Identical twins and the explosive influence of weight

A Track Your Plaque member, Eugene, brought this fascinating story to my attention.

Eugene has two nephews, identical twins aged 35 years. Despite their similar personalities and appearances, somehow these two drifted apart in weight with Steve outweighing Alfred by 30 lbs.

Eugene explains:

These guy's are big not, but overly fat. Just big. One is about 30 lbs heaver than the other. They live 2 blocks apart, they ate the same (together) meal the night before the blood work. Their mother is a type 2 diabetic with a heart condition. Steve does not eat as well as his twin, junk food and a lot of processed starches.


Their results:



LDL-Particle number
Alfred 900
Steve 2256

Small LDL-P
Alfred 400
Steve 1639

HDL-C
Alfred 44
Steve 36

Triglycerides
Alfred 85
Steve 355

Metabolic Syn.
Alfred no
Steve yes


Glucose

Fasting
Alfred 93
Steve 112

1hour
Alfred 134
Steve 206

2 hour
Alfred 105
Steve 172


Identical twins begin with the very same genetic background. As these two graphically illustrate, weight can have a profound influence in the genetically susceptible.

LDL particle number alone is 250% greater in the heavier twin. The dreaded small LDL particle is over 400% worse! Look also at the dramatic differences in blood sugar.

If you ever had any doubts about the importance of excess weight and nutrition, just remind yourself of this fascinating illustration.

Thanks, Eugene.

Low-fat diets raise triglycerides

Martin, a hospital employee, knowing that I fuss a great deal with lipids and lipoproteins, showed me his lipid panel because the result triggered a "panic value" for triglycerides at 267 mg/dl. He asked if he should go on a serious low-fat diet.

I asked Martin what he had for breakfast: a whole wheat bagel with no-added-sugar jam. Lunch: a turkey sub on whole grain bread, no mayonnaise. Snacks: baked chips, pretzels ("a low-fat snack!").

In years past, if person developed high triglycerides levels, a very low-fat diet was prescribed. Someone would come to the hospital, for instance, with abdominal pain from pancreatitis (an inflamed pancreas)due to the damaging effects of triglyceride levels >1000 mg/dl. For this reason, many people still believe that all instances of elevated triglycerides should be treated with a reduction in fat intake.

This is absolutely wrong. While a fat restriction may reduce triglycerides in genetically-programmed responses when triglycerides are >1000 mg/dl, lesser levels of high triglycerides of, say 250 or 300 mg/dl, do not respond to dietary fat restrictions as a sole strategy.

Yes, a reduction in unhealthy fats (saturated, trans, polyunsaturated) helps. But a reduction in fats of all sorts is not necessary and can, in fact, worsen the problem. We learned this lesson years ago with the Ornish diet and similar ultra low-fat approaches. When you reduce fat intake significantly to <10% of calories, triglycerides go way up. In those days, it wasn't uncommon to see triglycerides skyrocket past 200 or 300 mg/dl on these diets.

Why are triglycerides important? Triglycerides are an ingredient in creating the lipoproteins VLDL, IDL, small LDL. Elevated triglycerides trigger a drop in HDL, a shift towards small, ineffective HDL, and contribute to heightened inflammation. Higher triglycerides also tend to go hand in hand with lipoproteins that persist for extended periods (12-24 hours or longer) in the blood after a meal.

Triglycerides respond very nicely to a dramatic reduction in processed carbohydrates, especially wheat and corn. Of course, wheat is the bulk of the problem, since it has grown to occupy an enormous role in many people's diet, not uncommonly eaten 3,4, or 5 times per day in various forms, as it has in Martin's diet. Eliminating all sources of high-fructose corn syrup is also helpful, since high-fructose corn syrup shoots triglycerides way up. (Recall that high-fructose corn syrup is everywhere: ketchup, beer, low-fat or non-fat salad dressings, breads, fruit drinks, sports drinks, breakfast cereals, etc.)

Curiously, it is a fat that also powerfully reduces triglycerides in the form of fish oil. In the Track Your Plaque program, fish oil, taken at truly effective doses of 4000 mg per day or more (to provide at least 1200 mg EPA+DHA), is our number one choice after reduction of processed carbohydrates for reduction of high triglycerides.

The dreaded niacin "flush"

As most anybody who takes niacin knows, it can cause a hot flushed feeling over the chest and face that is generally harmless, though quite annoying.

