CoQ10 Combats Congestive Heart Failure

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Congestive heart failure is one of the most devastating forms of cardiovascular disease.1

More than 5.8 million people in the US are affected by congestive heart failure. If you’re diagnosed withcongestive heart failure today, you have a 50/50 chance of being dead within five years.1

Those aren’t good odds. But researchers have determined that with the help of CoQ10, you can beat these odds.

Mainstream medicine treats congestive heart failure with a barrage of medications including beta blockers, ACE inhibitors, diuretics, digoxin, nitrates, aldosterone antagonists, anticoagulants, and glucose-lowering drugs. These drug combinations have added considerable years of life to patients with congestive heart failure.2-7

Overlooked by most cardiologists, however, are published clinical studies showing that CoQ10 can dramatically improve treatment outcomes when properly used in conjunction with conventional treatments.

A recent international, multicenter study of patients with moderate-to-severe heart failure demonstrated, by the most conservative analysis, a 50% reduction in major cardiovascular events (strokes, heart attacks, etc.) and a 44% reduction in cardiovascular deaths, in response to CoQ10 supplementation.4

This dramatic outcome validates earlier studies demonstrating the utility of CoQ10 in managing heart disease. It also points to the potential role CoQ10 plays in the prevention, rather than treatment, of heart failure and other cardiovascular diseases.

What Is Congestive Heart Failure?

Congestive heart failure is the inability of the heart to pump sufficient blood to meet the needs of all organs in the body, and is frequently the result of other, preventable factors such as high blood pressure, diabetes, and coronary heart disease (which causes heart attacks).1

Congestive heart failure results from a progressive weakening of the heart muscle, which is usually a result of insufficient production of ATP (adenosine triphosphate), the energy that fuels your heart.34-36 In a healthy heart with ample energy in the form of ATP, the heart muscle is well-developed and thick, and it effortlessly pumps blood out of the left ventricle into the aorta and out into the body.1

But with inadequate ATP, which occurs from impaired energy transport, the robust heart muscle weakens and becomes flabby, resulting in relatively ineffective pumping action, so that blood pools in the heart.1 We refer to this slowed and inefficient movement of blood in the heart as “congestive” heart failure. The major symptoms of congestive heart failure arise from this backup of blood in the weakened left ventricle.

CoQ10 Helps Prevent Heart Failure

CoQ10 has been shown to prevent underlying pathological disorders that produce heart failure. This includes reducing atherosclerosis risk factors, improving endothelial function, and protecting against heart damage.8,9Here is a summary of the encouraging data supporting the role of CoQ10 in heart disease prevention:

CoQ10 Protects Against Arterial Occlusion

Atherosclerosis (“hardening of the arteries”) underlies virtually all heart attacks, strokes, and other blood vessel diseases.10-12 There are numerous risk factors that are associated with the onset of atherosclerosis, including LDL oxidation, chronic inflammation, elevated blood glucose, elevated lipid levels, and disordered growth factor signaling.13-17 Published studies show that CoQ10 combats many of those risks. For example:

  • Heart attack survivors who took 120 mg a day of CoQ10 for one year reduced the rate of total cardiac events and nonfatal heart attacks by 45 and 46%, respectively, compared to controls, while beneficial HDL cholesterol rose significantly.8
  • When compared to patients on statins, those taking 60 mg a day of CoQ10 favorably modified numerous atherosclerosis risk factors, including lipid profiles, platelet clumping, and oxidative stress.18
  • In adults at intermediate risk for atherosclerosis who took a combination of CoQ10 (120mg a day) and aged garlic extract (1,200 mg a day) for one year, atherosclerosis progression was 4-fold lower compared with control subjects, while markers of atherosclerosis-promoting inflammation were significantly reduced.19
  • CoQ10 helps prevent low-density lipoprotein (LDL) cholesterol from oxidizing and triggering arterial plaque formation.20
CoQ10 Treats And Prevents Heart Disease

CoQ10 Treats And Prevents Heart Disease

  • Cardiovascular disease remains the leading killer of American adults.
  • In particular, congestive heart failure, which can arise from hypertension, atherosclerosis, endothelial dysfunction, and heart attacks, prematurely sickens otherwise healthy people.
  • Some forms of cardiovascular disease involve some degree of energy mismanagement at the cellular level, leaving heart and blood vessel cells weakened and incapable of proper function.
  • CoQ10 is essential for transferring energy from food into ATP molecules, the universal cellular energy currency.
  • Studies show that supplementation with CoQ10 augments heart and vascular function, improves clinical status, and prevents further damage from cardiovascular disease.
  • CoQ10 may represent the single most vital supplement that everyone should take to sustain and support cardiovascular energy management.

CoQ10 Improves Endothelial Function

Dysfunction of the ultrathin cell layer lining arteries, the endothelium, is a major early risk factor for the development of atherosclerosis and cardiovascular disease.21,22 This endothelial dysfunction is especially prevalent in those with diabetes and/or lipid abnormalities.23 Numerous studies have demonstrated that CoQ10 directly addresses multiple causes of endothelial dysfunction:

  • In patients with diabetes, 12 weeks of supplementation with 200 mg a day of CoQ10 significantly increased endothelial function in a major artery.23
  • In a group of men with known endothelial dysfunction, CoQ10 supplementation improved endothelial function significantly compared with baseline.21
  • In patients with mild-to-moderate heart failure, 300 mg a day of CoQ10 improved endothelial function 38%, an effect comparable with that of exercise training.24
  • Blood vessel relaxation, a measure of endothelial function and blood flow, improved significantly in patients with known coronary artery disease at risk for heart attack who need optimal cardiac blood flow.25
New York Heart Association (NYHA) Functional Classification


