Shockwave Treatment for ED

National Institute for Health Conclusion on Low Intensity Extracorporeal Shock Wave Therapy:

LI-ESWT is a revolutionary treatment of ED, and probably possesses unprecedented qualities that can rehabilitate erectile tissue. The clinical improvement in subjective erectile function together with the significant improvement in penile hemodynamics following LI-ESWT confirm that LI-ESWT has unique properties that may create a new standard of care for men with ED. LI-ESWT is both feasible and tolerable and without any adverse or unwanted effects. Its main advantage is its ability to improve and potentially restore erectile function in men with ED without additional pharmacotherapy. Hence, LI-ESWT is an appealing addition to the armamentarium of existing treatment options for ED.

To read the entire article go to: towww.ncbi.nlm.nih.gov/pmc/articles/PMC3607492/

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ED / Vitamin D Deficiency Link

 

The prevalence of ED is 30% higher among men who have vitamin D levels below 20 ng/mL versus those with levels of 30 ng/mL or higher.
The prevalence of ED is 30% higher among men who have vitamin D levels below 20 ng/mL versus those with levels of 30 ng/mL or higher.
Vitamin D deficiency is associated with an increased prevalence of erectile dysfunction (ED) independent of risk factors for atherosclerotic cardiovascular disease (ASCVD), according to a new study.
Men with vitamin D deficiency—defined as a 25-hydroxyvitamin D [25(OH)D] level below 20 ng/mL—have a significant 30% and 80% greater prevalence of ED and severe ED, respectively, compared with men who have optimal levels (30 ng/mL or higher), after adjusting for comorbidities, lifestyle variables, and medication use, investigators reported in Atherosclerosis (2016;252:61-67). In addition, each 10 ng/mL decrease in 25(OH)D was associated with a significant 12% increased prevalence of ED.
“Our findings have potentially important clinical and public health implications for men,” Erin D. Michos, MD, of Johns Hopkins University School of Medicine in Baltimore, and colleagues wrote. “25(OH)D is an easy biomarker to screen for through simple commercially-available laboratory tests, and deficiencies can be treated with supplementation and/or modest sunlight exposure.”
They pointed out, however, that additional research, such as randomized controlled clinical trials, is needed to determine whether treating vitamin D deficiency can improve erectile function.
Dr Michos’ team studied 3390 men aged 20 years or older free of ASCVD who participated in the 2001–2004 National Health and Nutrition Examination Survey. For the study, investigators measured serum 25(OH)D using the DiaSorin radioimmunoassay and assessed self-reported ED using a single question from the Massachusetts Male Aging Study: “How would you describe your ability to get and keep an erection adequate for satisfactory intercourse?” Men who answered “never” or “sometimes able” were considered to have ED. Investigators defined severe ED as never being able to get and keep an erection.
The weighted prevalence of 25(OH)D deficiency and ED were 30% and 15.2%, respectively. Levels of 25(OH)D were significantly lower among men with versus without ED (mean 22.8 vs 24.3 ng/mL).
Dr Michos and her colleagues discussed various mechanisms that could explain a biologic relationship between vitamin D deficiency and ED. For example, vascular ED results from endothelial dysfunction and/or atherosclerosis. Diabetes mellitus is a strong risk factors for both of these conditions, diabetic men are 3 times more likely than non-diabetic men to have ED, they pointed out. “The association of 25(OH)D with ED and with ASCVD may be mediated by impaired glucose metabolism,” they stated.
The investigators also noted that men with ED have an increased prevalence of endothelial dysfunction, and vitamin D may improve endothelial function. “One mechanism linking low vitamin D levels with ED may be via reduced synthesis of nitric oxide,” they wrote. “Secretion of nitric oxide is needed for relaxation of the smooth muscles of the corpora cavernosa and subsequent penile erection, and vitamin D may be a regulator of endothelial nitric oxide synthase.”

Testosterone Therapy May Protect Against Heart Attacks

The past decade has seen a substantial increase in the number of older men receiving testosterone therapy—as well as a growing concern that it increases their risk for myocardial infarction (MI) and stroke.

But new research from the University of Texas Medical Branch at Galveston may ease some of those concerns.
“The most significant finding of our study was that older men who were treated with testosterone did not appear to have an increased risk of MI,” says lead study author Jacques Baillargeon, PhD, associate professor of epidemiology in UTMB’s Department of Preventive Medicine and Community Health. “In addition, for men with high MI risk, testosterone use appeared to be modestly protective against MI.”

