Originally published in Heart, Health & Nutrition, Vol. 15, No. 2, February 2009
The phone rang. Jim Roberts was on the line, the Toledo, OH, cardiologist who teamed with me to write Reverse Heart Disease Now in 2006. He wanted to know if I had seen the "big news" in the Journal of the American College of Cardiology. The "big news," he said, was a study saying that higher blood levels of CoQ10 may be related to longer life for heart failure patients.
This finding was hardly monumental for Jim and me. Rather, the "big news" was that the study was published in the "Bible" of orthodox cardiology, as I call that journal. That fact suggests a growing respect for supplemental CoQ10 by mainstream medicine. Integrative cardiologists – such as Richard Delaney in Milton, MA; Peter Langsjoen in Tyler, TX; Lee Cowden in Phoenix, AZ; Marc Silver in Oaklawn, IL; Stephen Devries in Deerfield, IL; Howard Elkin in Whittier, CA; and both Jim and I (of course) – have been preaching the CoQ10 message for years and recommending it to our patients with great success.
More than 20 years ago, Dr. Langsjoen, and his physician father before him, participated in some of the earliest clinical studies demonstrating CoQ10's outstanding benefits for heart failure. Since then, however, most cardiologists have either ignored or dismissed the evidence – even though it has been strengthened with subsequent published research showing that CoQ10 can prolong and save lives.
Heart failure (HF) is a diagnosis doctors apply to a patient with a tired, weak, energy-starved heart that is losing its ability to pump blood efficiently. More than two percent of the U.S. population, or almost five million people, have this condition. The prognosis for these patients remains poor despite improvements in conventional treatment. Unfortunately, 30 to 40 percent of patients die from HF within a year of diagnosis, and 70 percent die within 10 years.
It's well known among integrative cardiologists that HF patients have low blood concentrations of CoQ10. CoQ10 is an essential element in the cellular process that generates adenosine triphosphate (ATP), the body's fundamental source of internal energy. Ample ATP production is critical to all cells, but is particularly important to cells in the heart muscle because those cells never rest. Although CoQ10 is made naturally in the body, production falls off as we age. It is also blocked by certain medications, including statin drugs.
Against this background, a group of New Zealand doctors tested the hypothesis that CoQ10 blood levels are a predictor of total mortality in HF. They took blood samples from 236 hospitalized HF patients and then followed them for an average of 2.7 years. The researchers concluded that CoQ10 concentration in the blood is an independent predictor of mortality and that a deficiency is indeed associated with worse outcomes in HF.
Bravo to these New Zealand researchers. Their findings absolutely resonate with my clinical observations, which indicate that the bigger the deficiency, the more severe the symptoms. In fact, I find that my HF patients are less symptomatic and have improved quality of life when they have CoQ10 blood levels greater than 2.5 mcg/mL (0.6–0.8 mcg/mL is considered normal).
Back in 1992, I was Chief of Cardiology at Connecticut's Manchester Memorial Hospital. By sharing the data I had collected and the results with patients I had treated, I managed to convince the hospital formulary committee of physicians and pharmacists to add CoQ10 to the list of remedies that could be stocked at the facility. That was a big breakthrough! CoQ10 has now been on the formulary list at Manchester Memorial for 16 years, and it has helped many HF patients there.
In the next 10 years, HF is going to be a major medical challenge to, and a financial burden on, this country due to an aging population of baby boomers and the pervasive overprescribing of statin drugs for lowering cholesterol. We need more research like this latest study to make cardiologists aware of good, safe, natural options for dealing with HF (not just more pharmaceuticals). If they don't pay attention, heart failure could very well be to the medical field what subprime mortgages were to the housing industry. I'm doing my best to make sure that doesn't happen.
Lipitor depletes CoQ10 and heart pumping efficiency
For many years, integrative cardiologists have been sounding the alarm about the side effects of statin drugs, including how they interfere with CoQ10 synthesis in the body. We have been warning that the runaway use of statins is contributing to the sharp rise in the incidence of HF. When CoQ10 is depleted, energy production suffers. The repercussions are felt most notably in muscle tissue – including the heart muscle, where energy demands are the highest.
A new study conducted at Japan's Toyama University Hospital provides broader evidence for this connection. The researchers followed 29 patients with significant coronary artery disease (CAD), none of whom had overt HF. Twenty were on a statin before the study – 10 on Pravachol and 10 on Lescol – while the other nine had not been taking a statin for their CAD. The 20 patients taking Pravachol and Lescol were switched to Lipitor (another statin and the best-selling pharmaceutical in the world), and all 29 received either 5 or 10 mg of Lipitor once daily for three months.
At the end of the study, the researchers found that most participants had a lower blood level of CoQ10 than they had at the trial's start. They noted that as cholesterol goes down, so does CoQ10. The greater the reduction in cholesterol levels, the more significant the drop in vital CoQ10 levels.
