CHAPTER 7

HELP YOUR HEART WITH THESE SUPPLEMENTS

ASK YOUR TYPICAL MAINSTREAM DOCTOR ABOUT NUTRITIONAL SUPPLEMENTS and the first thing you’re likely to hear is this: “There’s no good research showing they work.” Both of us have heard this refrain time and time again when we discuss nutritional medicine with our more conservative colleagues.

It’s not true.

You or your doctor can go online to the National Institute of Medicine’s library (www.pubmed.com), enter into the search box the name of virtually any vitamin or herb you can think of, and, depending on what you choose, hundreds to thousands of citations will pop up. So the problem isn’t an absence of research.

The problem is twofold. One, the conventional training of medical doctors in this country is highly biased toward pharmaceuticals. From the time they enter med school, doctors are courted by the pharmaceutical companies in myriad ways, some subtle, some not so subtle. Free lunches, symposiums, honorariums, consulting and lecturing contracts, vacations, perky pharmaceutical reps showing up at offices with the latest studies that show their products in a favorable light, free samples, and pens and prescription pads bearing the company’s name—all create a culture in which pharmaceuticals are the first choice in any treatment plan. (Most docs will tell you these practices have no influence on them or what they choose to prescribe, but the research tells a very different story.¹)

The second part of the problem is that much of the research on vitamins flies beneath the radar. Your overworked doctor barely has time to scan the abstracts of the New England Journal of Medicine every month, let alone dig deeply into the hundreds of studies that are published every year on vitamins and nutrients in journals like the American Journal of Clinical Nutrition. The vast majority of doctors in this country get no training whatsoever in nutrition, and those who do receive only the most rudimentary and superficial introduction to the subject. Put this together with the built-in medical school bias in favor of patent medicines, and it’s easy to see why doctors often fail to think of natural substances as legitimate tools that can help keep people healthy.

Let’s be clear. Conventional medicine is simply terrific at keeping people alive in emergencies. Both of us know that if we were to be in a car accident, we wouldn’t want the ambulance rushing us to the nearest herbalist’s office. We’d want to go to the emergency room of the best hospital we could find. But as good as conventional medicine is at treating people in acute situations, it’s astonishingly bad at overall preventive care. It’s great at keeping your heart beating if you’ve just had a heart attack. It’s not nearly as good at keeping your heart healthy for the long run and keeping you, the heart’s owner, out of the hospital in the first place.

The supplements listed in this chapter are some of the superstars for heart health that Dr. Sinatra uses in his practice (as he has for decades) and that Dr. Jonny has recommended to clients and written about extensively in his books and newsletters. Neither of us is saying you should just throw out your prescriptions and start randomly taking vitamins. But we are saying that natural substances such as vitamins, antioxidants, omega-3 fats, and many of the thousands of compounds found in foods may affect the health of the heart in an even more profound way than many of the medicines routinely prescribed as the first order of business.

Even if you’re already on medication, nutritional supplements can still improve your health. In the case of coenzyme Q₁₀ (CoQ₁₀), for example, supplementation is an absolute must if you’re on a statin drug (more on that in a moment). Magnesium is often used in conjunction with blood sugar drugs such as metformin (Glucophage) or blood pressure medications such as beta blockers. And virtually everyone needs a little help in reducing oxidation and inflammation, two of the most important drivers in the development of heart disease. Omega-3 fatty acids, for example, can be used by just about anyone, whether he or she is on medication or not (check with your doctor for any possible contraindications, such as right before going into surgery).

The following list is far from exhaustive, but it will give you a good idea of how you can use supplements to keep your heart healthy, either alone or, in some cases, as an adjunct to conventional therapy.

COENZYME Q₁₀: THE SPARK OF LIFE

Coenzyme Q₁₀ is a vitamin-like substance found throughout the body and made in every cell. Among the many important things it does, CoQ₁₀ helps create energy from fuel (food) in the human body, just as a spark plug creates energy from fuel (gasoline) in a car.

A CoQ₁₀ deficiency affects your heart as profoundly as a calcium deficiency would affect your bones. We create less of it as we age, making it all the more important to supplement with CoQ₁₀ as we grow older.

Here’s how it works: Your body uses a molecule called adenosine triphosphate, or ATP, as a source of energy (which is why ATP is nicknamed “the energy molecule”). Much like gasoline is the fuel that allows you to actually drive a car to any of a million destinations, ATP is the fuel that allows your body to perform any of a million activities, ranging from cellular metabolism to doing bench presses to dancing the tango. The body makes ATP by stripping electrons—tiny subatomic particles that carry a negative electrical charge—from food and then delivering those electrons to oxygen, which is an electron receptor. CoQ₁₀ is one of the carriers of these electrons, so it essentially helps the cells use oxygen and create more energy. Bottom line: CoQ₁₀ has the ability to increase the body’s production of the energy molecule ATP, and this is a very good thing indeed.

Just as a gasoline engine can’t work without spark plugs, the human body can’t work without CoQ₁₀. It’s an essential component of the mitochondria, which is command central for the production of cellular energy (ATP). Not coincidentally, the heart is one of the two organs where the most CoQ₁₀ is concentrated (the other being the liver). The heart never sleeps, and it never takes a vacation. It beats more than one hundred thousand times a day, making it one of the most metabolically active tissues in the body, so it’s very dependent on the energy-generating power of CoQ₁₀.

A CoQ₁₀ deficiency affects your heart as profoundly as a calcium deficiency would affect your bones. We create less of it as we age, making it all the more important to supplement with CoQ₁₀ as we grow older. (Although it’s present in food, the only foods that have any CoQ₁₀ to speak of are organ meats such as heart and liver. It’s also easily destroyed by too much heat or overcooking.)

As we’ve said, one of the biggest problems with statin drugs is that they significantly deplete CoQ₁₀ levels. You may recall from the previous chapter on statins that the same pathway that produces cholesterol (the mevalonate pathway) also produces CoQ₁₀, so when you block that pathway at its virtual starting gate (as statin drugs do), you not only reduce the body’s ability to make cholesterol but you also interfere with its ability to make CoQ₁₀.

