text:
OHSU Physician Writes National and State-by-State Women's Report Card
Portland, Ore.
This is day 10 of the nursing strike at OHSU. Mixed messages and false accusations have muddied the truth about negotiations between OHSU and the Oregon Nurses Association. The following offers clarification of the facts surrounding the strike.
Here's what the OHSU nursing strike is and isn't about.
It's not about staffing.
Striking nurses say they walked off the job because they're sick of working long hours in overflowing hospitals. Most of OHSU's 1,000 full and part-time nurses work 28 to 36 hours per week. Nurses have requested twelve hour shifts so they can more days off. Management agrees this schedule helps ensure nurses get rest between work assignments.
The union claims OHSU nurses are intimidated to say no to overtime requests. In the more than two million hours nurses worked last year, they collectively worked about 600 hours of mandatory overtime, most of which occurred on two particularly busy weekends for Portland hospitals. OHSU nurses are always paid extra -- either time-and-a-half or double -- to work overtime.
Either these concerns are the issues for a fringe few, or the union is not adequately representing its members. During recent contract proposals, the ONA/AFL-CIO never asked for OHSU for staffing changes. The ONA's demands have always been about money.
It's not about patient safety.
Hospital managers adjust staffing constantly based on the number of patients and the severity of their illnesses. OHSU would never compromise patient care for any reason. That's why, when union nurses decided to strike, OHSU hired enough licensed professional replacement nurses to ensure safe, quality care. We also reduced our patient load to that which we could staff adequately.
It's not about earning a fair market wage.
The ONA has turned down every fair market wage offered by OHSU during recent negotiations. The combined wage and benefits package in OHSU's last offer would be the best nursing contract in the community.
The union has consistently demanded wages and benefits drastically higher than OHSU and the community can afford. OHSU values its nurses and the work they do, but the university has no pot of gold at the end of the rainbow. OHSU is bound by the limits of its budget.
It's not about OHSU's profit.
Profits are what private businesses pay to shareholders. As a not-for profit organization, OHSU has no profit and no shareholders. It is a public institution committed to everyone in Oregon.
Any money OHSU made last year goes into its reserve fund, to cushion the blow of unanticipated expenses -- such as a strike or an increase in our number of uninsured patients. Just as any fiscally-responsible person maintains an emergency savings account, all businesses have reserve funds as a safeguard.
It is about the economics of health care.
The pot of health care dollars shrinks as expenses and the ranks of the uninsured rise, forcing insurance premium increases for businesses and the government. OHSU and other public health institutions must help contain those costs or everyone loses.
It would be irresponsible of OHSU to pay what the union is asking, which is considerably higher than fair market wage. If OHSU resets the bar, other hospitals will be pressed to follow suit. Business and individuals would feel the pinch of this sudden wage inflation in the form of higher insurance premiums.
It is about OHSU's budget.
OHSU, which is not a state agency, struggles like any business in today's depressed economy. As Portland's largest employer and the state's fourth largest, OHSU has a responsibility to remain economically solvent. It must make sound business decisions to ensure fair wages for all of its 11,000 employees, many of whom work outside the patient care realm. OHSU is mandated by the state to serve Oregon through patient care, research, education and community service.
It is about training more nurses.
The obvious way to combat the nationwide nursing shortage is to educate more nurses. OHSU devotes a tremendous amount of energy to this effort. Enrollment in the School of Nursing's bachelor's program is up 15 percent from last year. Expanded online and video-based degree programs let working rural nurses pursue advanced training without leaving home. OHSU's School of Nursing, which is ranked among the top 10 schools in the nation, is launching new programs that focus squarely on this issue. In addition, the school constantly reinvigorates its curriculums to respond to the community's changing health care' needs.
It is about nurses having a greater say in health care.
OHSU nurses are integral to the university mission. Some striking nurses say that this is really about respect. OHSU wants to respond to them outside the context of a strike. The institution counts on nurses as partners in the ongoing effort to build a strong university and patient care community.
Previous Story OHSU Researchers Find Fourth and Perhaps Final Gene Involved in "Overheating" Disorder Next Story Facts About the OHSU Nursing Strike


Paysafecard is an industry leader in online prepaid payment methods in the gaming world. Learn how to make easy and instant deposits in online casinos with your Paysafecard.
Making payments for online games have been made possible through various casino deposit options. It is important to use a method that guarantees the security of your finances. The payment process is similar to any other online shopping practice. However, there are differing gaming laws across the globe. This means that when topping up your account, the regional differences may determine the kind of method you utilize for your payment. Of uttermost importance is the safety of the amount in your account.
PaysafeCard provides a unique electronic money payment mechanisms in the U.K and the globe at large. The service is provided by the Prepaid Services Company Limited. Its services are regulated by the Financial Conduct Authority (FCA) in the UK. The organization has an obligation under the UK Electronic Money Regulations 2011 in issuing electronic money and the payment instruments of plastic or online money.
The presence of PaysafeCard provides a plus as far as online and gaming payments are concerned. It provides a secure option for paying into your casino account for the purposes of playing the various games at Australia Casino. The method can be used from all over the globe where acceptable. Owing to its availability on the online platform, it is possible to have the account operated from anywhere as long as there is internet connectivity. You cannot miss your favourite play.
Can I Use PaysafeCard at Any Online Casino?
You must be asking yourself this question. The answer is YES and a resounding one for that matter. There is a selection of games that you will like and feel anxious playing at many. The beauty of it is that you get to play the trial game without worrying about any charge or fear of losing money. This will help you acquaint yourself with the basics of each ga me.