Baillargeon and colleagues studied more than 25,000 older men. They examined enrollment and claims Medicare data for 6,355 Medicare beneficiaries ages 66 and older who had been treated with at least 1 injection of intramuscular testosterone between January 1997 and December 2005.

They compared these patients to a control group of 19,065 men of the same age, race, Medicaid eligibility, and health status who did not receive testosterone therapy.

“This was a methodologically rigorous study of a large nationally representative cohort of ‘real-world’ older males,” Baillargeon says. “We believe it should be thoughtfully weighed and considered in the debate on the issue of testosterone and cardiovascular risks.”

Not only did their analyses show that testosterone therapy was not associated with an increased risk of heart attack, but it also suggested testosterone users with a higher MI risk had a lower rate of heart attacks compared to the control group. Baillargeon says there are some plausible biological mechanisms for this protective effect—but emphasizes that more research is needed.

“This finding was statistically significant, but I think it’s important to examine this finding in the context of the broader literature, including current and upcoming clinical trials,” he says. “On this issue, given the current state of conflicting evidence, it will be important to conduct more original research and systematic reviews of the entire body of evidence. Hopefully, over time with rigorous scientific assessment, clarity will be brought to this issue.”

Baillargeon and his colleagues would also like to conduct more research into the effects of long-term exposure to testosterone as well as evaluating testosterone therapy in younger men. “Given the increased number of middle-aged men receiving testosterone prescriptions, we’d like to examine risks and benefits in these younger age groups, particularly in men who are not clearly hypogonadal,” he says.

Colleen Mullarkey

Reference

Baillargeon J, Urban RJ, Kuo YF, Ottenbacher KJ, Raji MA, Du F, et al. Risk of myocardial infarction in older men receiving testosterone therapy. Ann Pharmacother. 2014 Jul 2. pii: 1060028014539918. [Epub ahead of print].

Eating Fruit Daily Reduces CV Risk by 40%

Fri, 09/05/14 – 16:16

Consuming fruit on a daily basis can cut the risk of cardiovascular disease (CVD) by up to 40%, according to research recently presented at the European Society of Cardiology Congress.

In a study of 451,681 participants in the China Kadoorie Biobank, the researchers found that, over the course of a 7-year follow-up period, the risk of cardiovascular disease declined the more fruit participants ate.

The study included individuals with no history of CVD and not on anti-hypertensive treatment at baseline. Habitual consumption was recorded at baseline according to 5 categories: never, monthly, 1 to 3 days per week, 4 to 6 days per week, and daily. Over the 7-year follow-up period, the researchers observed 19,300 cases of ischaemic heart disease (IHD), and 19,689 strokes. Eighteen percent of participants consumed fruit daily, while 6.3% never consumed fruit. The average amount of fruit eaten by those who reported consuming fruit daily was 1.5 portions.

Compared to those who never ate fruit, daily fruit eaters cut their CVD risk between 25% and 40% . More specifically, this number was around 15% for IHD, around 25% for ischaemic stroke, and 40% for hemorrhagic stroke. The authors also found a dose-response relationship between the frequency of fruit consumption and the risk of CVD. In addition, people who consumed fruit more often had much lower blood pressure. Eating fruit on a daily basis was associated with 3.4/4.1 mmHg lower systolic/diastolic blood pressure in comparison to those who indicated they never ate fruit.

“CVD, including ischaemic heart disease and stroke, is the leading cause of death worldwide,” according to Huaidong Du, MD, a physician in Oxford in the United Kingdom, and lead author of the study.

“Improving diet and lifestyle is critical for CVD risk reduction in the general population, but the large majority of this evidence has come from western countries and hardly any from China,” says Du.

“Our data clearly shows that eating fresh fruit can reduce the risk of cardiovascular disease, including ischaemic heart disease and stroke—particularly hemorrhagic stroke. And not only that, the more fruit you eat the more your CVD risk goes down. It does suggest that eating more fruit is beneficial compared to less or no fruit.”

The findings were originally presented at the European Society of Cardiology Congress, held Aug. 30 – Sept. 3 in Barcelona, Spain.