Many doctors are frightened by this response and will warn patients off from niacin. Some people who take niacin are so annoyed that they find it intolerable.

However, a very simple maneuver can relieve the hot flush in over 90% of instances: Drink water. Let me explain.

I usually instruct patients to take niacin at dinnertime. That way, food slows absorption modestly. I also ask them to drink water with dinner. If the flush occurs after dinner (usually 30-60 minutes later), then drinking two 8-12 oz glasses of water immediately breaks the flush within 3 minutes in the great majority of people. It's quite dramatic.

Doing this around dinner (lunch works just as well) allows sufficient time to clear the excess water from your body before bedtime and spare you the aggravation of disrupted sleep to urinate. Drinking plenty of water works most of the time. Only an occasional person will need to take a 325 mg uncoated aspirin to more fully break the flush. I generally suggest that patients keep the uncoated aspirin in reserve if the water doesn't provide relief within a few minutes.

Thankfully, the intensity of the niacin flush lessens, often disappears, with chronic use.

Why do some people develop the flush and other don't? It is believed that some people metabolize niacin more rapidly to a compound called nicotinuric acid, a niacin metabolite that causes dilation (relaxation) of skin capillaries--thus the flush. The rapidity of converting niacin to nicotinuric acid is determined genetically.

An occasional person really struggles with niacin to the point of intolerance. However, on the positive side, these people may also be "hyper-responders" to niacin, i.e., they show exagerated benefits in raising HDL, reducing small LDL, etc., from small doses such as 250 mg per day.

If you experience the hot flush of niacin, think water to put out the fire.

A cure for pessimism?

Followers of the Track Your Plaque program know that we place great value on having an optimistic outlook. Not only are you more likely to be happy and successful in life, you are also far more likely to drop your CT heart scan score. Virtually everyone who has succeeded in dropping their heart scan score dramatically has been an optimist, including our most recent record holder who dropped his score an astounding 51%.

But what if you are a pessimist, someone who gripes and complains about everything, sees the bad in other people, blames others for anything and everything that goes wrong--yet you still desire to drop your heart scan score? Are you a lost cause? Should you just give up?

I don't think so. I will admit that, of all the hurdles we encounter in trying to purposefully stop or reduce heart scan scores, overcoming a pessimistic attitude is probably the toughest. Tougher than being overweight, maybe tougher than even Lp(a).

Perhaps there's a solution in two years of psychotherapy sessions with a counselor, or exploring unresolved childhood conflicts with a psychologist, or an antidepressant drug. Pessimism is, after all, a deeply-ingrained pattern of behavior, something that can't be changed just by suggesting it or simple self-realization.

The closest thing I know of to a quick and relatively easy solution for converting a pessimist to an optimist is very simple:

Do good things for other people.

Something peculiar happens to the pessimist when he/she starts to help others. They are less threatened by other people (since much griping is really fear in disguise), begin to see others as vulnerable creatures who could use their help rather than sources of annoyance, and a kinship with others is acquired.

Doing good things can mean giving blood, donating money to the Sierra Club or other charity, volunteering with the Boy Scouts, tipping the hard working waitress trying to pay for college more generously, paying compliments to people around you, helping a neighbor carry the groceries when you see him struggling, showing a child how to make a paper airplane . . .

Good deeds can take a million different forms. But it must involve you personally. It can't mean delegating a helpful activity to your spouse. You must also do it frequently, not just once a year. It doesn't have to cost money, it doesn't have to involve a lot of time (though your personal bodily involvement does yield the greatest return in optimism). These are things anyone can do and help make the world around you a little better.

If taking these small steps towards an optimistic attitude are too much for you, then I would worry that you are destined to fail in dropping your heart scan score.

(Lack of ) Quality of nutritional supplements

In my last post, I blogged about how we must not confuse marketing with truth. They are often two different things.

A patient I saw today was absolutely convinced that his fish oil was the best available in the world: purer, uncontaminated by mercury or pesticides--"not like that other crap on the shelves." I asked him how he knew this. "They say so," he proudly declared.

Do you recognize this? He fell for the marketing. While there may be some truth in the manufacturer's claims, you can't believe it from the mouth of the manufacturer. True judgements about quality and purity have to come from an independent source like Consumer Reports, Consumer Lab, or the FDA.

But the FDA doesn't regulate the quality and purity of nutritional supplements. On the positive side, this has allowed supplement manufacturers to keep costs down, not having to navigate arcane and complex regulatory restrictions.