Now the other option comes when you want to play and to win real money; In paying for your bets and receiving your money in a secure money transfer mechanism is mandatory. PaysafeCard allows you to get such a platform. You will register your details and provide your preferred payment method. Your details will be verified to ascertain it's you and not a robot.
Online casinos and PaysafeCard are in a favourable collaboration that will allow customers to have a gaming experience free from online threats. Accounts phishing and unwelcome access are some of the many threats that are curbed by PaysafeCard. The platform has increased its security mechanisms that include the use of One Time passwords to confirm the customer. The online registration of customers on the PaysafeCard portal ensures that there is enhanced authentication process when making payments or receiving payments to the Casino.
The benefits of having PaysafeCard payment methods cannot be overemphasized. Previously gamblers and online game players encountered challenges of cyber-insecurity including fraudulent withdrawals from client's accounts. Having a PaysafeCard payment option, many online casinos became a secure place to link your cards and financial accounts when undertaking online games.
For instance, when you are paying for your favourite games, the payment you make will only be deducted per your order and no extra charges will be deducted from your account. You will be requested to confirm the details of your order before the process can go through. There are no middlemen processing where money has to get to another party before reaching the casino. This means that no agency fees may be placed on the charge.
Once you have generated real money, you may desire to withdraw some to enjoy some holiday with it or do some shopping. You will select the withdrawal option and PaysafeCard will guarantee you the secure transfer of your money. Once processed you are guaranteed of receiving your duly amount. This is what every gambler is looking for. A method that will not only be convenient for paying for online games but also for receiving money securely.
e-Wallets - There are several online payment modes. The most commonly used include Neteller, skrill casino payments, Payoneer and PayPal. These methods are considerably very convenient and they have minimal fees charged for the transaction. Most online casinos accept the use of e-wallets in depositing and withdrawing money.
e-Check - This is a transformation of cash-less transactions where the use of online checks has evolved from the former use of the paper check. It is an online version of the paper check. In order to make an e-check deposit, ensure your bank account and routing numbers have to be linked.
Credit and Debit Cards - Use of cards is a common thing in modern online shopping. The cards credit cards are pr-loaded and can be linked to someone's bank accounts. You link the card to the billing of your deposits. This makes it possible to have the off-checking process successful in paying your deposit to the online gaming account.
It is the simplest process that you can perform online. The first thing is to get registered with PaysafeCard. Have your correct details registered on their platform. Once authorized, you put the amount of money you want to use in playing. You can deposit money into your online casino account or one of these top new casinos through PaysafeCard and you are on your way to gaming for real money.
Register and play with PaysafeCard at your favorite online casino!
Don't be the last to know about latest bonuses, new casino launches or exclusive promotions. Join us today!
We hate spam too - unsubscribe any time!


Tocopilla 4 - San Pedro de Atacama Code: SPE013 Quote Questions?
Built over a place full of history and inspired in the circular geometric of Tulor´s village, it's a large house made of stone, wood and mud that gives to the passenger the real experience of being in desert. It has straw roofs, lamps and many other details that keep the rustic spirit of the place.
The lodging has adobe cabins, each one with a private backyard and spacious rooms. Outside has a breakfast bar, where the passengers can enjoy the landscape in the night and morning.
It organizes tours with individual vehicles and guides for each passenger, who can travel around Atacama trough adventures, horse riding, walks or just observe a place full of history and mystery.


text:
BENJAMIN FOLKE THOMAS – TOO CLOSE TO HERE
2013 – Bucketfull of Brains
This is a terrific debut album by a Swedish native who is London domiciled and has been immersed in the folk scene there for the last five years. His warm vocals are able to express a range of emotions, on occasions reminiscent of Irish folk great, Paul Brady. His songwriting is even more descriptive and includes some really strong memorable melodies whilst his guitar playing is subtle and highly skilled, similarly his Swedish backing band. Were English his native language his lyrical journeys through a range of emotions would be impressive but as it is not he deserves huge credit for all of the little lyrical nuances that are inserted into his songs. He is often compared to a young Bob Dylan, certainly something of an exaggeration on the strength of just one album, but not outrageously so!
'Roots music' is probably the most appropriate description of this album that sometimes has a country feel, at others is more folksy, perhaps even a little bluesiness and even the more mellow side of rock. He is obviously a man that pays little heed to generic boundaries, simply producing the music that he feels needs to be made. Whilst the songs are generally about various aspects of relationships, lyrically he delves deeper into the subject than simply writing lost or found love tales. In his world all relationships and emotions are complicated, something we all know, but most songwriters are content to keep to the straight line rather than exploring the off shoots and effects of whatever action is being taken or emotion explored.