We’ve said this before, but in case you missed it the first time, it’s important enough to repeat: If you are on a statin drug you must, repeat must, supplement with CoQ₁₀. We recommend at least 100 mg twice a day.

But CoQ₁₀ isn’t just essential for those on statin drugs. We believe it’s essential for everyone else as well, and especially for anyone at risk for heart disease.

CoQ₁₀ has been approved in Japan as a prescription drug for congestive heart failure since 1974. And even in the United States, the benefits of CoQ₁₀ for the heart have been well known since at least the mid-1980s. A study published in the Proceedings of the National Academy of Sciences of the United States of America in 1985 gave either CoQ₁₀ or a placebo to two groups of patients having class III or class IV cardiomyopathy according to the definitions put forth by the New York Heart Association (NYHA).2 These are seriously ill folks. Class III patients have marked limitation in activity because of symptoms and can basically only be comfortable at rest or with minimal activity; class IV patients have severe limitations and experience symptoms even while resting. (Most class IV patients are bedbound.)

So what happened when these very sick patients were given CoQ₁₀? Here’s how the researchers themselves summarized the results: “These patients, steadily worsening and expected to die within two years under conventional therapy, generally showed an extraordinary clinical improvement, indicating that CoQ₁₀ therapy might extend the lives of such patients. This improvement could be due to correction of a myocardial deficiency of CoQ₁₀ and to enhanced synthesis of CoQ₁₀-requiring enzymes.”³

Another study that lasted six years and was published in 1990 looked at 143 patients, 98 percent of whom were in the same two classes as the patients in the 1985 study.⁴ The participants were given 100 mg of CoQ₁₀ (orally), in addition to being treated in their conventional medical program. Eighty-five percent of the patients improved by one or two NYHA classes, and there was no positive evidence of toxicity or intolerance. “CoQ₁₀ is safe and effective long-term therapy for cardiomyopathy,” the study authors concluded.

CoQ₁₀ also has the ability to reduce blood pressure. A recent meta-analysis of CoQ₁₀ in the treatment of high blood pressure reviewed twelve different clinical trials and found that across the board patients who received CoQ₁₀ supplementation had significant reductions in blood pressure compared to control subjects who didn’t receive supplemention.⁵ It’s no wonder that several studies have demonstrated a strong correlation between severity of heart disease and severity of CoQ₁₀ deficiency.⁶

You might recall that oxidative damage (oxidation) is one of the four major culprits in heart disease, and you might also remember that cholesterol in the body is never a problem until it becomes oxidized. It’s only this oxidized cholesterol—specifically, pattern B LDL cholesterol—that is a problem, because pattern B LDL molecules are the ones that adhere to the cell walls and initiate or accelerate the process of inflammation. Why do we mention that here? Simple. CoQ₁₀ is a powerful antioxidant, inhibiting oxidative damage to LDL cholesterol and thus helping to prevent cholesterol from becoming a “problem” in the first place. It’s far smarter to prevent LDL from getting damaged and sticky in the first place than to use a sledgehammer pharmaceutical to reduce LDL as much as possible!

WHAT YOU NEED TO KNOW

• Coenzyme Q₁₀ (CoQ₁₀) is a kind of “energy fuel” for the heart.

• Statins deplete CoQ₁₀; supplementation is an absolute necessity if you’re on a statin drug, and it is a very good idea even if you’re not.

• D-ribose is one of the components of the energy molecule ATP, which the body uses to power all activity.

• L-carnitine supplementation after a heart attack increases survival rate and makes it less likely you’ll suffer a second heart attack.

• Magnesium relaxes the artery walls, reduces blood pressure, and makes it easier for the heart to pump blood and for the blood to flow freely.

• Niacin will lower both triglycerides and the “bad” kind of LDL cholesterol. It also reduces a toxic substance called lipoprotein(a)—Lp(a) for short—and raises HDL. Don’t use the time-release kind.

• Omega-3s—especially from fish—lower the death rate from heart disease. They also lower triglycerides, resting heart rate, and blood pressure.

• Omega-3s are highly anti-inflammatory.

• At least twenty-eight clinical trials in humans show that pantothenic acid (vitamin B₅) produces positive changes in triglycerides and LDL cholesterol. It also increases HDL.

• Nattokinase and lumbrokinase are natural “clot busters.”

• Other supplements worth considering include vitamin C, curcumin, resveratrol, and cocoa flavanols.

Coenzyme Q₁₀ and vitamin E have a strange, almost symbiotic relationship. In rats given supplemental vitamin E, increases in blood levels of CoQ₁₀ were observed; in baboons given supplemental CoQ₁₀, the anti-inflammatory effects of vitamin E were increased; and in one study, CoQ₁₀ plus vitamin E actually lowered C-reactive protein (CRP), a systemic measure of inflammation. We think it’s wise to make sure you’re getting about 200 IUs or so of vitamin E a day (from mixed tocopherols with a high gamma vitamin E formula) in addition to your CoQ₁₀ supplement. (But read the section on vitamin E, “The Good, the Bad, and the Ugly,” first!)

D-RIBOSE: THE MISSING LINK

D-ribose, a five-carbon sugar, is one of the components of ATP, the energy molecule the body uses to power all activities. Without D-ribose, there would be no ATP; without ATP, there would be no energy.

Both CoQ₁₀ and the nutritional supplement L-carnitine help facilitate the process by which the body manufactures ATP. Metaphorically speaking, they act like little elves, shuttling the material needed to make ATP to the factories where it’s made, resulting in more efficient production of this important energy molecule. CoQ₁₀ and L-carnitine can be said to function like very efficient trucks transporting building materials to the factories where stuff actually gets built, but D-ribose is one of the actual building materials. A shortage of D-ribose means a shortage of ATP, and a shortage of ATP, especially in the heart, is bad news indeed.

D-ribose is synthesized in every cell in the body, but only slowly and to varying degrees depending on the tissue. Tissues such as the liver, adrenal cortex, and adipose tissue make plenty of D-ribose because they produce chemical compounds used to synthesize fatty acids and steroids, which are in turn used to make hormones.