Patient Symptoms

Class I (Mild) No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).
Class II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.
Class III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.
Class IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

The New York Heart Association (NYHA) Functional Classification system has become the standard for measuring symptoms that affect functioning related to heart failure.81

CoQ10 Protects Against Heart Damage

Coronary artery disease typically refers to the consequences of atherosclerosis of the coronary arteries, which are the arteries that supply blood and nutrients to the heart muscle itself. Early disease may appear as painful and ominous angina (chest pain), while more advanced disease produces ischemia (lack of blood flow), and eventually infarction (death of heart muscle) in a classical heart attack.26 Numerous studies have shown that in the event of a heart attack, ample levels of CoQ10 may mitigate the amount of damage:

  • During open-heart surgery, when the heart is briefly stopped and ischemia is a major risk, CoQ10 protected heart muscle pumping and cardiac output.27
  • In functioning hearts from old rats, pretreatment with CoQ10 improved recovery of heart function following stress.28
  • In human atrial heart muscle tissue, CoQ10 treatment abolished the decreased ability to recover from ischemia seen in older hearts, producing a recovery pattern similar to that in younger hearts; this effect was shown to be related to improved mitochondrial energy efficiency in the treated tissue.28,29
  • In humans undergoing elective heart surgery, patients treated with CoQ10 had lower levels of markers of heart damage, improved pumping action, and shorter hospital stays, compared with untreated controls.28

When blood flow through the heart becomes congested, blood backs up throughout the body. The result is an accumulation of fluid that is squeezed out of the capillaries,82 the tiniest of blood vessels found in all tissues.

The most evident symptoms of congestive heart failure reflect this process: As the lungs become heavy and fluid-filled, patients experience shortness of breath during normal, non-strenuous activities, and have trouble breathing when lying down; as fluid builds up in the abdomen and extremities, patients experience weight gain, with swelling of the feet, legs, ankles, or stomach.1

Most patients also report feeling generally tired or weak, as the heart becomes less and less able to meet the body’s demand for oxygen and nutrients.

CoQ10 supplementation helps restore the heart’s normal energy economy, allowing heart muscle to regain its youthful strength, to resume its robust pumping action, and to reduce symptoms and disability induced by congestive heart failure.

CoQ10 And Cellular Energy

Some forms of cardiovascular disease involve energy mismanagement at the cellular level, weakening heart and blood vessel cells and leaving them incapable of proper function.30-33 This is especially true of congestive heart failure.

Despite its name, congestive heart failure is not a situation in which the heart stops beating. Rather, it results from a progressive weakening of the heart muscle, which is characterized by insufficient ATP (adenosine triphosphate) production.34-36

CoQ10 supplementation has repeatedly been shown to improve heart muscle function in patients with heart failure, supporting the scientific observation that heart failure is caused by a deficit in cellular energy.37,38 This includes improvement of heart muscle movement, increased cardiac output (the amount of blood pumped per minute), ejection fraction (proportion of blood pumped out with each stroke), and other technical measures.39-43

But are you taking the right amount—and the right type—of CoQ10 to extend your life span? Chances are, the answer is no.

Even fairly low doses of CoQ10 have been shown to reduce the symptoms associated with congestive heart failure. For example, in a three-month open study, an average daily dose of 100 mg a day of CoQ10 improved symptoms in a large majority of patients, including swelling, blueness (cyanosis), difficulty breathing, heart palpitations, sweating, insomnia, vertigo, and nighttime urination. In fact, 54% of patients experienced improvement in at least three such symptoms.44

But those low doses can be deceiving because even though they improve symptoms, ultimately few meaningful benefits in terms of survival or improved functioning were shown at CoQ10 doses of 100 mg a day.44 This is especially true for people who already have advanced congestive heart failure (Class IV) because fluid build-up in the walls of their intestines reduces the amount of a given dose that can be absorbed into the bloodstream.45

A study published in The Clinical Investigator shows us the difference that even modest increases in dosing makes: It demonstrated that an increased dose of CoQ10 produced more than just symptom reduction—it kept patients out of the hospital.

For this study, when patients with moderate-to-severe (class III and IV) heart failure took 2 mg/kg a day (about190 mg a day in an average-sized man, and about 150 mg a day for an average woman) of CoQ10 for one year, it significantly reduced hospitalization rates by 38%.38 In the same study, symptoms caused by fluid backing up into the lungs (pulmonary edema, “cardiac asthma”) were reduced by 61 and 51%, respectively.

But even with those increased doses and beneficial results, we’re still falling short of CoQ10’s full life-extending potential. Changing long-term outcomes (like reducing mortality) clearly requires higher doses for longer periods.


Mainstream medicine relies on drugs called statins to help lower cholesterol in an effort to prevent atherosclerotic heart disease. But a looming side effect of statins is that they deplete your heart muscle of CoQ10, in fact leaving you more vulnerable to congestive heart failure.83, 84

Fortunately, as shown by recent studies, people taking statins can benefit from supplemental CoQ10 at 200to 300 mg a day.84,85 Patients not only had improvements in CoQ10 levels and in natural free radical defense systems, but also had objective improvements in ejection fraction and in their NYHA functional classification as well.84, 85

CoQ10 And Longevity

To achieve benefits measured by longer life spans, you need to increase the dose and amount of CoQ10absorbed into the bloodstream.