Album opener Someday is a case in point, being an excellent mid tempo, incredibly descriptive song that
has quite an intensely dramatic feel on a dark tale of love and murder. It's a song that has a really nice flow to it and is easy to listen to but a long way from being 'easy listening.' Thematically it is as straightforward as love and
murder ever can be but on this song as with most others on this excellent album he explores some of the emotions that we would all feel if we were the songs characters, giving an impression that if you follow the various threads you will perhaps find that the causes and effects were unnecessary to begin with. It's not often a song with such specific subject matter can also be labeled as 'thought provoking,' but this is that rarity. Love Somebody is another really good mid tempo song that tells you, 'when love comes along grasp it with both hands and don't let go.' A simple tale but a very descriptive song that delves into the complexities of love, backed up by a lovely tinkling piano sound and excellent bass. Bye Bye Baby (Bye Bye) has a lovely twangy guitar sound on a really good song that tells of the regret and emotional confusion following a broken relationship, even name checking the late great Warren Zevon! Let Her Down starts with the eerie haunting tones of a musical saw on this moody tale that includes steel guitar and gorgeous female harmonies on a sad atmospheric tale of loneliness, followed by O.K Blues with the lovely tones of a dobro on a a terrific bluesy tale of the confusion that can be felt even with a lover that you know well! And so the
album goes on, with subtle variations in instrumentation, emotional content and atmosphere. There is nothing that can be attributed to any particular genre, just eleven excellent and varied songs performed with commitment and no little amount of skill.
Often you can listen to an album, sometimes even a great album, and yet feel that if the artist had done this or that a song or several songs could be improved upon but that is not the case on this exceptional recording. Buy the album and also see him live. You won't regret it!
http://benjaminfolkethomas.com/

redpajama_set_name: RedPajamaCommonCrawl


The plaintiff ("P") owned a third floor flat ("Flat 3A") in which she had lived with her family since 1996. In March 2008, the defendants ("Ds") purchased the flat immediately above ("Flat 4A") and leased it out. P claimed that in 2005, renovations carried out by the previous Flat 4A owner resulted in altered floor slabs and additional water pipes that transmitted loud sounds downstairs. Also, a toilet was constructed above P's bedroom and water had seeped into her ceiling, parts of which turned black with bubbles.
P sued Ds to solve the issues while seeking damages for repair costs and mental distress. The parties' joint surveying expert and a Food and Environmental Hygiene Department officer agreed that the problems had deteriorated before Ds purchased Flat 4A and continued until at least August 2009. However, the judge in the lower court, relying on P's evidence in her statement of claim as to the water seepage, found that it probably ceased shortly after Ds purchased Flat 4A and dismissed P's claim. P appealed.
The judge erred in her assessment of the water seepage and that Ds, as the current owners of Flat 4A, were liable for it. Her conclusion was contrary to the joint expert's evidence, though this went unexplained.
Further, the judge erred in her ruling on noise in that P's unusually sensitive hearing was not to be taken into account.


text:
Did You Hear That? I Think It Was A Walrus
By NPR Staff
Stand aside Beyonce, there's a new sound in town. More than 9,000 sounds, to be more precise. The Macaulay Library at the Cornell Lab of Ornithology has just finished digitizing its huge archive of wildlife sounds and made it available online.
"It represents the voice of the world — all the voices of the world," Greg Budney, audio curator for the archive, tells NPR's Scott Simon. Among the vast collection are birds, mammals, insects and amphibians, Budney says, all made available "to anyone who has an interest in nature, in conservation and in the world around them."
The library's holdings total more than 7,000 hours of sounds, the result of an 80-year collaboration between the scientific community and the library's "volunteer collaborators: private individuals who record for a hobby, really with no other purpose than engaging in science," Budney says.
Some highlights from the collection: the clarinet-like cry of the indri lemur, which the archive describes as the "best candidate to appear on a John Coltrane record," and the spine-tingling call of the common loon.
Ken Canning / iStockphoto.com
In compiling such a vast collection, Budney has hit upon a few favorites — like the tuneful call of the musician wren, a small brown bird found throughout the Amazon region. "It walks along the forest floor," Budney says, "flipping over leaves looking for insects."
Courtesy of John S. Dunning / VIREO
Then there's the walrus, one of Budney's favorite mammalian recordings. The sound produced to attract females, he says, "starts out with these methodical beats — and then what sounds like a gong or banging on a garbage can lid."
The brown-backed solitaire, found in Mexico and Central America, also has a distinct call — one that Budney considers among the world's most beautiful bird songs.
The brown-backed solitaire and musician wren images by John S. Dunning are from the VIREO Collection of The Academy of Natural Sciences of Drexel University. Audio files are courtesy of the Cornell Lab of Ornithology.
Science & TechnologyWeekend Edition
See stories by NPR Staff
Storm Chasers Search For Beauty In Nature's Fury
How Shark Week Became A Cultural Phenomenon
Local Amateur Radio Club Participates In National Field Day
The (Losing) Battle Against Mosquitoes In Texas


text:
CoQ10 Combats Congestive Heart Failure
bostontestosterone	Uncategorized	boston testosterone, coq10, core medical group, core new england, heart disease, hormones, men's health	Leave a comment
By Martin Stein
Source: http://www.lifeextension.com/magazine/2015/4/coq10-combats-congestive-heart-failure/page-01
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
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 CLASSIFICATION81
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
SYMPTOMS OF CONGESTIVE HEART FAILURE
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.
FIGHT BACK AGAINST STATIN-INDUCED COQ10 DEFICIENCY
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.
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.
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.
USE OF UBIQUINOL IN CLINICAL STUDIES
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
Contact us for information on all of our therapies.
BTP/CORE New England
Men's Health Centers
Available at: http://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_failure.htm. Accessed December 21, 2014.
Thadani U, Ripley TL. Side effects of using nitrates to treat heart failure and the acute coronary syndromes, unstable angina and acute myocardial infarction. Expert Opin Drug Saf. 2007 Jul;6(4):385-96.
Andrey JL, Romero S, García-Egido A, et al. Mortality and morbidity of heart failure treated with digoxin. A propensity-matched study. Int J Clin Pract. 2011 Dec;65(12):1250-8.