But molecules of D-ribose made by these tissues are the opposite of rollover minutes on your cell phone—they have to be used right then and there and can’t be “transferred” to other tissues that might need them, such as the heart. The heart, as well as the skeletal muscles and brain, can only make enough ribose for their day-to-day needs. They have no D-ribose saving account. When the cells of the heart, for example, encounter a stressor such as oxygen deprivation, they lack the metabolic machinery needed to quickly whip up some badly needed D-ribose ribose. Tissues that are stressed because they don’t get enough blood flow or oxygen can’t make enough D-ribose to replace lost energy quickly. And when oxygen or blood flow deficits are chronic—as in heart disease—tissues can never make enough D-ribose, and cellular energy levels are constantly depleted.

The D-ribose connection to cardiac function was first discovered by the physiologist Heinz-Gerd Zimmer at the University of Munich. In 1973, Zimmer reported that energy-starved hearts would recover much faster if D-ribose was given prior to or immediately following ischemia (an insufficient supply of blood to the heart, usually as a result of blockage). Five years later, Zimmer demonstrated that the energy-draining effects of certain drugs used to make the heart beat stronger (called inotropic agents) could be significantly lessened if D-ribose was given along with the drugs.

The most important finding from Zimmer’s research was that D-ribose plays an enormous part in both energy restoration and the return of normal diastolic cardiac function. (Diastolic dysfunction is basically a kind of heart failure.) One 1992 clinical study from Zimmer’s group showed that administering D-ribose to patients with severe but stable coronary artery disease increased their ability to do exercise and delayed the onset of moderate angina (chest pain). Since then, the benefits of D-ribose have been reported for heart failure, cardiac surgery recovery, restoration of energy to stressed skeletal muscles, and control of free radical formation in tissues that have been deprived of oxygen.

Here’s one dramatic story from Dr. Sinatra’s practice that illustrates the almost miraculous power of D-ribose supplementation to improve the quality of life of cardiac patients:

Dr. Sinatra: The Case of Louis and D-Ribose

Louis came to my office suffering from severe coronary artery disease. He had been previously treated by having a stent placed in a major coronary artery, but he still had severe blockage in a small arterial branch that was difficult to dilate with a stent and next to impossible to bypass with surgery. He had what’s called refractory angina, which means he experienced chest pain even with normal activities such as walking across a room. He’d also feel chest pain anytime he had even mild emotional stress. Louis had visited a number of cardiologists for his heart problem and had been placed on a number of common heart drugs, but his problems persisted.

When Louis came to my office I noticed high levels of uric acid in his blood, indicating faulty ATP metabolism. At the time, he was already taking L-carnitine and CoQ₁₀ at “maintenance doses.” Realizing that it would help him enormously if he could build up his ATP stores, I immediately recommended D-ribose as well as increased doses of L-carnitine and CoQ₁₀. In just a few short days, Louis showed remarkable improvement. His son-in-law, a dentist, called me a few days later and reported, “You fixed Louis!”

An adequate dose of D-ribose usually results in symptom improvement very quickly, sometimes within days, as in Louis’s case. If initial response is poor, the dose should be increased to 5 g (1 teaspoon) three times a day. Logically, those who are the sickest and the most energy depleted will notice the most improvement in the quickest time.

Despite accumulating scientific evidence of the benefit of D-ribose, very few physicians in the United States have even heard of it outside of their first-year med school biochemistry class. Fewer still recommend it to their patients. Those who are familiar with it have the wonderful gratification of seeing it help patients on a regular basis.

Although the optimal level of D-ribose supplementation will differ depending on the person and the particular condition, here are some good recommended starting points for supplementation:

• 5 g daily for cardiovascular prevention, for athletes on maintenance, and for healthy people who engage in strenuous activities or hard-core workouts

• 10 to 15 g daily for most patients with heart failure, ischemic cardiovascular disease, or peripheral vascular disease; for individuals recovering from heart attacks or heart surgery; for treatment of stable angina; and for athletes who engage in chronic bouts of high-intensity exercise

• 15 to 20 g daily for patients with advanced heart failure, dilated cardiomyopathy, or frequent angina; for individuals awaiting heart transplant; and for individuals with severe fibromyalgia, muscle cramps, or neuromuscular disease

Reported side effects are minimal and infrequent, and there are no known adverse drug or nutritional interactions associated with D-ribose use. The toxicology and safety of D-ribose have been exhaustively studied, and the supplement is 100 percent safe when taken as directed. (Thousands of patients have taken D-ribose at doses of up to 60 g a day with minimal, if any, side effects.)

However, even though there are no known contraindications for supplementation with D-ribose, we recommend that pregnant women, nursing mothers, and very young children refrain from taking D-ribose simply because there is not enough research on using it in these populations.

L-CARNITINE: THE SHUTTLE BUS FOR FATTY ACIDS

As previously stated, the best way to conceptualize L-carnitine is to think of it as a transportation system. It acts as a kind of shuttle bus, loading up fatty acids and transporting them into tiny structures within each cell called mitochondria, where they can be burned for energy. Because the heart gets 60 percent of its energy from fat, it’s very important that the body has enough L-carnitine to shuttle the fatty acids into the heart’s muscle cells.

Studies of patients being treated for various forms of cardiovascular disease provide the strongest evidence for the benefit of L-carnitine supplementation. One study showed that people who took L-carnitine supplements after suffering heart attacks had significantly lower mortality rates compared to those of a control group (1.2 percent of the L-carnitine takers died versus 12.5 percent of the subjects in the control group).7 One randomized, placebo-controlled study divided eighty heart failure patients into two groups. One group received 2 g of L-carnitine a day, and the other group received a placebo. There was a significantly higher three-year survival rate in the group receiving L-carnitine.⁸

L-carnitine improves the ability of those with angina to exercise without chest pain.⁹ In one study, the walking capacity of patients with intermittent claudication—a painful cramping sensation in the muscles of the legs because of a decreased oxygen supply—improved significantly when they were given oral L-carnitine. In another study, patients with peripheral arterial disease of the legs were able to increase their walking distance by 98 meters when they supplemented with L-carnitine; they were able to walk almost twice as far as those who were given a placebo. Further, congestive heart failure patients have experienced an increase in exercise endurance on only 900 mg of L-carnitine a day.