On the negative side, a fair number of supplement manufacturers get away with 1) producing supplements that fail to contain the stated amounts of ingredients, occasionally containing none of the essential ingredient(s), 2) contain contaminants like lead, and 3) make extravagant and often unfounded claims like "superior", "more effective", and "purer". (DHEA, for instance, is a particular landmine of poor quality. I recently suggested that a patient take DHEA; despite consistently taking 50 mg of a specific brand for several months, the blood level of DHEA-S didn't budge one bit--there was likely little or none in the capsule.)

The Fanatic Cook at http://fanaticcook.blogspot.com has posted some very insightful discussions on this issue and the proposed FDA regulations of supplements. They're worth perusing.

I really wish regulation weren't necessary and that the industry could have policed itself. But it clearly has failed and perhaps federal oversight is not such a bad thing, as long as the FDA regulations restrict themselves to oversight over quality and purity and not to efficacy. It's the efficacy regulation that could hogtie innovation in supplement development.

Marketing and truth are not the same

I often remind people: Don't confuse marketing with the truth.

Today, I spent a total of probably an hour and a half dissuading patients that some crazed piece of marketing trying to sell them something was not the same as truth.

I spent approximately 40 minutes alone with a woman who was absolutely convinced that:

--Nattokinase would cure her of all heart disease. It does not. Despite the promising health benefits of natto and vitamin K2 supplementation, nattokinase is a scam with no basis in science nor logic.

--Niacin destroys your liver and homeopathic remedies are superior. Quite simply, homeopathy = quackery. No rational thinking scientist endorses the utter nonsense practiced in this strange and outrageous set of practices that requires you to suspend all reason.

--Sufficient vitamin D is obtainable through a "potent" multivitamin. I know of no multivitamin preparation that even begins to provide the dose of vitamin D that is actually required by adults, nor is it absorbed since these D preparations are powder based.

--Fish oil will poison you with mercury. Accordingly, one brand of fish oil claims to be the only safe form. Those of you following these posts, or the reports of the USDA and FDA, as well as the reports of Consumer Reports and Consumer Lab (www.consumerlab.com) know that, unlike fish itself, there is no mercury in fish oil capsules.

--All coronary atherosclerotic heart disease is caused by heavy metal poisoning. Thus chelation with EDTA represents a cure for heart disease.


People are inundated with marketing that promise extravagant cures, remove need for any medication, make you smarter, sexier, thinner, and on and on.

If you see a TV ad for Ford that says they make the best cars in the U.S., do you immediately run out and put a For Sale sign on your GM car and buy a Ford? No, of course not. You recognize the ad for what it is: marketing. It may be true, but a TV commercial is not enough to convince you.

Then why would an ad promising extraordinary cures for cancer or heart disease convince you that this is true? It should not. Marketing ads should only serve to alert you to the possibility of value or benefit, but should never-- never--stand alone as proof. Take marketing for what it is: marketing of a product or service, not a scientific report, not a factual report, not news.

Marketing is advertising. Period.

More on erectile dysfunction

Several facts on erectile dysfunction and coronary plaque:


If you have erectile dysfunction, there's at least a 50% chance you also have coronary plaque.

If you have coronary plaque by a CT heart scan, there's a 50% chance you have erectile dysfunction.

If you have symptomatic coronary disease (chest pains, breathlessness, prior heart attack), there's a 90% chance you also have erectile dysfunction.


Coronary disease is characterized by a dysfunctional state of the "endothelium", or inner lining of the coronary arteries. Erectile dysfunction is characterized by dysfunction of the endothelium of the penile circulation. Same phenomenon, different territories. (There are other differences, of course, but the two conditions share this fundamental phenomenon.)


If you have any doubts about the physiologic effects of the supplement, l-arginine, just give it a try if you have erectile dysfunction. The erection enhancing effects alone should convince you that a genuine artery-dilating effect is exerted by this very powerful nutritional supplement.

If l-arginine fails by itself to restore full erectile capacity, there are additional strategies, both nutritional and medical, that you can consider.

Our newest Track Your Plaque Special Report on erectile dysfunction is coming out any day now.

High LDL cholesterol--only

As a sequel to my last post, just how often can we blame an isolated high LDL cholesterol as the cause of coronary plaque and a heart scan score?

In other words, how often does someone prove to have only LDL cholesterol as the cause of a heart scan score . . . and nothing else? No low HDL, small LDL, lipoprotein(a), a post-prandial (after-eating) intermediate-density lipoprotein, inflammatory responses, phospholipase A2, high triglycerides, vitamin D deficiency, etc.