Eurich DT, McAlister FA, Blackburn DF, et al. Benefits and harms of antidiabetic agents in patients with diabetes and heart failure: systematic review. BMJ. 2007 Sep 8;335(7618):497.
Tabrizchi R. Guidelines for choosing drugs in chronic heart failure. Vasc Health Risk Manag. 2005;1(3):171-2.
Miller AB. Aldosterone antagonism in heart failure. Vasc Health Risk Manag. 2007;3(5):605-9.
Hernandez AF, Liang L, Fonarow GC, et al. Associations between anticoagulation therapy and risks of mortality and readmission among patients with heart failure and atrial fibrillation. Circ Cardiovasc Qual Outcomes. 2014 Sep;7(5):670-9.
Singh RB, Neki NS, Kartikey K, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction. Mol Cell Biochem. 2003 Apr;246(1-2):75-82.
Gao L, Mao Q, Cao J, Wang Y, Zhou X, Fan L. Effects of coenzyme Q10 on vascular endothelial function in humans: a meta-analysis of randomized controlled trials. Atherosclerosis. 2012 Apr;221(2):311-6.
Marzilli M, Merz CN, Boden WE, et al. Obstructive coronary atherosclerosis and ischemic heart disease: an elusive link! J Am CollCardiol . 2012 Sep 11;60(11):951-6.
Pepine CJ, Douglas PS. Rethinking stable ischemic heart disease: is this the beginning of a new era? J Am Coll Cardiol. 2012 Sep 11;60(11):957-9.
Arenillas JF. Intracranial atherosclerosis: current concepts. Stroke. 2011 Jan;42(1 Suppl):S20-3.
Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med. 2011 Nov 7;17(11):1410-22.
Lusis AJ. Atherosclerosis. Nature. 2000 Sep 14; 407(6801): 233-41.
Aronson D, Rayfield EJ. How hyperglycemia promotes atherosclerosis: molecular mechanisms.Cardiovasc Diabetol. 2002 Apr 8;1:1.
Choy PC, Siow YL, Mymin D, O K. Lipids and atherosclerosis. Biochem Cell Biol. 2004 Feb;82(1):212-24.
Celletti FL, Waugh JM, Amabile PG, Brendolan A, Hilfiker PR, Dake MD. Vascular endothelial growth factor enhances atherosclerotic plaque progression. Nat Med. 2001 Apr;7(4):425-9.
Chapidze G, Kapanadze S, Dolidze N, Bachutashvili Z, Latsabidze N. Prevention of coronary atherosclerosis by the use of combination therapy with antioxidant coenzyme Q10 and statins. Georgian Med News. 2005 Jan (118):20-5.
Zeb I, Ahmadi N, Nasir K, et al. Aged garlic extract and coenzyme Q10 have favorable effect on inflammatory markers and coronary atherosclerosis progression: a randomized clinical trial. J Cardiovasc Dis Res. 2012 Jul;3(3):185-90.
Singh RB, Wander GS, Rastogi A, et al. Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction. Cardiovasc Drugs Ther. 1998 Sep;12(4):347-53.
Kuettner A, Pieper A, Koch J, Enzmann F, Schroeder S. Influence of coenzyme Q(10) and cerivastatin on the flow-mediated vasodilation of the brachial artery: results of the ENDOTACT study. Int J Cardiol. 2005 Feb 28;98(3):413-9.
Perez-Vizcaino F, Duarte J, Andriantsitohaina R. Endothelial function and cardiovascular disease: effects of quercetin and wine polyphenols. Free Radic Res. 2006 Oct;40(10):1054-65.
Watts GF, Playford DA, Croft KD, Ward NC, Mori TA, Burke V. Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus. Diabetologia. 2002 Mar;45(3):420-6.
Belardinelli R, Mucaj A, Lacalaprice F, et al. Coenzyme Q10 and exercise training in chronic heart failure.Eur Heart J. 2006 Nov;27(22):2675-81.
Tiano L, Belardinelli R, Carnevali P, Principi F, Seddaiu G, Littarru GP. Effect of coenzyme Q10 administration on endothelial function and extracellular superoxide dismutase in patients with ischaemic heart disease: a double-blind, randomized controlled study. Eur Heart J. 2007 Sep;28(18):2249-55.
Available at: http://www.nhlbi.nih.gov/health/health-topics/topics/cad. Accessed December 16, 2014.
Chen YF, Lin YT, Wu SC. Effectiveness of coenzyme Q10 on myocardial preservation during hypothermic cardioplegic arrest. J Thorac Cardiovasc Surg. 1994 Jan;107(1):242-7.
Rosenfeldt FL, Pepe S, Linnane A, et al. The effects of ageing on the response to cardiac surgery: protective strategies for the ageing myocardium. Biogerontology. 2002;3(1-2):37-40.
Rosenfeldt F, Marasco S, Lyon W, et al. Coenzyme Q10 therapy before cardiac surgery improves mitochondrial function and in vitro contractility of myocardial tissue. J Thorac Cardiovasc Surg. 2005 Jan;129(1):25-32.
Kakinuma Y, Miyauchi T, Yuki K, Murakoshi N, Goto K, Yamaguchi I. Mitochondrial dysfunction of cardiomyocytes causing impairment of cellular energy metabolism induces apoptosis, and concomitant increase in cardiac endothelin-1 expression. J Cardiovasc Pharmacol. 2000 Nov;36(5 Suppl 1):S201-4.