And if that were not enough to establish L-carnitine’s bonafides, it has been shown to be a powerful cardio-protective antioxidant. One paper published in the International Journal of Cardiology found that L-carnitine had a direct stimulatory effect on two important oxidative stress–related compounds (HO-1 and ecNOS). Both of these markers have antioxidant, antiproliferative (meaning they have an inhibitory effect on tumor cells), and anti-inflammatory properties, so ratcheting up their activity a notch is a very good thing indeed. The researchers concluded that this action of L-carnitine “would be expected to protect from oxidative stress related to cardiovascular and myocardial damage.”10

Dr. Sinatra: L-Carnitine and CoQ₁₀

Eighty-five percent of my patients with congestive heart failure have improved significantly on CoQ₁₀. But I was concerned about the 15 percent who, despite supplementation with CoQ₁₀, still had symptoms that severely compromised their quality of life.

These folks were supplementing with CoQ₁₀ and had excellent blood levels to show for it, typically 3.5 ug/mL or higher (the normal level of CoQ₁₀ is 0.5 to 1.5 ug/mL.) Nonetheless, these folks seemed to be unable to utilize what was in their own bodies.

As I read more about L-carnitine, I came to see that it might work in synergy with coenzyme Q₁₀, stoking the fire in the ATP production phase of the Krebs cycle (a sequence of reactions by which living cells generate energy). I finally got comfortable enough to recommend to some of my worrisome patients that they give it a try in combination with CoQ₁₀, and wow, what a difference!

These treatment-resistant folks came in with better color, breathed easier, and walked around the office with minimal difficulty. I was genuinely amazed. It was as if the L-carnitine provided a battery, working perfectly with the coenzyme Q₁₀.

The bottom line is that the heart is the most metabolically active tissue in the body, and thus it requires a huge and constant amount of energy molecules, or ATPs.

Remember, the heart has to pump sixty to one hundred times a minute, twenty-four hours a day, for years and years with no time off for good behavior! Cardiac muscle cells burn fats for fuel, so the heart is especially vulnerable to even subtle deficiencies in the factors contributing to ATP supply: coenzyme Q₁₀, D-ribose, and L-carnitine.

These nutrients make up three of what Dr. Sinatra calls the “Awesome Foursome” in metabolic cardiology. Now let’s introduce the fourth.

MAGNESIUM: THE GREAT RELAXER

Dr. Robert Atkins once referred to magnesium as a “natural calcium channel blocker,” and he was 100 percent correct. A few paragraphs from now, you’ll understand just why magnesium’s ability to block the channels by which calcium gets into the cells is so important for the health of your heart.

Recent research strongly suggests that calcium in the heart can be a huge problem. One meta-analysis examined fifteen eligible trials with the objective of investigating the relationship between calcium supplements and cardiovascular disease. The researchers concluded that calcium supplements (administered without vitamin D) were associated with a modest but significant increase in the risk of cardiovascular disease—an increase, they noted, that might well translate into “a large burden of disease in the population.” The authors called for a reassessment of the role of calcium supplements in the management of osteoporosis.11

A second study had a different purpose, one particularly relevant to our story.¹² The researchers began with the premise that statins reduce cardiovascular risk and slow the progression of coronary artery calcium. The purpose of the study, then, was to determine whether lowering LDL cholesterol (as statins do) is in some way complementary to slowing the progression of coronary artery calcium. The researchers basically wanted to illuminate the relationship of these two phenomena as they relate to heart disease.

Here’s what they did. They measured the change in coronary artery calcium in 495 patients who were basically symptom-free at the beginning of the study. They did this by using a method known as electron beam tomography scanning. Right after their first scan, the patients were started on statin drugs, and they were followed for an average of 3.2 years, during which time their cholesterol was checked and they were scanned on a regular basis. Over the course of the 3.2-year follow-up period, 41 of the patients had heart attacks.

On average, the 454 patients who did not suffer heart attacks saw their arterial calcium go up by approximately 17 percent every year. But the 41 patients who did experience heart attacks saw a whopping 42 percent increase per year in their arterial calcium. According to the researchers, having a faster progression of coronary artery calcium gives you an astonishing 17.2-fold increase in your heart attack risk.¹³

And get this: LDL cholesterol did not differ between the two groups. Ironically, the LDL levels of the folks who did not suffer heart attacks were slightly higher (though not significantly so) than the average LDL levels of the folks who did suffer heart attacks.

So let’s summarize the results. Both groups—the 41 folks who had heart attacks and the 454 folks who didn’t—essentially had the same LDL levels. (So if you were using patients’ LDL levels to predict heart attacks, you’d get no better accuracy than you would by reading their horoscopes!) But if instead of LDL levels you looked at the levels of calcium in the arteries, it would be a whole different story. Those who suffered myocardial infarctions were the most likely to have higher calcium levels in their arteries, especially when the arteries became totally blocked.

Coronary artery calcification has long been recognized as a big risk factor for heart disease, but for some reason we continue to obsessively focus on cholesterol, while few people have heard much about the calcium connection.

Arthur Agatston, M.D., a Florida cardiologist best known as the author of The South Beach Diet, actually invented a scoring method to determine the severity of calcification in the arteries—it’s known as the Agatston score. (Research shows that people with Agatston scores higher than 400 are at a significantly increased risk for coronary “events”—myocardial infarctions—as well as for most coronary artery procedures [bypasses, angioplasty, etc.].14)

Calcium in the bones? Very good. Calcium in the arteries? Not so good.

Enter magnesium.

Magnesium and calcium have an interesting, symbiotic relationship. When magnesium is depleted, intracellular calcium rises. Magnesium also inhibits platelet aggregation, an important step in the development of clots. Calcium channel blockers widen and relax the blood vessels by affecting the muscle cells found in the arterial walls, which is exactly what magnesium does—splendidly, we might add. Magnesium dilates the arteries, thus reducing blood pressure and making it far easier for the heart to pump blood and for the blood to flow freely.