Moreover, the study also measured levels of brain natriuretic peptide (BNP) and found that it increased with Lipitor therapy. BNP is an amino acid compound secreted in the heart's ventricles (the two lower pumping chambers) in response to excessive stretching of cardiac muscle tissue in that area. This often happens with a failing heart. The left ventricle is the chamber that pumps blood into the aorta for general circulation, and it is the section that becomes compromised, stretched, and sometimes dilated during HF. Thus, in cardiology, we recognize a higher level of BNP as a marker associated with HF.
Not only did this study re-confirm that regular treatment with Lipitor depletes CoQ10 (which all statins do, not just Lipitor), but it also showed that statin therapy may deteriorate the left ventricle function in patients with CAD – and possibly lead to heart failure. The message here for statin users is this: You must supplement with CoQ10! In fact, I strongly recommend that anyone – and especially those with any known cardiac condition like hypertension, blocked coronary arteries, or arrhythmia – supplement their statin therapy with at least 200 mg of CoQ10 daily, in divided doses.
The BNP findings dovetail with the clinical research of Drs. Silver and Langsjoen – cardiologists who aggressively use CoQ10 in their treatment of CAD and HF. In 2004, they published a study, also in the American Journal of Cardiology, which showed that Lipitor worsened left ventricular diastolic function and that CoQ10 supplementation reversed this side effect.
The term they used – diastolic dysfunction, or DD – describes a problem with the diastolic phase of the cardiac cycle. During diastole, the heart muscle stretches as the chamber fills with blood. Diastolic dysfunction means the chamber's muscle stiffens (which could be a result of heart attack scars, longstanding high blood pressure, or viral attack) and is less receptive to filling. Most people think that pumping blood out of the heart demands more dynamic energy than is needed to fill it. In fact, the opposite is true – it takes more energy to fill the heart than to empty it. That's why diastolic dysfunction is so important. The cascade effect that results from statin therapy goes something like this: Lower CoQ10 levels lead to decreased ATP production, which leads to diastolic dysfunction of the left ventricle, which leads to heart failure.
This stiffness phenomenon is insidious, and it may brew under the surface for years. A patient duly taking his or her statin drug may not experience any sign of trouble until one day fatigue and shortness of breath suddenly develop. In 40 percent of these cases, early diastolic dysfunction will eventually lead to HF. Unless a doctor is familiar with the statin-CoQ10 connection (and most are not), the cause goes unaddressed. So, please share this article with everyone you know who is taking a statin so that they can protect themselves.
Fish oil makes waves in heart failure treatment
As my longtime readers know, I'm a big fan of fish oil and I routinely recommend it for its many cardiovascular benefits. Just for starters, it reduces blood pressure; it protects against arrhythmias, sudden death, and plaque rupture; and it has a powerful positive effect on heart rate variability.
Now, a new study shows that just 1 g of fish oil a day yields significant benefits for symptomatic HF patients – a challenging population because of weakened cardiac pumping efficiency. The revelation emerged from the large GISSI database in Italy, where heart researchers monitor thousands of cardiovascular patients at more than 300 medical facilities. In this particular study, nearly 7,000 patients receiving standard care were assigned to also take either a daily fish oil supplement or a placebo. The researchers specifically wanted to know if supplementation could improve morbidity and mortality.
In contrast to participants in the placebo group, those taking fish oil had an eight percent lower risk of cardiovascular-related death or hospitalization. Over four years, this finding meant that one cardiovascular death or hospital admission was averted for every 44 patients – just by taking a simple, safe, and inexpensive fish oil supplement.
The results don't surprise me. Fish oil reduces high blood pressure and coronary artery disease – two of the top contributors to HF. If you have HF, be sure to get on the fish oil bandwagon. I would even suggest a higher dosage than what was used in the study. I recommend taking 2-4 g a day in divided doses. I've had excellent results with that higher dosage, and no problems.
Statin (Crestor) fails heart failure test
In another recent GISSI study involving HF patients, Italian researchers tested the most powerful cholesterol-lowering statin drug on the market – Crestor (rosuvastatin). In this investigation, they enlisted more than 2,300 patients and randomly assigned half of them to take a typical daily dose of 10 mg of Crestor and half of them to take a placebo pill. After about four and a half years, the results showed no impact on clinical outcomes for the statin-takers. In fact, there was a very slight advantage for the group taking the placebo. The two pharmaceutical companies who helped fund the trial – AstraZeneca (the maker of Crestor) and Pfizer (the maker of Lipitor) – had to be disappointed.
This finding brings up an obvious question: If the strongest statin has no effect on HF, why prescribe statins for these patients? In these cases, doctors are interested in the drugs' ability to reduce inflammation, not lower cholesterol. The purpose of this study was to see if heart failure patients would respond favorably to that effect. They didn't.