Surprisingly few studies have bothered to measure blood levels of CoQ10 in patients, a basic step in gauging the effectiveness of a dosing program. What we do know is that leaders in the field have demonstrated that blood levels of more than 3.5micrograms/mL are required to reliably produce improvements in cardiac function.24,46,47 Doses of standard CoQ10 (also called ubiquinone) of at least 240 mg a day may produce such elevations in blood levels, while lower doses rarely do so.47,48

A better way to achieve optimal blood levels of CoQ10 is to use a superior form of CoQ10 called ubiquinol. In one particularly impressive study, patients with severe heart failure (average of class IV) had mean CoQ10 levels of just 1.6 micrograms/mL even though they were taking 450 mg a day of standard CoQ10. Once they changed to an average of 580 mg a day of ubiquinol, their blood CoQ10 levels shot up to 6.5 micrograms/mL and their mean ejection fraction improved 77.3% from baseline. In addition, their NYHA class improved from a mean of class IV to a mean of class II, demonstrating substantial improvement in their ability to carry out tasks of daily living.45

Dramatic proof of the effectiveness of higher doses of standard CoQ10 for longer periods comes from the most recent large clinical trial, conducted by an international group of cardiologists.49 In this study, patients with moderate-to-severe heart failure took either a placebo or 300 mg a day of CoQ10 (in the lesser absorbable form called ubiquinone) for two years. Patient data was examined at 16 weeks (short term) and at the end of the study (long term). No meaningful changes were seen in any patients at the short-term data point (16 weeks) using the ubiquinone form of CoQ10.

In the same study, by the two-year mark, however, supplemented patients were half as likely to experience a major adverse cardiovascular event, compared with placebo recipients.49 In addition, significantly more placebo patients died a cardiovascular death compared with supplemented subjects (16 versus 9%), whiledeaths from all causes were 18% in placebo patients, and just 10% in supplemented ones. The rate of heart failure-related hospital stays was also significantly lower in patients taking CoQ10 than in controls.

These studies indicate that making energy safely and abundantly available to heart muscle through CoQ10 supplementation at reasonable doses for a prolonged period is a powerful way to reduce the impact of congestive heart failure.

It is important to note here that in all studies, patients remained on their regular medications. This is important to emphasize as people with existing heart failure should use CoQ10 as a long-term heart-strengthener and not as a replacement for prescription medications.

Ubiquinol: The Optimal Form Of CoQ10

Whenever tissues are deficient in CoQ10, their energy-providing mitochondria throughout the body suffer.87 That’s because CoQ10 is an essential component in the transfer of electrons, nature’s tiniest unit of energy, from chemical bonds in food molecules to chemical bonds in the ATP molecules all tissues use as an immediate energy supply.88,89 CoQ10 deficiency has been found in a number of age-related disorders, prominently including heart failure.88,89

Supplementing with CoQ10 has been found to be a highly effective means of increasing tissue CoQ10 activity, with improvements in function of heart muscle, brain cells, and other energy-intensive tissues. Increasingly, research is proving that not all forms of CoQ10 are the same; some are better absorbed than others. Better absorption means more benefit for you.87

There’s evidence indicating that CoQ10 in the form of ubiquinol may be a better-absorbed, more readily available form of the coenzyme, compared with the more common ubiquinone.87 Ubiquinol is also the form of CoQ10 found naturally in the body, where it protects mitochondria and cell membranes.90,91

Research supports the idea that ubiquinol has a faster and more powerful effect—that it is morebioavailable.92 Animal studies have found higher tissue levels of CoQ10 when ubiquinol is the supplement used, and in one study ubiquinol was the only form that could increase CoQ10 in brain mitochondria.87When CoQ10 was combined with the adaptogen shilajit, there was a 56% increase in energy production in the brain.93 The compounds in shilajit have been shown to stabilize CoQ10 in its ubiquinol form and help facilitate more efficient delivery of CoQ10 to the mitochondria.93-96 And a human study showed that both a single oral dose of 150 or 300 mg of ubiquinol and long-term administration of ubiquinol were rapidly absorbed, and no safety concerns or laboratory abnormalities were seen.97

Laboratory studies show that ubiquinol is highly effective in reducing the disastrous effects of shock induced by blood loss, a leading killer following major trauma.98 The effect was attributed to ubiquinol’s powerful ability to clean up products of oxidation and thereby decrease inflammatory changes.99 Similarly, ubiquinol is the preferred supplement for use in certain forms of congestive heart failure.88 And ubiquinol is showing great promise in a host of other conditions and health concerns for which oxidant damage is a major predisposing factor, such as male infertility due to weakened sperm,100 blood markers of cardiovascular disease,90 and autism in children.101 There is also animal evidence supporting ubiquinol supplementation to prevent trauma-associated kidney damage.102

The beneficial effects of ubiquinol are so universal throughout the body that the compound is being explored for its effects on overall longevity. When age-accelerated mice (a model of human old age) were supplemented with high-dose ubiquinol (equivalent to about 1,680 mg in humans), their performance on a treadmill was improved by more than 15%, and they had a significant increase in their natural free radical defense systems, further adding to their protection against aging.103 Revolutionary data published in mid-2014 showed that ubiquinol has a direct antiaging effect by supporting actions of the SIRT family of proteins that slow senescence through multiple biochemical activities.104

All of us face the age-accelerating effects of poor mitochondrial function, oxidant damage, and inflammation that arise from deficient CoQ10 levels. For those who seek the extra added benefits of greater bioavailability and enhanced expression of anti-aging genes, reduced CoQ10 in the form of ubiquinol may be the answer.

