The more procedures generated from an internist’s or family practitioner’s practice, the greater the end-of-year productivity bonus will be, not uncommonly totaling tens of thousands of dollars. Dr. Ted Phillips (not his real name, since he declined to allow me to use it) received a bonus check of $9,437 this year for his “productivity,” defined murkily as the return on specialist referrals. While the bonus may have helped him pay for his son’s college tuition, it clearly was a situation that made him acutely uncomfortable when asked.

Several primary care physicians are also quietly dismissed every year from the ranks of employed physicians for not maintaining a minimum flow of patients into the system.

Another hazardous point of entry: Many patients enter the hospital through the emergency room (ER). A patient in the emergency room is at his or her most vulnerable, seeking help for an urgent complaint and usually willing to accept whatever the ER physician advises. Hospitals know this. That’s why many systems insist that the ER physicians be employees of the hospital, with their practice habits subject to control. A patient goes to the ER with chest pain or breathlessness. The worst thing that can happen from a financial standpoint is for the patient to be evaluated and discharged. For this reason, a growing number of hospitals employ ER physicians, then proceed to legislate practice patterns. Consulting a cardiologist is strongly encouraged, since they generally provide access to the downstream revenue-producing procedures offered in the hospital. That way, what might have been a four hour, $2500 ER visit is converted into a $10,000 to $40,000 hospital stay, even when nothing was wrong in the first place. There are millions of people nationwide who have the hospital bills to prove it after being discharged with a diagnosis of indigestion.

Caveat emptor: Buyer beware.