In most of the epidemiologic and clinical trials, a high dietary intake of magnesium (at least 500 to 1,000 mg a day) resulted in reduced blood pressure.¹⁵ These studies showed an inverse relationship between magnesium intake and blood pressure; people who consumed more magnesium had lower blood pressure. One study of 60 hypertensive subjects who were given magnesium supplementation showed a significant reduction in blood pressure over an eight-week period.¹⁶

So basically, you can think of magnesium as a “relaxer.” One of the most relaxing things you can do is to bathe in Epsom salts, which is basically a compound of magnesium with a little bit of sulfur and oxygen. If you’ve ever worked with an integrative medicine practitioner who happens to use vitamin drips, you might have found that the most amazing and restful sleep you’ve ever had occurred after getting a magnesium-heavy vitamin push.* Just as magnesium has a relaxing effect on your body, it also has a relaxing effect on your arteries. And that’s a very good thing from the perspective of the heart, which instead of having to push blood through a narrow or constricted vessel (dangerously raising blood pressure) now has the much easier task of pumping it through a relaxed, widened vessel that doesn’t put up so much resistance. Your heart doesn’t have to work as hard, your blood pressure goes down, and all is well with the world.

There’s another interesting connection between magnesium and the heart, and if you’ve followed our argument so far, you’ll love the elegance of how it all comes full circle. The connection? Sugar.

You’ll recall from chapter 4 that sugar is one of the worst things you can eat if you want to have a healthy heart. (To save you the trouble of looking it up, here’s why: Sugar is highly inflammatory. It also creates dangerous compounds known as advanced glycation end products, or AGEs, which play a pivotal role in atherosclerosis.17) AGEs play a role of particular importance in type 2 diabetes, which, as you know, is a condition in which blood sugar and insulin are essentially at unhealthy levels and have to be brought under control. (And diabetes is one way to fast-track your path to heart disease.)

One of the very best things magnesium does is help manage blood sugar. In several studies of diabetic patients, magnesium supplements of 400 to 1,000 mg per day, given for anywhere from three weeks to three months, improved a number of measures of glycemic (blood sugar) control, including the requirement for insulin.¹⁸ One study measured serum concentrations of magnesium in 192 people with insulin resistance and found that the prevalence of a low magnesium level was about 65 percent among those with insulin resistance, as opposed to only 5 percent of those in a control group.¹⁹

Clearly, there’s a strong association between magnesium deficiency and insulin resistance. You’ll recall that people with insulin resistance are at great risk for diabetes, which in turn puts them at great risk for heart disease. Helping to control blood sugar and insulin is just one more important way in which magnesium is critical for heart health.

Magnesium is necessary for more than three hundred biochemical reactions in the body, and many of these are enzymatic reactions, essential for heart health (or what scientists call myocardial metabolism).²⁰ Even borderline deficiencies of magnesium can negatively affect the heart, and not surprisingly, there is a considerable amount of evidence associating low levels of magnesium with cardiovascular disease.²¹

Bottom line: Magnesium supplements are a must for those who want to protect their hearts. Magnesium lowers blood pressure, helps control blood sugar, and relaxes the lining of the blood vessels. And almost all dietary surveys show that Americans aren’t getting nearly enough.²² We recommend supplementing with at least 400 mg per day.

NOTE: Magnesium supplementation is not recommended for anyone with renal insufficiency (kidney disease).

NIACIN AND ITS EFFECT ON CHOLESTEROL

Even if your doctor hasn’t studied nutrition and is skeptical (or worse) when it comes to supplements, chances are he or she will be familiar with the benefits of niacin. It’s been known since 1955 that cholesterol can be effectively lowered with doses of 1,000 to 4,000 mg of niacin daily.²³ Subsequent studies have shown that niacin will lower triglycerides by 20 to 50 percent and LDL cholesterol by 10 to 25 percent.²⁴

Niacin is one of two major forms of vitamin B₃—the other is nicotinamide. Although both forms can be used for different things in the body, only the niacin form has an effect on your cholesterol, triglycerides, and related compounds. And the effect is not just on overall cholesterol. Studies have shown that when LDL cholesterol is reduced with niacin, there is a preferential reduction of the really nasty LDL molecules, the hard, small, BB gun pellet–type particles that stick to the artery walls, get oxidized, and cause damage.

Niacin also reduces lipoprotein(a), or Lp(a). Lipoprotein(a) is basically a special kind of LDL, and it’s a really bad one. This, folks, is the real cholesterol story! Lp(a) is an independent risk factor for heart disease and for heart attacks, yet it doesn’t get as much attention as cholesterol does because there aren’t effective drug treatments for lowering it, and no one really knows what to do about it. Niacin lowers Lp(a) levels by a remarkable 10 to 30 percent.25

Equally terrific, if not more so, is the fact that niacin raises HDL cholesterol. That alone would be worth shouting from the rooftops, because we consider HDL cholesterol to be a much undervalued player in the heart disease story. (We’ll delve into this topic later on in the book.) Niacin raises HDL levels by 10 to 30 percent.²⁶ But even better is the fact that it preferentially increases HDL-2, which is the most beneficial of the HDL subclasses.²⁷ (HDL-3 is actually pro-inflammatory, even though it’s a member of the so-called “good” cholesterol family—HDL—once again demonstrating how obsolete and ridiculous the classification of cholesterol into just “good” and “bad” really is!)

The most clinically important side effect of too much niacin is that it can be very taxing on the liver (a condition known as hepatotoxicity), although as Dr. Alan Gaby points out in his exhaustive review of nutritional supplements and disease, this is almost never seen in patients taking 3 g or less per day.²⁸

Abram Hoffer, M.D., the great pioneer of nutritional and integrative medicine, stated that his thirty years of experience with niacin therapy (usually 3 g a day or more) showed that one out of every two thousand patients will develop hepatitis from large doses of this vitamin. However, Hoffer also pointed out that in all of his patients who developed hepatotoxicity, liver function returned to normal after treatment was discontinued.²⁹

Sustained-release niacin is actually more hepatotoxic than regular niacin, and liver problems may occur at lower doses.³⁰ Nausea may be an early warning sign of niacin-induced hepatotoxicity; if nausea occurs, the dose should be reduced, or treatment should be stopped.³¹ For folks taking therapeutic doses of niacin, it’s a good idea to have your doctor check your liver enzymes periodically using a standard liver function test.