Potential Of CoQ10 In Noncardiac Disorders

Heart muscle and blood vessel cells are of course not the only tissues that require ample CoQ10 for efficient energy utilization. In reality, every cell in your body runs better when ample CoQ10 is available. This is especially true for the eyes, kidneys, and brain, which is why CoQ10 has shown such tremendous benefits for each of these organs.50-53

Promising studies have demonstrated that CoQ10 protects cells in the eye—specifically the energy-intense retina and the oxygen-exposed cornea.54-63 These effects may prevent common causes of blindness in old age, such as macular degeneration, glaucoma, and cataracts.

The kidney, like the eye, heart, and blood vessels, is an organ with tremendous blood flow, high oxygen exposure, and a crucial need for maximum energy efficiency. Studies in humans and animals reveal powerful protective effects of CoQ10 on kidney tissue structure and function, potentially adding years to the lives of people who might otherwise succumb to kidney failure.64-71

The human brain is the body’s largest consumer of oxygen and utilizer of energy. The major neurodegenerative diseases, including Alzheimer’s, Parkinson’s, ALS, and Huntington’s, and many of their associated cognitive deficits, are beginning to show small signs of yielding to CoQ10 supplementation, at least in their earliest stages.72-80

The High Cost Of Heart Disease

$818 billion … That’s the estimated annual cost, in the United States alone, for total direct medical costs of cardiovascular disease by 2030.86

That represents a tripling, from about $273 billion, over a 20-year period, and a failure of the American health system to accomplish a major goal, which is the reduction of heart attacks and strokes by a million patients by 2017.1

During that time, real indirect costs from lost productivity will increase by 61%, from $172 billion to $276 billion.86 That’s more than a trillion dollars a year in total.

With those kinds of figures, we can’t afford to NOT get heart disease under control.

Studies show that supplementation with CoQ10 augments heart and vascular function, improves clinical status, and prevents further damage from cardiovascular disease.

CoQ10 may represent the single most vital supplement that everyone should take to sustain and support the cardiovascular energy management essential for a healthy heart.


Cardiovascular disease has many faces, but a central mechanism is loss of energy efficiency at the level of heart muscle and the coronary arteries that feed it.

CoQ10 is essential for transferring energy from food into ATP molecules, the universal cellular energy currency.

Studies show that CoQ10 levels are diminished in heart disease, particularly congestive heart failure. Supplementing with CoQ10 improves heart and vessel function in lab experiments, animal studies, and clinical trials.

If you suffer from existing heart disease, add a daily supplement of CoQ10, preferably the ubiquinol form, to your medication regimen after discussion with your doctor. If you are not yet a victim of overt cardiovascular disease, you are even better positioned to take advantage of CoQ10’s preventive effects.

It is impossible to overstate the importance of CoQ10 supplementation in maintaining healthy bioenergetics in the heart, brain, kidney, eye, and other energy-intensive tissues. There is every reason to believe that regular CoQ10 supplementation will add to both your life span and your health span.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.


Ubiquinol has now been shown to be important and effective in management of a number of chronic, age-related, oxidation-driven diseases, due to its potent effects in smoothing mitochondrial energy transfer and reducing the collateral damage to cells and tissues. For example:

  • In diabetic retinopathy, a higher ratio of ubiquinol to ubiquinone was shown to be protective.105
  • In diastolic heart failure, or heart failure with relatively normal pumping ability in the heart, ubiquinol is in growing use to improve patient outcomes and improve the function of the heart’s left ventricle during its relaxation phase, when it recovers from energy-intensive contractions.106
  • In men with impaired fertility due to weak or defective sperm, ubiquinol exerted favorable changes on sperm structure and motility, changes that favor fertility.100
  • In cardiovascular diseases, an early marker of dangerous oxidative damage to heart cells is a rise in levels of a normally intracellular enzyme called GGT; ubiquinol was shown in a human study to reduce GGT activity, probably through complex effects on gene expression.90
  • In autism, a childhood disorder thought to have roots in oxidative damage to brain tissue, ubiquinol supplementation improved communication with parents, verbal communication, game playing with other children, sleep, and food rejection, all common findings in autistic children.101

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Men with ‘low testosterone’ have higher rates of depression

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WASHINGTON (July 1, 2015) — Researchers at the George Washington University (GW), led by Michael S. Irwig, M.D., found that men referred for tertiary care for borderline testosterone levels had much higher rates of depression and depressive symptoms than those of the general population.

“In an era where more and more men are being tested for “Low T” — or lower levels of testosterone — there is very little data about the men who have borderline low testosterone levels,” said Irwig, associate professor of medicine and director of the Center for Andrology at the GW School of Medicine and Health Sciences. “We felt it important to explore the mental health of this population.”

The research, slated to publish online on July 1 in the Journal of Sexual Medicine, involved 200 adult men, aged 20-77, with a mean age of 48 years old, who were referred for borderline total testosterone levels between 200 and 350 ng/dL. Information gathered included demographics, medical histories, medication use, signs and symptoms of hypogonadism, and assessments of depressive symptoms and/or a known diagnosis of depression or use of an antidepressant.

Depression and/or depressive symptoms were present in 56 percent of the subjects. Furthermore, one quarter of the men in the study were taking antidepressants and that the men had high rates of obesity and low rates of physical activity. The most common symptoms were erectile dysfunction, decreased libido, fewer morning erections, low energy, and sleep disturbances.

While more research is needed in this area of study, the researchers concluded that clinicians should consider screening for depression and depressive symptoms, overweight and unhealthy lifestyle factors in men who are referred for tertiary care for potential hypogonadism.


“High Rates of Depression and Depressive Symptoms Among Men Referred for Borderline Testosterone Levels” is available at

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AACE releases new position statement on testosterone replacement therapy in men

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Rigorous studies have not linked testosterone replacement therapy to heart attack or stroke, and the decision to prescribe testosterone replacement therapy should be based on a full diagnostic work-up – not the underlying cause of hypogonadism, according to a new position statement from the American Association of Clinical Endocrinologists.