Ventura-Clapier R, Garnier A, Veksler V. Energy metabolism in heart failure. J Physiol. 2004 Feb 15;555(Pt 1):1-13.
Huss JM, Kelly DP. Mitochondrial energy metabolism in heart failure: a question of balance. J Clin Invest. 2005 Mar;115(3):547-55.
Harvey PA, Leinwand LA. The cell biology of disease: cellular mechanisms of cardiomyopathy. J Cell Biol. 2011 Aug 8;194(3):355-65.
Sinatra ST. Metabolic cardiology: the missing link in cardiovascular disease. Altern Ther Health Med. 2009 Mar-Apr;15(2):48-50.
Sheeran FL, Pepe S. Energy deficiency in the failing heart: linking increased reactive oxygen species and disruption of oxidative phosphorylation rate. Biochim Biophys Acta. 2006 May-Jun;1757(5-6):543-52.
Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G. Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators.Mol Aspects Med. 1994;15 Suppl:s287-94.
Mortensen SA, Vadhanavikit S, Muratsu K, Folkers K. Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. Int J Tissue React. 1990;12(3):155-62.
Morisco C, Trimarco B, Condorelli M. Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. Clin Investig. 1993;71(8 Suppl):S134-6.
Sacher HL, Sacher ML, Landau SW, et al. The clinical and hemodynamic effects of coenzyme Q10 in congestive cardiomyopathy. Am J Ther. 1997 Feb-Mar;4(2-3):66-72.
Munkholm H, Hansen HH, Rasmussen K. Coenzyme Q10 treatment in serious heart failure. Biofactors.1999;9(2-4):285-9.
Molyneux SL, Florkowski CM, Richards AM, Lever M, Young JM, George PM. Coenzyme Q10; an adjunctive therapy for congestive heart failure? N Z Med J. 2009 Oct 30;122(1305):74-9.
Fotino AD, Thompson-Paul AM, Bazzano LA. Effect of coenzyme Q(1)(0) supplementation on heart failure: a meta-analysis. Am J Clin Nutr. 2013 Feb;97(2):268-75.
Belardinelli R, Mucaj A, Lacalaprice F, et al. Coenzyme Q10 improves contractility of dysfunctional myocardium in chronic heart failure. Biofactors. 2005;25(1-4):137-45.
Hofman-Bang C, Rehnqvist N, Swedberg K, Wiklund I, Astrom H. Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. The Q10 Study Group. J Card Fail. 1995 Mar;1(2):101-7.
Langsjoen PH, Langsjoen AM. Supplemental ubiquinol in patients with advanced congestive heart failure.Biofactors. 2008;32(1-4):119-28.
Langsjoen PH, Langsjoen AM. Overview of the use of CoQ10 in cardiovascular disease. Biofactors.1999;9(2-4):273-84.
Langsjoen PH. Lack of effect of coenzyme Q on left ventricular function in patients with congestive heart failure. J Am Coll Cardiol. 2000 Mar 1;35(3):816-7.
Zita C, Overvad K, Mortensen SA, Sindberg CD, Moesgaard S, Hunter DA. Serum coenzyme Q10 concentrations in healthy men supplemented with 30 mg or 100 mg coenzyme Q10 for two months in a randomised controlled study. Biofactors. 2003;18(1-4):185-93.
Mortensen SA, Rosenfeldt F, Kumar A, et al. The effect of coenzyme Q on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail. 2014 Sep 25.
Noh YH, Kim KY, Shim MS, et al. Inhibition of oxidative stress by coenzyme Q10 increases mitochondrial mass and improves bioenergetic function in optic nerve head astrocytes. Cell Death Dis. 2013 Oct 3;4:e820.
Matthews RT, Yang L, Browne S, Baik M, Beal MF. Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8892-7.
Gazdíková K, Gvozdjáková A, Kucharská J, Spustová V, Braunová Z, Dzúrik R. Effect of coenzyme Q10 in patients with kidney diseases. Cas Lek Cesk. 2001 May 24;140(10):307-10.
Ishikawa A, Kawarazaki H, Ando K, Fujita M, Fujita T, Homma Y. Renal preservation effect of ubiquinol, the reduced form of coenzyme Q10. Clin Exp Nephrol. 2011 Feb;15(1):30-3.
Chen CC, Liou SW, Chen CC, et al. Coenzyme Q10 rescues ethanol-induced corneal fibroblast apoptosis through the inhibition of caspase-2 activation. J Biol Chem. 2013 Apr 26;288(17):11689-704.
Kernt M, Hirneiss C, Neubauer AS, Ulbig MW, Kampik A. Coenzyme Q10 prevents human lens epithelial cells from light-induced apoptotic cell death by reducing oxidative stress and stabilizing BAX / Bcl-2 ratio.Acta Ophthalmol. 2010 May;88(3):e78-86.
Lee D, Kim KY, Shim MS, et al. Coenzyme Q10 ameliorates oxidative stress and prevents mitochondrial alteration in ischemic retinal injury. Apoptosis. 2014 Apr;19(4):603-14.
Lee D, Shim MS, Kim KY, et al. Coenzyme Q10 inhibits glutamate excitotoxicity and oxidative stress-mediated mitochondrial alteration in a mouse model of glaucoma. Invest Ophthalmol Vis Sci. 2014 Feb;55(2):993-1005.