Dr. Jonny: Niacin Flush

The first time I experienced the “niacin flush” I was working as a personal trainer. It was five o’clock in the morning, and I was getting ready for my six a.m. client. I remember drinking my protein shake, swallowing my vitamins, and then, a very short time later while getting dressed, having the distinct feeling that I was going to die. My skin was flushed, warm to the touch, and my cheeks (and arms) were pinkish red. It wasn’t painful, but it was deeply unpleasant.

My six a.m. client happened to be the president of a high-end makeup company whose husband was an equally well-known Manhattan dermatologist (as well as the only doctor I knew who was likely to be awake at this ungodly hour). I called my client, and she immediately put her husband on the line. I described my symptoms, and he asked me if I’d taken or eaten anything unusual. “Just my vitamins,” I said, to which he replied without hesitation, “Oh, it’s just the niacin. Nothing to worry about, it’ll pass in a few. I’m going back to bed now.”

So that was my first encounter with the infamous “niacin flush.” It’s basically a temporary flushing of the skin, not at all dangerous (especially if you know it’s coming!), and it’s actually a result of the dilation of the blood vessels in the skin (which is why my skin turned pink). Some people experience itching as well or even a mild burning sensation. It typically goes away within a couple of weeks and can usually be counteracted with a baby aspirin taken beforehand.

NOTE: If you are diabetic or have a liver ailment, be sure to check with your doctor before supplementing with niacin.

Dr. Sinatra’s Niacin Know-How

• Look for straight, non-time-release niacin (also known as nicotinic acid). Take after meals at dosages of 500 mg to 3 g daily (see below).

• Start slowly at 100 mg. Work your way up gradually to a higher level, in divided doses.

• If the flush is too uncomfortable, take a baby aspirin before the first meal of the day and then take the niacin after the meal. Use the aspirin only as long as you experience the flush and whenever you increase your niacin dosage, which will trigger a flush.

• You can also try taking an apple pectin supplement with the niacin to reduce a flush.

• Niacin may increase the enzyme levels in liver function tests. This does not necessarily mean that niacin is causing a liver problem, but have your doctor keep an eye on it. He or she may suggest stopping the niacin for five days before your next liver test to avoid possible confusion. Be aware, though, that when you resume the niacin you will develop a flush.

VITAMIN E: THE GOOD, THE BAD, AND THE UGLY

For decades, the nutritional world revered vitamin E as something of a heart savior, a major antioxidant that defended against lipid peroxidation, which was thought to be the cause of cardiovascular disease. (Lipid simply means fat, and peroxidation is a fancy way of saying oxidative damage from free radicals.) During the 1990s the adulation for vitamin E even extended to mainstream medicine, going as far as the American Heart Association. In 1996, for instance, vitamin E was celebrated in a well-publicized study for significantly reducing cardiovascular events over the course of one year among some 2,000 patients with documented heart disease.

The successes and reputation of vitamin E prompted many to believe that if a little vitamin E was good, then more would be even better! Critical studies that followed, however, began demonstrating that daily doses of vitamin E at 400 IUs and above didn’t necessarily generate beneficial results, and, in fact, might be detrimental to health. (As early as 2003, Dr. Sinatra wrote in his newsletter about his own reluctance to back high-dose vitamin E because the emerging research indicated possible pro-oxidant effects.)

That said, both of us found ourselves puzzled by the negative study results that have popped up since then. Sure, problems could come from using the synthetic form of vitamin E (designated dl-alpha-tocopherol) instead of the “natural” form (designated d-alpha-tocopherol). But a pro-oxidant effect from natural vitamin E, considered one of the powerhouses in the anti-oxidant armamentarium? How could that be?

Sharp-eyed readers may have noticed that we put quotation marks around the word natural when referring to natural vitamin E in the above paragraph. That’s because d-alpha-tocopherol by itself is only one part of natural vitamin E. Vitamin E is actually a collection of eight related compounds that are divided into two classes: tocopherols and tocotrienols. The tocopherols come in four forms: alpha, delta, beta, and gamma. Of these four forms, the best known is alpha. When you purchase a “natural” vitamin E supplement, most of the time it is 100 percent alpha-tocopherol.

And therein lies the problem.

Gamma-tocopherol is turning out to be the most potent of the four tocopherols, and the one most responsible for vitamin E’s positive effects as an anti-oxidant. Thus, people taking high-dose alpha-tocopherol alone and not getting enough gamma-tocopherol in their diets, or in their supplements, could run the risk of experiencing a pro-oxidant effect from vitamin E. Moreover, large doses of alpha-tocopherol could also deplete the body’s existing gamma-tocopherol stores.

A 2011 study provided an even sharper image of the two faces of vitamin E. In laboratory experiments, researchers in Belfast found that vitamin E (alpha-and gamma-tocopherol) protects very low-density lipoprotein (VLDL) and LDL cholesterol against oxidation. That’s a good thing! Yet they found a “surprising” pro-oxidant effect on HDL (high-density lipoprotein), the cholesterol particle that acts like a garbage truck, picking up harmful oxidized LDL and transporting it back to the liver for removal. Anything that can hinder HDL is of real concern.

Worth noting is that the researchers referenced a previous study in which taking a small amount of vitamin C along with your alpha-tocopherol helped prevent the negative, pro-oxidant effect of vitamin E on HDL. That wouldn’t be the first time one nutrient helped another one out. We already know that CoQ₁₀ helps protect vitamin E in the body and gives it a hand by recycling it back to an active form after it’s been oxidized in biochemical reactions. (We are big fans of the synergistic effects of nutrients.)

The other half of the vitamin E story concerns the four components known as the tocotrienols. Tocotrienols are turning out to be the real heavy lifters in the vitamin E family, at least when it comes to benefits for the heart. They have more potent antioxidant activity than tocopherols do.32 They also increase the number of LDL receptors, which helps with LDL removal.³³ Tocotrienols provide significant lipid-lowering effects in experimental animals, and most prospective studies have demonstrated the same thing in humans.³⁴

If you take vitamin E, we recommend that you always get it from a supplement labeled “mixed tocopherols” in order to avoid the problems that can occur with pure alpha-tocopherol supplementation. A vitamin E supplement that is 100 percent alpha-tocopherol is less effective and may even be problematic in high doses. Virtually all the studies showing negative results used the alpha-tocopherol form or, worse, the synthetic dl-alpha-tocopherol form. (The dl-alpha-tocopherol form should be left on the shelf to rot!)