—Mark McGraw

EMA Panel Says No Heart Risk With Testosterone

A European Medicines Agency (EMA) review committee has concluded that there’s no consistent evidence that testosterone increases the risk of heart problems in men with hypogonadism.
The agency’s Pharmacovigilance Risk Assessment Committee (PRAC) said the drug’s benefits outweigh its risks but warned that it should only be used in patients with confirmed hypogonadism.
The decision follows an FDA advisory committee meeting last month that called for a tightening of label indications and renewed efforts to curb off-label use.
European regulators decided that the evidence about testosterone’s risks and benefits is inconsistent. Several studies have shown an increased risk of heart problems, while others did not, the agency said in a press release.
A group of American endocrinologists has called for one of those papers, published in the Journal of the American Medical Association, to be retracted.
PRAC recommended that testosterone only be used if hypogonadism has been confirmed by symptoms and laboratory testing — and this should be added to the European product information for all testosterone-containing drugs, the group said.
Label information should also include warnings against the drug’s use in men who have heart, liver, or kidney problems, as well as the fact that there are limited data on safety and efficacy in patients over 65, PRAC said.
Although the group acknowledged that a lack of testosterone could increase the risk of heart problems, it still called for further investigation and monitoring of the safety of testosterone drugs.
EMA launched its review of testosterone products in April. PRAC’s recommendations will now go to the Coordination Group for Mutual Recognition and Decentralized Procedures – Human (CMDh) for a final position.
The FDA has not yet given a final ruling on its testosterone review, which began in January. In June, the agency issued a warning that testosterone products could cause venous thromboembolism (VTE), but it said this action was not related to the review.

Testosterone & Cardiac Risk

ISSUE: FDA is investigating the risk of stroke, heart attack, and death in men taking FDA-approved testosterone products. We have been monitoring this risk and decided to reassess this safety issue based on the recent publication of two separate studies that each suggested an increased risk of cardiovascular events among groups of men prescribed testosterone therapy. FDA is providing this alert while it continues to evaluate the information from these studies and other available data. FDA will communicate final conclusions and recommendations when the evaluation is complete.

BACKGROUND: Testosterone is a hormone essential to the development of male growth and masculine characteristics. Testosterone products are FDA-approved only for use in men who lack or have low testosterone levels in conjunction with an associated medical condition.

RECOMMENDATION: At this time, FDA has not concluded that FDA-approved testosterone treatment increases the risk of stroke, heart attack, or death. Patients should not stop taking prescribed testosterone products without first discussing any questions or concerns with their health care professionals. Health care professionals should consider whether the benefits of FDA-approved testosterone treatment is likely to exceed the potential risks of treatment. The prescribing information in the drug labels of FDA-approved testosterone products should be followed.

Healthcare professionals and patients are encouraged to report adverse events or side effects related to the use of these products to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program:

Is Testosterone Replacement Safe?

Dear Patients,
Recently there has been a great deal of press regarding the safety of Testosterone replacement. Two recent studies have suggested that Testosterone replacement therapy is associated with a higher risk of heart attack and stroke. The first study was first reported in November of 2013. This study was debated at the Sexual Medicine Society of North America’s meeting shortly after it was published. The conclusions by some of the most noted authorities in the country is reproduced for you below. It suggests that the study was poorly designed and fraught with technical errors. It was my suggestion at the time that patients on testosterone replacement therapy should continue on with their treatment.
A new study has just been published last week, that again claims that T replacement can be harmful to patients with heart disease. Like the previous study, it will have to be examined for its credibility. I will update you as soon as we have a consensus of opinion from medical experts in the field of T therapy.
Yours in good health,
George Carroll MD

Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels, Editorial Commentary by Ravi Kacker, MD and Abraham Morgentaler, MD