The statement challenges several aspects of a recent Food and Drug Administration safety announcement warning about “possible” increased risks of heart attack and stroke with testosterone replacement therapy (TRT) and approving its use only for testicular, pituitary, or brain disorders that cause low testosterone, not for age-associated hypogonadism.

In fact, AACE rejoined, randomized controlled trials have lacked the power to assess whether TRT increases the chances of cardiovascular events or death. Data linking TRT to cardiovascular problems come from a few retrospective studies, the “major flaws” of which limit their ability to assess risk. “Large-scale prospective randomized controlled trials on testosterone therapy, focusing on cardiovascular benefits and risks, are clearly needed. As with therapeutics in general, common sense, experience, and an individualized approach are recommended” (Endocr Pract. 2015;21:1066-73).

The benefits and risks of TRT in age-associated hypogonadism remain uncertain, according to both the FDA and AACE. Until better studies are available, AACE recommends that clinicians consider TRT for men with signs and symptoms that are consistent with hypogonadism, regardless of cause, and who have at least two “unequivocally low” testosterone levels in samples drawn before 10 a.m.

Clinicians also should educate patients about the possible cardiovascular risks of TRT, should be “extra cautious” when considering TRT for symptomatic elderly men with low testosterone levels, and should avoid TRT entirely in frail elderly men “until better outcome data are available,” AACE also recommended. Furthermore, clinicians should avoid TRT for patients with uncontrolled or poorly controlled heart failure, a history of heart attack or cerebrovascular accident within the past 6 months, an individual or family history of a procoagulant state, or an individual history of thromboembolism, AACE stated.

Although TRT can improve some cardiovascular risk factors by promoting muscle gain and fat loss, decreasing insulin resistance, and potentially reversing metabolic syndrome, it remains unclear whether low testosterone is a marker of cardiovascular illness or a causal factor, AACE noted. Replacement therapy is most likely to benefit men with very low testosterone levels, not those whose levels are just below normal, according to AACE.

The American Urological Association has echoed several recommendations from AACE, emphasizing in its own statement that “testosterone therapy in the absence of hypogonadism is inappropriate” and calling for more federal and industry funding for studies of the indications, benefits, and risks of approved treatments for hypogonadism as well as studies of new potential therapies. “Current evidence does not provide any definitive answers regarding the risks of testosterone therapy on prostate cancer and cardiovascular disease, and patients should be so informed,” noted the statement from the AUA, which was last updated in August 2015.

The AACE Reproductive Endocrinology Scientific Committee listed the following disclosures: first author Dr. Neil Goodman reported serving on the AbbVie speaker bureau for AndroGel and senior author Dr. Glenn Cunningham reported receiving research support from Abbvie, having served on advisory panels for Abbvie, Apricus, Clarus Therapeutics, Endo Pharma, and Lilly and having consulted for Clarus Therapeutics, Endo Pharma, Ferring, Purdue Pharma, and Repros Therapeutics. Two other coauthors declared financial relationships with Abbvie, GlaxoSmithKline, Merck, Sanofi-Aventies, and a number of other pharmaceutical companies. The other two coauthors declared no competing interests.

By: AMY KARON, Clinical Endocrinology News Digital Network

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Lipotropic Injections and Medical Weight loss

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Merriam-Webster Online dictionary defines the word ‘Lipotropic’ as something that promotes “the physiological utilization of fat.” In other words, lipotropic injections help your body burn fat. Lipotropics are essential for a healthy liver because they help reduce the amount of dangerous fat in that organ. Without lipotropic compounds, fat and bile could accumulate and rise to dangerous levels in your liver, putting you at risk for cirrhosis and other serious liver diseases. Scientists classify several substances as lipotropic compounds. Three lipotropic compounds in particular – Choline, Inositol and Methionine – help you lose weight.


This is an essential amino acid, meaning it cannot be produced by the body itself. Therefore, it is necessary to ensure an intake through nutrition and/or supplementation. Methionine has a fat-dissolving effect and reduces the depositing of fat in the liver. By helping prevent the accumulation of fat in the liver it ensures normal liver function, which is essential for the elimination of toxins from the body. Methionine also supports liver function by regulating glutathione supplies; glutathione is needed to help neutralize toxins in the liver. The body also needs plenty of Methionine to produce two other sulfur-containing amino acidsCysteine and Taurine, which help the body eliminate toxins, build strong, healthy tissues, and promote cardiovascular health.


Inositol benefits your body in a number of ways by transporting fat throughout your body and it also aids the neurons in your central nervous system to make sure everything is running smoothly. One major health benefit of Inositol is that when combined with Choline, they produce lecithin. Lecithin is fundamental in breaking down fats in your body and this means that it can prevent fat build ups in the cell walls of your heart, arteries and brain by breaking down the fatty deposits.  Less fat in your arteries, means lower cholesterol!

One of the most talked about Inositol benefits is how it benefits your hair. It’s a member of the B complex family which, are known to promote strong, healthier hair, and faster growth.


Choline serves various functions in our bodies. Over the past few years, there has been a rush of research, and there are now hints that Choline may be essential not only for the brain development of fetuses and infants, but may help prevent memory loss associated with aging.

Choline has been shown to protect the liver from certain types of damage, and can help reverse damage that has already occurred. Additionally, it may help lower cholesterol and homocysteine levels associated with cardiovascular disease, and may also help protect against some types of cancers.