If you add 200 IUs of mixed tocopherols or high-gamma vitamin E to a regimen that also includes vitamin C and CoQ₁₀, you should be fine!

FISH OIL’S OMEGA-3: THE ULTIMATE WELLNESS MOLECULE

If you’ve read this book sequentially, you’re already familiar with omega-3 fatty acids from our extensive discussion of them in chapter 5, so here we’ll highlight just a few of the many studies demonstrating the value of omega-3 fats for the heart. (We should also point out that there is equally compelling research documenting the positive effect of omega-3s on the brain as well,³⁵ but because this is a book on cholesterol and cardiovascular disease, we’ll focus on the heart.)

More than thirty years ago, scientists began to notice very low rates of cardiovascular disease among Greenland Eskimos compared to age- and sex-matched Danish control subjects. Shortly afterward, they were able to link these low rates of heart disease to high consumption of omega-3s in the Greenland diet.³⁶ This discovery triggered an enormous amount of research on the role of fish oil in preventing heart disease. (On the day of writing this—December 7, 2011—a National Library of Medicine search for the term “omega-3 fatty acids cardiovascular” produced 2,524 citations.)

One recent review of omega-3s and cardiovascular disease by Dariush Mozaffarian, M.D., of the Harvard School of Public Health, concluded that omega-3 consumption “lowers plasma triglycerides, resting heart rate, and blood pressure and might also improve myocardial filling and efficiency, lower inflammation, and improve vascular function.”³⁷ Mozaffarian also noted that the benefits of omega-3s seem most consistent for coronary heart disease mortality and sudden cardiac death.

In case your eyes were beginning to glaze over from all the medical journal speak, let’s sum it up in plain English: There is reliable and consistent research evidence demonstrating that omega-3 fats, mainly from fish, lower the death rate from heart disease and lower the risk of sudden cardiac death. This is hardcore evidence that fish oil saves lives.

One of the landmark clinical studies of omega-3 supplementation in a high-risk population was published in 1999 and was known as the GISSI-Prevenzione trial.³⁸ More than 11,000 patients who had suffered a heart attack within the past three months were randomly assigned to receive either 1 g a day of omega-3s, 300 mg of vitamin E, both, or neither, in addition to whatever standard therapy they were receiving. Vitamin E had no effect, but omega-3s were associated with a 20 percent reduction in mortality and a whopping 45 percent reduction in the risk of sudden death. These effects were apparent within a mere three months of therapy.³⁹

International guidelines recommend 1 g of omega-3 fats daily for all people who’ve already had a heart attack or for patients with elevated triglycerides.⁴⁰ Experts believe these guidelines will soon be extended to patients with heart failure as well.⁴¹

It’s worth mentioning that the overwhelming majority of research on omega-3s and heart disease was done using the two omega-3s that are found in fish, EPA and DHA. But other studies have also found that ALA—the omega-3 found in plant foods such as flax and flaxseed oil—has benefits for the heart as well. One review of the literature pointed out that both in vitro (test-tube) studies and animal studies have shown that ALA can prevent ventricular fibrillation, the chief mechanism of cardiac death, and that it might be even more efficient at preventing this than EPA and DHA are. The review also noted that ALA was effective at lowering platelet aggregation, which is an important step in thrombosis (a stroke or nonfatal heart attack).42

Even if you’re already on a statin drug and have decided to remain on one, fish oil can still help you. One study found that among more than 3,600 people with a history of cardiovascular disease—many of whom were on antiplatelet drugs, antihypertensive agents, and nitrates—daily fish oil supplementation led to a statistically significant 19 percent reduction in major coronary events compared to the control group.⁴³

Omega-3 fats, particularly from healthy, wild fish, are your heart’s best friend, whether you’re recovering from a heart attack or hoping to prevent one. They lower triglycerides. And they lower blood pressure. And best of all, omega-3s are among the most anti-inflammatory compounds on the planet, meaning they have a beneficial effect on the root causes of heart disease.

We recommend that you take 1 to 2 g of fish oil daily, and that you eat cold water fish (such as wild salmon) as often as you can. (We both recommend Vital Choice, an impeccable source of wild salmon from pristine Alaskan waters that is reasonably priced and shipped in dry ice directly to your door.)

When you supplement with fish oil, remember that the total amount of omega-3s is not what’s important. Bargain-basement omega-3 supplements often tout on their labels how much omega-3 they contain. This number by itself is meaningless. You want to know specifically how much EPA and DHA are contained within each capsule. These are the gold nuggets in the prospector’s tin—you don’t care about the total amount of stones in that pan, you care about the gold. EPA and DHA are the gold. Try to get at least 1 g daily of combined EPA and DHA. (For many of his patients, Dr. Sinatra prefers higher DHA, as it penetrates more into the heart, brain, and retina than EPA does, so he frequently uses squid or algae oil in addition to fish oil because of its higher DHA content.)

PANTETHINE: YOUR SECRET WEAPON

Pantethine is a metabolically active (and somewhat more expensive) form of vitamin B₅ (pantothenic acid). The blood tests of patients with dyslipidemia—a fancy way of saying that their blood levels of cholesterol are too high—significantly improve with pantethine supplementation. And although this can’t be seen on a blood test, pantethine also reduces the oxidation of LDL.⁴⁴

No fewer than twenty-eight clinical trials in humans have shown that pantethine produces significant positive changes in triglycerides, LDL cholesterol, and VLDL, along with increases in HDL cholesterol.⁴⁵ In all of these trials, virtually no adverse effects were noted. The mean dose of pantethine in these studies was 900 mg per day given as 300 mg three times daily. This appears to be the optimal dosage, and it is the one we recommend.