I prescribe statins to lower inflammation and to improve blood viscosity. I prescribe them for men with calcium deposits in their coronary arteries as well as for diabetic men and women who have been diagnosed with arterial disease and who have high levels of C-reactive protein, a potent inflammatory marker. However, I also emphasize my "Awesome Foursome" of CoQ10, carnitine, ribose, and magnesium to help revive energy production in starved heart muscle cells.
Lowering cholesterol proves risky in patients with acute heart failure
A study published recently in the American Heart Journal examined the relationship between lower cholesterol and hospitalized patients with acute HF – the key word being acute as opposed to the GISSI analysis I just mentioned in which chronic HF patients were studied.
In this study of patients with acute HF, some new – as well as old – evidence related to the fast-deteriorating nature of the disease was brought to light. Keep in mind that lower cholesterol levels have already been associated with increased mortality in chronic HF patients – a fact that always makes me question overly aggressive cholesterol lowering. After all, the heart's main fuel is fat. Given this, does lowering cholesterol too much negatively affect energy production in weak hearts?
This study seems to answer my question. Researchers from UCLA, Duke, and Baylor looked at data collected from nearly 18,000 patients at 236 hospitals that participated in a database registry called Get With the Guidelines – Heart Failure. The patients were divided into four groups (Q1–Q4) based on their cholesterol levels – Q1 (118 mg/dL and less), Q2 (119–135 mg/dL), Q3 (146–179 mg/dL), and Q4 (180 mg/dL and above).
Fifty-eight percent of the Q1 group, that is, the folks with the lowest cholesterol, were taking a statin drug. Of the groups Q2, Q3, and Q4, 50 percent, 43 percent, and 34 percent, respectively, were taking statins. The analysis revealed that for each 10-point increase in total cholesterol there was an associated four percent decrease in the risk of in-hospital death. In short, the higher the total cholesterol among patients in this acute group, the less chance they had of dying in the hospital. The researchers concluded, "In patients hospitalized with heart failure, lower total cholesterol levels independently predict increased in-hospital mortality risk."
This finding is huge. It clearly shows that cholesterol is protective, and that lowering cholesterol – which has become an absurd medical pastime – is patently dangerous for this fragile population. I have long said that a total cholesterol level of less than 150 is an invitation for trouble. For example, I've mentioned before that cholesterol is a necessary component of cell membranes and a raw material for the body's steroid hormones. However, something else I have only learned recently is that cholesterol appears to bind and detoxify endotoxins that enter the circulatory system via the gut.
Endotoxins are substances made of fat and sugar constituents – the remnants of certain pathogens destroyed in the gut. Researchers think that HF patients develop a "leaky" intestinal barrier that allows these poisons to enter the bloodstream where they trigger an inflammatory response. The resultant inflammatory compounds can weaken and undermine the sensitive inner endothelial layer of blood vessels that is critical for cardiovascular health. The more endotoxins that make their way into the blood, the greater the risk of disease and death. Therefore, by lowering cholesterol, you take away a key detox weapon for the HF patient.
My bottom line is to avoid statin drugs for HF unless you also have diabetes and have been diagnosed with arterial disease. However, statins are a great weapon for someone with progressive angina and active coronary artery disease. In those cases, statins provide an important benefit by reducing inflammation and thinning the blood. As I said earlier, though, statins must always be accompanied by CoQ10 supplementation.
Heart failure – Sinatra's nutritional recommendations
My "Awesome Foursome" are at the core of my nutritional strategy. I've written about them a number of times, most recently last September. They are CoQ10, magnesium, L-carnitine, and ribose. These potent metabolic supplements provide nutrients that are necessary for peak energy production in the heart, and they help support overall heart function.
Here are my Awesome Foursome dosage recommendations:
- CoQ10 – at least 200 mg daily of hydrosoluble softgels for best absorption (not the capsules)
- Magnesium – 400–800 mg
- L-carnitine – 1 g on an empty stomach two to three times a day (2-3 g total)
- Ribose – 5 g up to three times daily, depending on need
Along with these four supplements, I also recommend a high-quality daily multivitamin along with 2-4 g of fish oil.
GISSI-HF Investigators. Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet. 2008;Aug 29. [Epub ahead of print]. Presented at the European Society of Cardiology Congress.
GISSI-HF Investigators. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet. 2008;Aug 29. [Epub ahead of print]
Horwich T, et al. Cholesterol levels and in-hospital mortality in patients with acute decompensated heart failure. Am Heart J. 2008; published online 10 Sept 2008.
Molyneux SL, et al. Coenzyme Q10: An independent predictor of mortality in chronic heart failure. J Am Coll Cardiol. 2008;52:1435–1441.
Sandek A, et al. The emerging role of the gut in chronic heart failure. Curr Opin Clin Nutr Metab Care. 2008;11(5):632–639.
Silver MA, et al. Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction. Am J Cardiol. 2004;94(10):1306–1310.
Suzuki T, et al. Atorvastatin-induced changes in plasma coenzyme Q10 and brain natriuretic peptide in patients with coronary artery disease. Int Heart J. 2008;49:423–433.