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UTMB study finds that testosterone therapy is not linked with blood clot disorders in veins

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A new study from The University of Texas Medical Branch at Galveston of more than 30,000 commercially insured men is the first large comparative analysis to show that there is no link between testosterone therapy and blood clots in veins. The study found that middle-aged and older men who receive testosterone therapy are not at increased risk of this illness. The findings are detailed in Mayo Clinic Proceedings.

Venous thromboembolism is a disease where blood clots form in the veins and cause blockages. The most common forms of VTE are deep vein thrombosis, which occurs often in the legs and pulmonary embolism, which is a clot in the lungs. VTE is the third most common cardiovascular illness, after heart attack and stoke.

“In 2014, the Federal Drug Administration required manufacturers to add a warning about potential risks of VTE to the label of all approved testosterone products,” said Jacques Baillargeon, professor of epidemiology in the department of preventive medicine and community health and lead author of the study. “The warning, however, is based primarily on post-marketing drug surveillance and case reports. To date, there have been no published comparative, large-scale studies examining the association of testosterone therapy and the risk of VTE.”

As a result of this conflicting evidence and the broad media attention it has received, there are many men with medically confirmed low testosterone who are afraid to receive testosterone therapy and there may be physicians who are reluctant to prescribe testosterone therapy based on this conflicting information.

The case-control study included 30,572 men 40 years and older who were enrolled in one of the nation’s largest commercial insurance programs between Jan. 1, 2007 and Dec. 31, 2012. Cases were defined as men who had a primary diagnosis of VTE and received an anticoagulant drug or an intravascular vena cava filter in the 60 days following their diagnoses. Cases were matched with three control subjects on age, geographic region, diagnosis of low testosterone and diagnosis of any underlying pro-clotting condition.

The researchers found that having a prescription for testosterone therapy was not associated with an increased risk of VTE. In addition, none of the specific routes of administration examined — topical creams, transdermal patches or intramuscular injections — were associated with an increased risk. There were no differences between men who received the therapy 15, 30 or 60 days before being diagnosed with VTE.

“It is important to acknowledge, for a man who has medically-diagnosed low testosterone, that there are clear risks to not receiving testosterone therapy, including osteoporosis, sexual dysfunction, increased amounts of fat tissue, decreased lean muscle mass, possible metabolic syndrome and cardiovascular disease,” said Baillargeon. “It’s also important to note that further research needs to be conducted to rigorously assess the long-term risks of testosterone therapy.

These findings may help to inform the benefit-risk assessment for men with testosterone deficiency considering treatment.


Other authors include UTMB’s Randall J. Urban, Gwen Baillargeon, Gulshan Sharma and Yong-Fang Kuo; Abraham Morgentaler from Men’s Health Boston at Harvard Medical School and Charles J. Glueck from Jewish Hospital at Mercy Medical Physicians in Cincinnati, OH.

This research was supported by the National Institutes of Health.


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Low testosterone linked to heightened risk of early death

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Low testosterone levels seem to be linked to a heightened risk of premature death from heart disease and all causes, suggests research published online in Heart.

The finding refutes received wisdom that the hormone is a risk factor for cardiovascular disease.

The researchers base their findings on 930 men, all of whom had coronary artery heart disease, and had been referred to a specialist heart centre between 2000 and 2002. Their heart health was then tracked for around 7 years.

On referral, low testosterone was relatively common. One in four of the men was classified as having low testosterone, using measurements of either bioavailable testosterone (bio-T) – available for tissues to use – of under 2.6 mmol/l or total testosterone (TT) of under 8.1 mmol/l.

These measures indicate clinically defined testosterone deficiency, referred to as hypogonadism, as opposed to a tailing off in levels of the hormone as a result of ageing.

During the monitoring period almost twice as many men with low testosterone died as did those with normal levels. One in five (41) of those with low testosterone died, compared with one in eight (12%) of those with normal levels.

The only factors that influenced this risk were heart failure (left ventricular dysfunction), treatment with aspirin or a high blood pressure drug (beta blocker) and low bio-T levels.

A low bio-T level was an independent risk factor for premature death from all causes and from heart disease, after taking account of other influential factors, such as age, other underlying health problems, smoking and weight.

Borderline levels of low total testosterone (15.1mmol/l) also increased the risk of an early death.

While high doses of testosterone found in anabolic steroids are harmful to health, the evidence suggests that low, rather than high, levels of the hormone, are associated with obesity, risky blood fats, and insulin resistance, all of which are risk factors for diabetes and heart disease, say the authors.

Men at high risk of these diseases may stand most to gain from testosterone replacement, they suggest.

An accompanying editorial points out that there is increasing interest in looking at the impact of testosterone replacement.

“There has been a marked increase in prescription of testosterone over recent years. While the long term cardiovascular impact of testosterone supplements in those with low levels remains to be demonstrated, accumulating evidence suggests there is a sound basis for examining this,” write the authors.

Research into testosterone has taken a back seat for many years, in favour of looking at the impact of oestrogens on heart disease, they conclude, adding: “Recent data suggest that this important pathway warrants a lot more attention.”


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Low testosterone levels may indicate worsening of disease for men with prostate cancer

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For men with low-risk prostate cancer, low levels of testosterone may indicate a worsening of their disease. That’s the conclusion of a new study published in BJU International. The findings may help physicians identify patients with low-risk prostate cancer who should receive aggressive anticancer treatment.

Men with prostate cancer that is not life threatening and is only slowly progressing, can often forego treatment and instead undergo active surveillance. This involves close monitoring to ensure that their disease does not become serious and jeopardize their health. Unfortunately, doctors currently have no reliable way of predicting which men will develop evidence of worsening or more aggressive disease during active surveillance.