According to a review of the literature on pantethine published in Progress in Cardiovascular Diseases, Mark Houston, M.D., noted that in most studies, at the end of four months pantethine reduced total cholesterol by 15.1 percent, LDL by 20.1 percent, and triglycerides by 32.9 percent, with an increase in HDL of 8.4 percent.46 Houston also noted that in studies of longer duration, there appeared to be continued improvement. (The only adverse reactions were mild gastrointestinal side effects in less than 4 percent of the subjects.) As previously stated, we recommend 900 mg of pantethine divided into three daily doses of 300 mg each.

OTHER SUPPLEMENTATION YOU SHOULD CONSIDER

Picking the “top” supplements for treating any health issue is always difficult. In trying to keep the list from being too overwhelming, you’re always going to leave a few good things out. There’s also the very real issue of compliance. Most people don’t like to take a lot of pills, even if the pills in question are natural substances that will boost or protect their health. We consider the following supplements important, and we suggest that you read about what they do and consider using them in addition to the key supplements discussed above.

Vitamin C. Vitamin C is one of the most powerful antioxidants in the world, and because heart disease is initiated by oxidative damage (damage caused by free radicals), any help you can get in the antioxidant department is a good thing. And the evidence is not just theoretical: A large 2011 study published in the American Heart Journal found that the lower the level of vitamin C in the blood, the higher the risk for heart failure.⁴⁷ Take 1,000 to 2,000 mg a day.

Worth knowing: Vitamin C is extremely safe, and side effects are rare because the body can’t store the vitamin. (In some cases, doses exceeding 2,000 mg a day can lead to a little harmless stomach upset and diarrhea.) The bigger danger is the fact that vitamin C increases the amount of iron absorbed from foods. People with hemochromatosis, an inherited condition in which too much iron builds up in the bloodstream, should not take more than 100 mg of supplemental vitamin C.

Curcumin. This extract from the Indian spice turmeric has multiple benefits, not the least of which is that it’s highly anti-inflammatory. Scientific research has demonstrated its anti-inflammatory, antioxidant, anti-thrombotic, and cardiovascular protective effects.⁴⁸ Curcumin also reduces oxidized LDL cholesterol.⁴⁹ In animal studies, it was shown to protect the lining of the artery walls from damage caused by homocysteine.⁵⁰ The synergistic relationship of curcumin with resveratrol is espeically important.

Resveratrol. Resveratrol is the ingredient in red wine that’s best known for its “anti-aging” activity. It helps protect the arteries by improving their elasticity, inhibits blood clots, and lowers both oxidized LDL and blood pressure.⁵² Not a bad résumé! It’s both a strong antioxidant and a strong anti-inflammatory, inhibiting a number of inflammatory enzymes that can contribute to heart disease. It also inhibits the ability of certain molecules to stick to the arterial walls, where they can take up residence and contribute to inflammation.⁵³ The recommended daily dose is 30 to 200 mg of trans-resveratrol, the active component of resveratrol. Read labels carefully to see what percentage of the capsule is actually the “trans” variety, because that’s the only kind you care about.

NATURAL CLOT BUSTERS: NATTOKINASE AND LUMBROKINASE

Hyperviscosity refers to sticky, or sludgy, blood. When blood thickens, it bogs down as it moves through the blood vessels, causing platelets to stick together and clump. Blood vessels become more rigid, less elastic, and frequently calcified. The danger lies in the tendency to form clots that can block vessels leading to vital organs.

Nattokinase is extracted from the traditional fermented soy food natto, believed by many researchers to contribute to the low incidence of coronary heart disease in Japan. It provides a unique, powerful, and safe way to eliminate clots, or reduce the tendency to form clots, and thus decrease the risk of heart attack and stroke.51

Lumbrokinase, developed in both Japan and China, comes from an extract of earthworm, a traditional source of healing in Asian medicine. These two separate products of dynamic Asian research share a powerful and common property of great interest to anyone who wants to protect their cardiovascular system: They are natural clot eaters.

Here’s how it works: Your body naturally produces fibrin, a fibrous protein formed from fibrinogen. (A fibrinogen test is one of the blood tests we recommend—see chapter 9—because it is a good marker of how much fibrin you’re making.) Fibrin is both good and bad. Its clot-forming action is immediately activated when bleeding occurs, so that’s a good thing. But excess fibrin activity can produce consistently thick blood, and that’s a big problem.

To offset the danger—and to create thinner blood—the body produces another substance called plasmin, an enzyme whose job is to break down excess fibrin. A nice system of checks and balances. But if plasmin, the natural anticlotting agent, becomes overwhelmed and can’t keep up with the job, there’s trouble in River City. And that’s where nattokinase and lumbrokinase come in. If blood clots in an already narrowed blood vessel, you’re basically screwed. So if you can dissolve the clotted material, you can open arteries and improve blood flow. If you reduce the clot even just a tiny bit, you get a significant blood flow boost.

Nattokinase and lumbrokinase are natural blood thinners. They can literally turn your blood from the consistency of ketchup to the consistency of red wine! Best of all, they work pretty quickly, within minutes to hours.

If you take these supplements preventively, you may not form clots in the first place.

Cocoa flavanols. Plant chemicals in cocoa known as flavanols help the body synthesize a compound called nitric oxide, which is critical for healthy blood flow and healthy blood pressure. Nitric oxide also improves platelet function, meaning it makes your blood less sticky. It also makes the lining of the arteries less attractive for white blood cells to attach to and stick around. Researchers in Germany followed more than 19,000 people for a minimum of ten years and found that those who ate the most flavanol-rich dark chocolate had lower blood pressure and a 39 percent lower risk of having a heart attack or stroke compared to those who ate almost no chocolate.54

Cocoa flavanols now come in supplement form, so if you prefer not to eat a couple squares of dark chocolate a day, consider a supplement.

CONVINCING YOUR DOCTOR

If you show this chapter to your doctor, and he or she is still skeptical, we suggest you direct him or her to the superb review paper on nonpharmacological treatment for dyslipidemia written by Mark Houston, M.D., and published in Progress in Cardiovascular Diseases.⁵⁵ This paper has 421 citations and should go a long way toward reassuring him or her that there is plenty of research to support the use of these natural, non-toxic substances.