Lulli M, Witort E, Papucci L, et al. Coenzyme Q10 instilled as eye drops on the cornea reaches the retina and protects retinal layers from apoptosis in a mouse model of kainate-induced retinal damage. Invest Ophthalmol Vis Sci. 2012 Dec;53(13):8295-302.
Mencucci R, Favuzza E, Boccalini C, et al. CoQ10-containing eye drops prevent UVB-induced cornea cell damage and increase cornea wound healing by preserving mitochondrial function. Invest Ophthalmol Vis Sci. 2014 Oct 9;55(11):7266-71.
Nakajima Y, Inokuchi Y, Nishi M, Shimazawa M, Otsubo K, Hara H. Coenzyme Q10 protects retinal cells against oxidative stress in vitro and in vivo. Brain Res. 2008 Aug 21;1226:226-33.
Nucci C, Tartaglione R, Cerulli A, et al. Retinal damage caused by high intraocular pressure-induced transient ischemia is prevented by coenzyme Q10 in rat. Int Rev Neurobiol. 2007;82:397-406.
Qu J, Kaufman Y, Washington I. Coenzyme Q10 in the human retina. Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1814-8.
Russo R, Cavaliere F, Rombola L, et al. Rational basis for the development of coenzyme Q10 as a neurotherapeutic agent for retinal protection. Prog Brain Res. 2008;173:575-82.
Carrasco J, Anglada FJ, Campos JP, Muntane J, Requena MJ, Padillo J. The protective role of coenzyme Q10 in renal injury associated with extracorporeal shockwave lithotripsy: a randomised, placebo-controlled clinical trial. BJU Int. 2014 Jun;113(6):942-50.
Gokbel H, Atalay H, Okudan N, Solak Y, Belviranli M, Turk S. Coenzyme Q10 and its relation with oxidant and antioxidant system markers in patients with end-stage renal disease. Ren Fail. 2011;33(7):677-81.
Ishikawa A, Homma Y. Beneficial effect of ubiquinol, the reduced form of coenzyme Q10, on cyclosporine nephrotoxicity. Int Braz J Urol. 2012 Mar-Apr;38(2):230-4; discussion 34.
Persson MF, Franzen S, Catrina SB, et al. Coenzyme Q10 prevents GDP-sensitive mitochondrial uncoupling, glomerular hyperfiltration and proteinuria in kidneys from db/db mice as a model of type 2 diabetes. Diabetologia. 2012 May;55(5):1535-43.
Saiki R, Lunceford AL, Shi Y, et al. Coenzyme Q10 supplementation rescues renal disease in Pdss2kd/kd mice with mutations in prenyl diphosphate synthase subunit 2. Am J Physiol Renal Physiol. 2008 Nov;295(5):F1535-44.
Sakata T, Furuya R, Shimazu T, Odamaki M, Ohkawa S, Kumagai H. Coenzyme Q10 administration suppresses both oxidative and antioxidative markers in hemodialysis patients. Blood Purif.2008;26(4):371-8.
Triolo L, Lippa S, Oradei A, De Sole P, Mori R. Serum coenzyme Q10 in uremic patients on chronic hemodialysis. Nephron. 1994;66(2):153-6.
Levy G, Kaufmann P, Buchsbaum R, et al. A two-stage design for a phase II clinical trial of coenzyme Q10 in ALS. Neurology. 2006 Mar 14;66(5):660-3.
Mischley LK, Allen J, Bradley R. Coenzyme Q10 deficiency in patients with Parkinson's disease. J Neurol Sci. 2012 Jul 15;318(1-2):72-5.
Muller T, Buttner T, Gholipour AF, Kuhn W. Coenzyme Q10 supplementation provides mild symptomatic benefit in patients with Parkinson's disease. Neurosci Lett. 2003 May 8;341(3):201-4.
Shults CW, Flint Beal M, Song D, Fontaine D. Pilot trial of high dosages of coenzyme Q10 in patients with Parkinson's disease. Exp Neurol. 2004 Aug;188(2):491-4.
Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. 2002 Oct;59(10):1541-50.
Dumont M, Kipiani K, Yu F, et al. Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease. J Alzheimers Dis. 2011;27(1):211-23.
Orsucci D, Mancuso M, Ienco EC, LoGerfo A, Siciliano G. Targeting mitochondrial dysfunction and neurodegeneration by means of coenzyme Q10 and its analogues. Curr Med Chem. 2011;18(26):4053-64.
Salama M, Yuan TF, Machado S, et al. Co-enzyme Q10 to treat neurological disorders: basic mechanisms, clinical outcomes, and future research direction. CNS Neurol Disord Drug Targets. 2013 Aug;12(5):641-64.
Shetty RA, Forster MJ, Sumien N. Coenzyme Q(10) supplementation reverses age-related impairments in spatial learning and lowers protein oxidation. Age (Dordr). 2013 Oct;35(5):1821-34.
The Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels. 9th ed. Boston: Little, Brown & Co.; 1994.
Glaus T, Schellenberg S, Lang J. Cardiogenic and non cardiogenic pulmonary edema: pathomechanisms and causes. Schweiz Arch Tierheilkd. 2010 Jul;152(7):311-7.
Andalib S, Shayanfar A, Khorrami A, Maleki-Dijazi N, Garjani A. Atorvastatin reduces the myocardial content of coenzyme Q10 in isoproterenol-induced heart failure in rats. Drug Res (Stuttg). 2014 May;64(5):246-50.
Lee BJ, Tseng YF, Yen CH, Lin PT. Effects of coenzyme Q10 supplementation (300 mg/day) on antioxidation and anti-inflammation in coronary artery disease patients during statins therapy: a randomized, placebo-controlled trial. Nutr J. 2013;12(1):142.