Ignacio San Francisco, MD, of the Pontificia Universidad Católica de Chile, and his colleagues looked to see if testosterone levels might provide any indication. After following 154 men with low-risk prostate cancer for 38 months, the investigators found that low levels of free testosterone were significantly linked with an increased risk of developing more aggressive disease. They found no significant association with total testosterone concentrations, although there was a general trend towards increased risk with lower levels. Free testosterone comprises one to two percent of total testosterone and is considered a useful surrogate for the biologically active portion of circulating testosterone.

“These results suggest low levels of testosterone are associated with more aggressive prostate cancer. This contradicts long-held beliefs that high testosterone is risky for prostate cancer, and low testosterone is protective,” said Dr. San Francisco.

The results of this study provide valuable information to clinicians and their patients concerning risk factors for prostate cancer progression in men undergoing active surveillance. “In borderline cases, the presence of low values of free testosterone may help determine whether it is more prudent to initiate treatment rather than continue observation,” said Dr. San Francisco.

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Study of 83,000 veterans finds cardiovascular benefits to testosterone replacement

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A Veterans Affairs database study of more than 83,000 patients found that men whose low testosterone was restored to normal through gels, patches, or injections had a lower risk of heart attack, stroke, or death from any cause, versus similar men who were not treated.

The study also found that men who were treated but did not attain normal levels did not see the same benefits as those whose levels did reach normal. The study was published online Aug. 6, 2015, in the European Heart Journal.

The findings may sway the ongoing debate over testosterone therapy’s benefits and risks, especially for the heart. Studies over the past few years have yielded mixed results, although part of that might stem from differing patient populations and research methods.

For example, the new VA study excluded men with a history of heart attacks or strokes, although it did include those with existing heart disease. A much-cited VA database study that was published in JAMA in 2013 looked specifically at men with coronary artery disease; about 20 percent of the total study group of around 8,700 men had suffered a prior heart attack.

So far, the medical community lacks results from any definitive clinical trial that might provide clear guidance. Meanwhile, the Food and Drug Administration issued guidance earlier in 2015 advising clinicians about the over-use of testosterone therapy, and pointing to a possible increased risk of heart attack and stroke.

The new VA study is likely to draw attention because of its large size and relatively long follow-up period.

Dr. Rajat Barua, the paper’s corresponding author, says the study is also noteworthy because of its finding that administering the right dose is critical: Treating “low T” but not restoring levels to normal doesn’t appear to impart much benefit, at least in terms of cardiovascular risk. Testosterone isn’t prescribed with the goal of improving heart health, but that is a consideration in many cases.

“It is the first study to demonstrate that significant benefit is observed only if the dose is adequate to normalize the total testosterone levels,” Barua and his coauthors wrote. “Patients who failed to achieve the therapeutic range after testosterone replacement therapy did not see a reduction in [heart attack] or stroke and had significantly less benefit on mortality.”

Barua is with the Kansas City (Mo.) VA Medical Center. He’s also an assistant professor of medicine at the University of Kansas.

The study team looked at national data on more than 83,000 men with documented low testosterone, all age 50 or above, who received care in VA between 1999 and 2014.

The researchers divided the men into three clinical groups: those who were treated to the point where their total testosterone levels returned to normal (Group 1); those who were treated but without reaching normal (Group 2); and those who were untreated and remained at low levels (Group 3).

Importantly, all three groups were “propensity matched” so the comparisons would be between men with similar health profiles. The researchers took into account a wide array of factors that might affect cardiovascular and overall risk. They included, for example, age, body mass index, various chronic diseases, LDL cholesterol levels, and the use of aspirin, beta blockers, and statins.

The average follow-up across the groups ranged from 4.6 to 6.2 years.

The sharpest contrast emerged between Group 1 (those who were treated and attained normal levels) and Group 3 (those whose low testosterone went untreated). The treated men were 56 percent less likely to die during the follow-up period, 24 percent less likely to suffer a heart attack, and 36 percent less likely to have a stroke.

The differences between Group 1 and Group 2 (those who were treated but did not attain normal levels) were similar but less pronounced.

Little difference emerged between Groups 2 and 3, except for a slight benefit in survival for those who were treated.

Barua and colleagues say they don’t know the exact reasons for testosterone’s apparent benefits for the heart and overall survival. “The mechanisms for these effects remain speculative,” they write. Possible explanations, they say, could involve body fat, insulin sensitivity, lipids, blood platelets, inflammation, or other biological pathways. More research is needed, they say, to clarify how testosterone affects the cardiovascular system.

While the new study results do seem to advocate for testosterone replacement therapy, Barua stresses the need for “appropriate screening, selection, dosing, and follow-up of patients to maximize the benefit of testosterone therapy.”

The authors also caution that “off-label” use remains a concern. In other words, doctors should not write a prescription simply because an older man is complaining of symptoms such as low energy and low sex drive. According to the FDA, “Testosterone products are FDA-approved only for use in men who lack or have low testosterone levels in conjunction with an associated medical condition. Examples of these conditions include failure of the testicles to produce testosterone because of reasons such as genetic problems or chemotherapy. … None of the FDA-approved testosterone products are approved for use in men with low testosterone levels who lack an associated medical condition.”

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Testosterone therapy may prevent Alzheimer’s disease

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Researchers at the University of Southern California have discovered a direct link between loss of testosterone and the development of an Alzheimer’s-like disease in mice. They also discovered that testosterone treatment slows progression of the disease.

The study, published in the December 20 issue of The Journal of Neuroscience, predicts that testosterone-based hormone therapy may be useful in the treatment and prevention of Alzheimer’s disease in aging men.