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BERKELEY, CA (UroToday.com) – Considerable concern has been expressed regarding the safety of testosterone (T) therapy since the recent publication in JAMA of a study alleging increased risk of death, and cardiovascular events in men who received testosterone. However, a careful reading of this study by Vigen, et al. reveals this concern is misplaced, and that the data appear to support the opposite conclusion.
The authors retrospectively investigated rates of death, myocardial infarction (MI), and stroke in a large cohort of men in the VA hospital system who had undergone coronary angiography and had a documented serum T < 300ng/dl.[1] The authors reported that men who were treated with T therapy had a greater risk of events than untreated men.
To anyone familiar with the testosterone field, this conclusion was surprising as it contradicts a rich literature spanning more than 20 years demonstrating a beneficial effect of T on cardiovascular function.[2] The discrepancy between the conclusion of this study and prior literature is explained by the highly statistical nature of the paper, and by a serious methodological error.
The raw data was as follows. Among 1 223 men who received T therapy, there were 67 deaths, 23 MIs, and 33 strokes for an event rate of 10.1% (123 of 1 223 men). For 7 486 men who did not receive T therapy, there were 681 deaths, 420 MIs, and 486 strokes for a rate of 21.2% (1 587 of 7 486 men), or roughly twice the rate of events for men on T therapy. Despite this, the authors wrote, “The absolute rate of events were 19.9% in the no testosterone therapy group vs 25.7% in the testosterone therapy group” at 3y following angiography. This is mathematically impossible, and the authors have since been obligated to revise their article, replacing “absolute risk” with “Kaplan-Meier estimated cumulative percentages with events.” The significance of this change is that it accurately reflects the fact that the conclusion was based on statistical estimates rather than compelling raw data. By the end of the study, the estimated event rate was approximately 30% for the T-group, a threefold multiple of what actually occurred, greatly magnifying potential errors.
The rationale for such a high degree of statistical manipulation becomes evident when one looks at the study design. All men began in the no-T group until some of them filled a prescription for testosterone, at which point they were assigned to the T group. However, men in this group also contributed survival data to the no-T group for the period prior to initiating T therapy. There was also a significant delay (mean 531d) in initiating treatment. An MI was attributed to the T group if a man filled his testosterone prescription the same day, but to the no-T group if he hadn’t yet filled it. Moreover, the two groups were dissimilar in important ways at baseline, with greater coronary artery disease burden in the no-T group, and lower serum T concentration in the T-group, each of which could influence outcomes. Clearly, a sophisticated statistical approach was necessary to accommodate these and other complex issues, causing the investigators to adjust for more than 50 variables. While understandable, this degree of complexity undermines the reliability of the results.
However, our greatest concern is the incorrect exclusion of 1 132 men who were placed on T therapy after MI or stroke. For the purposes of the study, once the event occurred it was irrelevant what happened subsequently to these men. All these events should have been attributed to the no-T group, which would have increased events in that group by 71.8%. Corrected for that serious methodological error, it seems likely that the results of this study would be consistent with two previous reports showing a substantial reduction in mortality with T therapy.[3, 4]
Shores, et al. also investigated the use of T therapy in a VA population of men with T< 300ng/dl. In that study, mortality in T-treated men was 10.3% compared with 20.7% in untreated men (P < 0.0001). Muraleedharan, et al. performed a similar investigation in diabetic men with T< 300ng/dl, and reported mortality of 8.4% in T-treated men and 19.2% in untreated men (P=0.002).
Defining the cardiovascular risk of T therapy is important, and will ultimately require a large, prospective trial. In the meantime, we must make do with available data, indicating on the whole that men with T deficiency are at increased risk for diabetes, metabolic syndrome, cardiovascular disease, and mortality.[5, 6] The conclusions of Vigen et al notwithstanding, early retrospective results suggest that T therapy may actually reduce cardiovascular events and mortality.
References:
  1. Vigen R, O’Donnell CI, Baron AE, et al. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA : The journal of the American Medical Association. Nov 6 2013;310(17):1829-1836.
  2. Traish AM, Kypreos KE. Testosterone and cardiovascular disease: an old idea with modern clinical implications. Atherosclerosis. Feb 2011;214(2):244-248.
  3. Shores MM, Smith NL, Forsberg CW, Anawalt BD, Matsumoto AM. Testosterone treatment and mortality in men with low testosterone levels. Journal of Clinical Endocrinology and Metabolism. Jun 2012;97(6):2050-2058.
  4. Muraleedharan V, Marsh H, Kapoor D, Channer KS, Jones TH. Testosterone deficiency is associated with increased risk of mortality and testosterone replacement improves survival in men with type 2 diabetes. European Journal of Endocrinology / European Federation of Endocrine Societies. 2013;169(6):725-733.
  5. Tajar A, Huhtaniemi IT, O’Neill TW, et al. Characteristics of androgen deficiency in late-onset hypogonadism: results from the European Male Aging Study (EMAS). The Journal of Clinical Endocrinology and Metabolism. May 2012;97(5):1508-1516.
  6. Stellato RK, Feldman HA, Hamdy O, Horton ES, McKinlay JB. Testosterone, sex hormone-binding globulin, and the development of type 2 diabetes in middle-aged men: prospective results from the Massachusetts male aging study. Diabetes Care. Apr 2000;23(4):490-494.
Additional Recommended Reading:
  • Carson CC, 3rd, Rosano G. Exogenous testosterone, cardiovascular events, and cardiovascular risk factors in elderly men: a review of trial data. The Journal of Sexual Medicine. Jan 2012;9(1):54-67.
  • Kelly DM, Jones TH. Testosterone: a vascular hormone in health and disease. The Journal of Endocrinology. Jun 2013;217(3):R47-71.
Written by:
Ravi Kacker, MD and Abraham Morgentaler, MD, Men’s Health Boston, Brookline, MA USA
JAMA Nov 6 2013;310(17):1829-1836
doi: 10.1001/jama.2013.280386