Rarely. In fact, I can truly count the number of people who have only LDL cholesterol as their sole cause of coronary atherosclerotic plaque on one hand. It is really an infrequent situation.

Far more commonly, people have 5, 6, 7 or more reasons for coronary plaque.

Thus, the idea that a statin drug to reduce LDL will cure heart disease is completely folly. It does happen--but rarely. I think I've seen it happen twice. Much more commonly, a program that addresses all the causes of coronary plaque yields far superior benefits.

In my view, an effort to identify all the causes is relatively easy, makes far better sense, and provides you much greater assurance that you will succeed in conquering heart disease and removing its evil influence from your life.

Heart disease = statin deficiency

Judging from the conversations I hear from colleagues, what I hear from the media, and drug company advertising, you'd think that heart disease has one cause--a deficiency of statin drugs.

As their thinking goes, if you have coronary disease, you need a statin drug (Lipitor, Zocor, Crestor, pravachol, etc.). If you have progressive coronary disease, you need more statin drug. If you have a heart attack while on a statin drug, you need even more statin drug.

Some "experts" have even proposed that we do away with LDL cholesterol and we just give everybody a statin drug at high doses.

Does this make any sense to you?

Doesn't it make better sense that if someone has progressive heart disease or heart attack while on a statin drug, then target the other causes largely unaffected by a statin drug? Perhaps if LDL cholesterol remains high on the statin drug, then a higher dose is justified. But more often than not, it's not a high LDL on statin drugs that responsible, it's other causes. And there's many of them: low HDL, VLDL, IDL, Lp(a), deficiency of omega-3 fatty acids, inflammatory processes, vitamin D deficiency, among others. (An important exception to this is when the conventional calculated LDL substantially underestimates true LDL as measured by LDL particle number by NMR, apoprotein B, or 'direct' LDL.)

Imagine someone has pneumonia. After 2 weeks of antibiotics, they are only partly better. The solution: a higher dose of the same antibiotic--but never question if it was the right antibiotic in the first place. That's what is going on in heart disease.

The doctors have been brainwashed into believing this $22 billion dollar per year bit of propaganda. The drug companies actively try to recruit the public into believing the same. Don't fall for it.

The statin drugs do indeed have a role. But they are not the complete answer. More of the same when disease progresses makes no sense at all.

Fish oil and mercury

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, 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.

Kitchen sink approach for Lp(a)


Lipoprotein(a), Lp(a), can be a tough nut to crack.

Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern.

I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.

Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others.

Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a).

Even with this multi-agent approach, not everybody gains control over Lp(a).

That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).

While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on.

Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency.

There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years.

Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.

Making Dr. Friedewald an honest man

Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)

In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day.

By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.

So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc.

Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction.

Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number.

It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.

The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug.

As I've warned many times before: Beware the Friedewald calculated LDL.

Some basic vitamin D issues

The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

I think it is important to stress that vitamin D supplementation needs to be continued long term.

I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times.


Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking?

If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life.


Twinb asked:

How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?

We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level.


Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level.


Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests?

Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute.


Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)

Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.

“How much vitamin D should I take?”

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong.

The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”

Utter nonsense.

The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach.

Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child.

It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors.

It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place.

As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized.

Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t.

Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.)

With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody.

Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved.

Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined.

But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)

Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized.

There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level.

Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period.

Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it.

I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor.

If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.)

So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)

You probably don't take enough fish oil

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:


Zero--I don't take any
17 (7%) of respondents

Less than 1000 mg per day
24 (10%) of respondents

1000-2000 mg per day
91 (38%) of respondents

2000-3000 mg per day
44 (18%) of respondents

3000-4000 mg per day
40 (16%) of respondents

More than 4000 mg per day
20 (8%) of respondents



Based on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more.

Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans.

But what dose is sufficient? What dose is ideal?

Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.)

If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary.

But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque?

This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:

--The Inuits (aka Eskimos) of Greenland and northern Canada
--The Japanese
--The Bantus of Tanzania who live along Nyasa Lake

All three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)).

The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids.

I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change.

We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change.

As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.

Vitamin D and HDL

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies


At first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduce
processed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL.

Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke.

Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so.

Add niacin, HDL increases another 5-10 mg/dl.

Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great.

Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl.

The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl.

Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude.

Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation.

Why? How?

That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.

An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years?

Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)

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.