“We’ve known that low testosterone is a risk factor for Alzheimer’s disease but now we know why,” said Christian Pike, senior author and associate professor at the Leonard Davis School of Gerontology at USC. “The implication for humans is that testosterone therapy might one day be able to block the development of the disease.”

In order to investigate testosterone’s role in the development of Alzheimer’s disease, the team took away the ability of male mice to produce testosterone. Some mice were then given a form of testosterone while others were given none.

The mice with lowered testosterone showed increases in levels of the protein beta-amyloid, which has been widely implicated as playing a role in the development of Alzheimer’s disease. They also showed signs of behavioral impairment.

The mice that were given testosterone showed reduced accumulation of beta-amyloid and less behavioral impairment.

“These results are exciting because they tell us that we are on to something that is worth pursuing,” said Pike. “The next step is to look at what the long term effects of testosterone therapy are in aging men.”

This study adds valuable new information to understanding the role of hormones in aging and disease. Recent evidence has suggested that testosterone may be useful in other neurological conditions. In a presentation at the Society of Neuroscience’s annual meeting this fall, Chien-Ping Ko, professor of biological sciences at USC reported that testosterone therapy improved muscle coordination in mice suffering from a form of Amyotrophic Lateral Sclerosis, Lou Gehrigs Disease.


Pike’s co-authors on the Journal of Neuroscience study were Emily R. Rosario and Jenna Carroll of the USC Neuroscience Graduate Program and Salvatore Oddo and Frank M. LaFerla of the University of California, Irvine. The Alzheimer’s Association and the National Institutes of Health provided funding.


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Beet juice boosts muscle power in heart patients

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Scientists have evidence that Popeye was right: Spinach makes you stronger. But it’s the high nitrate content in the leafy greens — not the iron — that creates the effect.

Building on a growing body of work that suggests dietary nitrate improves muscle performance in many elite athletes, researchers at Washington University School of Medicine in St. Louis found that drinking concentrated beet juice — also high in nitrates — increases muscle power in patients with heart failure.

“It’s a small study, but we see robust changes in muscle power about two hours after patients drink the beet juice,” said senior author Linda R. Peterson, MD, associate professor of medicine. “A lot of the activities of daily living are power-based — getting out of a chair, lifting groceries, climbing stairs. And they have a major impact on quality of life. We want to help make people more powerful because power is such an important predictor of how well people do, whether they have heart failure, cancer or other conditions. In general, physically more powerful people live longer.”

Based on research in elite athletes, especially cyclists who use beet juice to boost performance, the study’s corresponding author, Andrew R. Coggan, PhD, assistant professor of radiology, suggested trying the same strategy in patients with heart failure.

In the September issue of the journal Circulation: Heart Failure, the scientists reported data from nine patients with heart failure. Two hours after the treatment, patients demonstrated a 13 percent increase in power in muscles that extend the knee. The researchers observed the most substantial benefit when the muscles moved at the highest velocities. The increase in muscle performance was significant in quick, power-based actions, but researchers saw no improvements in performance during longer tests that measure muscle fatigue.

Patients in the study served as their own controls, with each receiving the beet juice treatment and an identical beet juice placebo that had only the nitrate content removed. There was a one- to two-week period between trial sessions to be sure any effects of the first treatment did not carry over to the second. Neither the trial participants nor the investigators knew the order in which patients received the treatment and placebo beet juice.

The researchers also pointed out that participants experienced no major side effects from the beet juice, including no increase in heart rates or drops in blood pressure, which is important in patients with heart failure.

Heart failure can have various triggers, from heart valve problems to viral infections, but the result is the heart’s gradual loss of pumping capacity.

“The heart can’t pump enough in these patients, but that’s just where the problems start,” said Peterson, a cardiologist and director of Cardiac Rehabilitation at Washington University and Barnes-Jewish Hospital. “Heart failure becomes a whole-body problem because of the metabolic changes that happen, increasing the risk of conditions such as insulin resistance and diabetes and generally leading to weaker muscles overall.”

While the trial was not designed to find out whether patients noticed an improved ability to function in daily life, the researchers estimated the size of the benefit by comparing the improvement in muscle power with what is seen from an exercise program.

“I have compared the beet-juice effect to Popeye eating his spinach,” said Coggan, who specializes in exercise physiology. “The magnitude of this improvement is comparable to that seen in heart failure patients who have done two to three months of resistance training.”

The nitrates in beet juice, spinach and other leafy green vegetables such as arugula and celery are processed by the body into nitric oxide, which is known to relax blood vessels and have other beneficial effects on metabolism.

With the growing evidence of a positive effect from dietary nitrates in healthy people, elite athletes and now heart failure patients, the researchers also are interested in studying dietary nitrates in elderly populations.

“One problem in aging is the muscles get weaker, slower and less powerful,” Coggan said. “Beyond a certain age, people lose about 1 percent per year of their muscle function. If we can boost muscle power like we did in this study, that could provide a significant benefit to older individuals.”


This work was supported by The Foundation for Barnes-Jewish Hospital, the Washington University Mentors in Medicine and C-STAR programs, and Washington University Institute of Clinical and Translational Sciences grant UL1 TR000448 from the National Center for Advancing Translational Sciences of the National Institutes of Health (NIH).

Coggan AR, Leibowitz JL, Spearie CA, Kadkhodayan A, Thomas DP, Ramamurthy S, Mahmood K, Park S, Waller S, Farmer M, Peterson LR. Acute dietary nitrate intake improves muscle contractile function in patients with heart failure: a double-blind, placebo-controlled, randomized trial. Circulation: Heart Failure. September 2015.

Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient-care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.

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