Pourmoghaddas M, Rabbani M, Shahabi J, Garakyaraghi M, Khanjani R, Hedayat P. Combination of atorvastatin/coenzyme Q10 as adjunctive treatment in congestive heart failure: A double-blind randomized placebo-controlled clinical trial. ARYA Atheroscler. 2014 Jan;10(1):1-5.
Heidenreich PA, Trogdon JG, Khavjou OA, et al. Forecasting the future of cardiovascular disease in the United States: a policy statement from the American Heart Association. Circulation. 2011 Mar 1;123(8):933-44.
Garcia-Corzo L, Luna-Sanchez M, Doerrier C, et al. Ubiquinol-10 ameliorates mitochondrial encephalopathy associated with CoQ deficiency. Biochim Biophys Acta. 2014 Jul;1842(7):893-901.
Bates A, Shen Q, Hiebert JB, Thimmesch A, Pierce JD. Myocardial energetics and ubiquinol in diastolic heart failure. Nurs Health Sci. 2014 Dec;16(4):428-33.
Molyneux SL, Young JM, Florkowski CM, Lever M, George PM. Coenzyme Q10: is there a clinical role and a case for measurement? Clin Biochem Rev. 2008 May;29(2):71-82.
Onur S, Niklowitz P, Jacobs G, et al. Ubiquinol reduces gamma glutamyltransferase as a marker of oxidative stress in humans. BMC Res Notes. 2014;7:427.
Bhagavan HN, Chopra RK. Plasma coenzyme Q10 response to oral ingestion of coenzyme Q10 formulations. Mitochondrion. 2007 Jun;7 Suppl:S78-88.
Failla ML, Chitchumroonchokchai C, Aoki F. Increased bioavailability of ubiquinol compared to that of ubiquinone is due to more efficient micellarization during digestion and greater GSH-dependent uptake and basolateral secretion by Caco-2 cells. J Agric Food Chem. 2014 Jul 23;62(29):7174-82.
Bhattacharyya S, Pal D, Gupta AK, Ganguly P, Majumder UK, Ghosal S. Beneficial effect of processed shilajit on swimming exercise induced impaired energy status of mice. Pharmacologyonline. 2009;1:817-25.
Ghosal S. Shilajit in Perspective. Oxford, UK: Narosa Publishing House; 2006.
Islam A, Ghosh R, Banerjee D, Nath P, Mazumder U, Ghosal S. Biotransformation of 3-hydroxydibenzo-pyrone into 3,8 dihydroxydibenzo-pyrone and aminoacyl conjugates by Aspergillus niger isolated from native "shilajit." Electro J Biotechno. 2008 Jul 15;11(3):2-10.
Bhattacharyya S, Pal D, Banerjee D, et al. Shilajit dibenzo—pyrones: Mitochondria targeted antioxidants.Pharmacologyonline. 2009; 2:690-8.
Hosoe K, Kitano M, Kishida H, Kubo H, Fujii K, Kitahara M. Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers. Regul Toxicol Pharmacol. 2007 Feb;47(1):19-28.
Makley AT, Goodman MD, Friend LA, et al. Resuscitation with fresh whole blood ameliorates the inflammatory response after hemorrhagic shock. J Trauma. 2010 Feb;68(2):305-11.
Shen Q, Holloway N, Thimmesch A, Wood JG, Clancy RL, Pierce JD. Ubiquinol decreases hemorrhagic shock/resuscitation-induced microvascular inflammation in rat mesenteric microcirculation. Physiol Rep.2014 Nov 1;2(11).
Cakiroglu B, Eyyupoglu SE, Gozukucuk R, Uyanik BS. Ubiquinol effect on sperm parameters in subfertile men who have astheno-teratozoospermia with normal sperm concentration. Nephrourol Mon. 2014 May;6(3):e16870.
Gvozdjakova A, Kucharska J, Ostatnikova D, Babinska K, Nakladal D, Crane FL. Ubiquinol improves symptoms in children with autism. Oxid Med Cell Longev. 2014;2014:798957.
Peerapanyasut W, Thamprasert K, Wongmekiat O. Ubiquinol supplementation protects against renal ischemia and reperfusion injury in rats. Free Radic Res. 2014 Feb;48(2):180-9.
Maruoka H, Fujii K, Inoue K, Kido S. Long-term effect of ubiquinol on exercise capacity and the oxidative stress regulation system in SAMP1 mice. J Phys Ther Sci. 2014 Mar;26(3):367-71.
Tian G, Sawashita J, Kubo H, et al. Ubiquinol-10 supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal. 2014 Jun 1;20(16):2606-20.
Ates O, Bilen H, Keles S, et al. Plasma coenzyme Q10 levels in type 2 diabetic patients with retinopathy.Int J Ophthalmol. 2013;6(5):675-9.
