The Great Cholesterol Myth (24 page)

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
dys
function 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:

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 CoQ
₁₀
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 CoQ
₁₀
. 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.

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

Eighty-five percent of my patients with congestive heart failure have improved significantly on CoQ
₁₀
. But I was concerned about the 15 percent who, despite supplementation with CoQ
₁₀
, still had symptoms that severely compromised their quality of life.

These folks were supplementing with CoQ
₁₀
and had excellent blood levels to show for it, typically 3.5 ug/mL or higher (the normal level of CoQ
₁₀
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 Q
₁₀
, 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 CoQ
₁₀
, 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 Q
₁₀
.

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 Q
₁₀
, 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.

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.