Men with 'low testosterone' have higher rates of depression
bostontestosterone	Uncategorized	andropause, boston testosterone, core medical group, core new england, depression, hormones, hrt, low t, men's health, testosterone, trt	Leave a comment
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 http://onlinelibrary.wiley.com/doi/10.1111/jsm.12937/full.
http://www.eurekalert.org/pub_releases/2015-07/gwum-mw070115.php
To request a free informational packet on all our Men's Health therapies, visit us at www.BostonTestosterone.com
For for more information and appointments, please contact Clinic Director Charlie Blaisdell at CBlaisdell@CoreNewEngland.com
BTP/CORE New England/ Core Medical Group
Clinic: 781-269-5953
AACE releases new position statement on testosterone replacement therapy in men
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 http://www.clinicalendocrinologynews.com/specialty-focus/men-s-health/single-article-page/aace-releases-new-position-statement-on-testosterone-replacement-therapy-in-men/be703dd9532765177582f453158e98e1.html
A Message from Dr. Lach:http://www.bostontestosterone.com/doc…/DoctorLachMessage.pdf
Lipotropic Injections and Medical Weight loss
bostontestosterone	Uncategorized	boston testosterone, core medical group, core new england, fat loss, fitness, HCG B12 MIC, weight loss	Leave a comment
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.
Methionine:
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 acids, Cysteine and Taurine, which help the body eliminate toxins, build strong, healthy tissues, and promote cardiovascular health.
Inositol:
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:
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.
UTMB study finds that testosterone therapy is not linked with blood clot disorders in veins
bostontestosterone	Uncategorized	andropause, boston testosterone, core medical group, core new england, hormones, hrt, low t, men's health, testosterone, trt	Leave a comment
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.
Source: http://www.eurekalert.org/pub_releases/2015-07/uotm-usf071615.php
Low testosterone linked to heightened risk of early death
bostontestosterone	Uncategorized	boston testosterone, core medical group, core new england, hormones, hrt, men's health, testosterone, trt	Leave a comment
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."
Source: http://www.eurekalert.org/pub_releases/2010-10/bmj-ltl101910.php
Low testosterone levels may indicate worsening of disease for men with prostate cancer
bostontestosterone	Uncategorized	andropause, boston testosterone, core medical group, core new england, hormones, hrt, men's health, prostate cancer, prostate health, testosterone, trt	Leave a comment
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.
Article Source: http://www.eurekalert.org/pub_releases/2014-05/w-ltl050214.php
Contact us for information on getting your levels checked and more information on our therapies.
Study of 83,000 veterans finds cardiovascular benefits to testosterone replacement
bostontestosterone	Uncategorized	andropause, boston testosterone, cardiovascular health, core medical group, core new england, hormones, hrt, low t, men's health, testosterone, trt	Leave a comment
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."
http://www.eurekalert.org/pub_releases/2015-08/varc-so8081015.php
Testosterone therapy may prevent Alzheimer's disease
bostontestosterone	Uncategorized	Alzheimers, andropause, boston testosterone, core medical group, core new england, disease, hormones, hrt, men's health, testosterone, trt	Leave a comment
New USC study shows loss of testosterone speeds the development of Alzheimer's disease in mice, while hormone replacement prevents it; findings are first to show how lowered testosterone increases the risk of Alzheimer's disease.
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.
Source: http://www.eurekalert.org/pub_releases/2006-12/uosc-ttm121506.php
Beet juice boosts muscle power in heart patients
bostontestosterone	Uncategorized	andropause, boston testosterone, core medical group, diabetes, diet, hrt, men's health, muscle, strength, testosterone therapy, trt	Leave a comment
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."
http://www.eurekalert.org/pub_releases/2015-09/wuso-bjb091615.php
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.
Contact us for more information on on our therapies.


Interior house painting ideas with color combination picture is just one of the many collections of images or photos on this website. There are approximately 137014 images that exist in our database associated with this post. This post of "interior house painting ideas with color combination picture" was uploaded by louis on 22-08-2018 and posted on the wallsumo.com website with category Interior House Painting Ideas and has been viewed some 831,659 times.
This pictures of "interior house painting ideas with color combination picture" is from the above 1463x918 resolutions which is part of the Interior House Painting Ideas directory, Download this wallpapers for free in HD resolution the choice "download button" below. If you do not find the exact resolution you are looking for, then go for a native or higher resolution.
We hope you can find what you need here. We always effort to show a picture with HD resolution or at least with perfect images. Interior house painting ideas with color combination picture can be beneficial inspiration for those who seek an image according specific categories, you can find it in this site. Finally all pictures we have been displayed in this site will inspire you all. Thank you for visiting.
This is a background related to interior house painting ideas with color combination picture, there are approximately 137014 wallpaper related to this interior house painting ideas photos gallery. Please see the details below and click on the title for more information..
Interior house painting ideas with color combination picture is wallpaper about Interior House Painting Ideas was uploaded by francis on 22 August 2018.
Superior interior house painting ideas color photo of room with is image about Interior House Painting Ideas was uploaded by cody on 18 September 2018.
Interior painting color ideas new house with power painters of is background about Interior Painting Color Ideas was uploaded by philip on 07 September 2018.
Interior painting color ideas pictures photo uhyx house decor picture is image about Interior Painting Color Ideas was uploaded by curtis on 14 September 2018.
Home interior painting color ideas also enchanting combination house is post about Interior Painting Color Ideas was uploaded by darren on 12 August 2018.
Interior painting color ideas pictures photo ygmi house decor picture is post about Interior Painting Color Ideas was uploaded by scott on 22 August 2018.
Interior painting color ideas pictures house decor picture is photos about Interior Painting Color Ideas was uploaded by william on 11 August 2018.
Interior painting color ideas picture house decor picture is pictures about Interior Painting Color Ideas was uploaded by clarence on 04 October 2018.
Interior painting color ideas pictures photo xuqe house decor picture is wallpapers about Interior Painting Color Ideas was uploaded by maurice on 12 September 2018.