Combination treatment with CDK4/6 inhibitor improves progression-free survival in HR breast cancer patients

The addition of the CDK4/6 inhibitor ribociclib to letrozole therapy significantly improves progression-free survival in postmenopausal women with hormone receptor-positive advanced breast cancer, researchers reported today at the ESMO 2016 Congress in Copenhagen.

The first interim analysis of data from the randomized, double-blind MONALEESA study showed a 44% improvement in progression-free survival with ribociclib plus letrozole as a first-line treatment combination.

"This was THE definitive study to demonstrate the superiority of the combination of ribociclib and letrozole over letrozole alone," said principle investigator, Professor Gabriel Hortobagyi, from the University of Texas MD Anderson Cancer Center in Houston, Texas, US.

Researchers randomized 668 postmenopausal women with hormone receptor-positive, HER2-negative advanced breast cancer, who had not undergone any prior systemic treatment, to ribociclib (600 mg/day, 3 weeks on/1 week off) and letrozole (2.5 mg/day, continuous), or letrozole plus placebo.

                                

ribociclib                                                                                  letrozole

In the ribociclib arm, there was a 44% improvement in the primary objective of progression-free survival compared to the placebo arm (HR: 0.556, p = 0.00000329). Median progression-free survival was 14.7 months in the placebo arm, but was not reached in the ribociclib arm at data cut-off.

"The results of this trial represent a compelling proof of principle, and suggest a paradigm shift in metastatic, HR+ breast cancer. They also suggest that testing combinations of ribociclib with other inhibitors of various signaling pathways might lead to additional progress in the management of several subtypes of breast cancer," Hortobagyi said.

Patients with measurable disease at baseline showed a significantly higher objective response rate to ribociclib plus letrozole compared to letrozole alone (53% vs. 37%; p=0.00028), and improved clinical benefit rate (80% vs. 72% p=0.02).

Serious adverse events occurred in fewer than 5% of patients in both arms but other adverse events were significantly more common in the ribociclib arm. Neutropenia occurred in 59% of patients in the ribociclib arm compared to 1% of the placebo arm; leukopenia occurred in 21% vs 1%; lymphopenia in 7% vs. 1%, and patients in the ribociclib arm had a higher incidence of elevated alanine aminotransferase and elevated aspartate aminotransferase.

The number of deaths in the study was too low to enable a reliable analysis of the impact of ribociclib therapy on overall survival.

Commenting on the findings, Professor Giuseppe Curigliano, Director of the New Drugs and Early Drug Development for Innovative Therapies Division at the European Institute of Oncology, Milan, Italy, said, "I believe the results of this study are significant because now we have a new CDK4/6 inhibitor for patients with estrogen-receptor positive metastatic breast cancer, in addition to palbociclib (already FDA approved) and abemaciclib (under development)."

"The addition of ribociclib to letrozole does increase the rate of toxicity, but overall, if we evaluate the magnitude of clinical benefit, there is definitely a benefit to be gained from adding ribociclib."

Curigliano also suggested that further studies of ribociclib should examine the use of cancer biomarkers to better identify patients who would respond to the combination.

Researchers report high response rate with single drug in phase I/II trial of paediatric brain cancer

In continuation of my update on Dabrafenib

A high response rate with a single drug in a phase I/II trial of paediatric brain tumour has set the stage for combination therapy with higher response and lower toxicity, researchers reported at the ESMO 2016 Congress in Copenhagen.

"The likelihood of curing a child with a low-grade glioma is very high," said lead author Dr Mark Kieran, Director, Paediatric Medical Neuro-Oncology, Dana-Farber Boston Children's, Boston, US. "In fact many children don't suffer lifelong from the tumour but rather from the cognitive damage and secondary malignancies caused by radiation therapy."

He continued: "The development of drugs that target the specific causative mutation of the tumour and avoid long-term toxicities may revolutionise the treatment of paediatric brain cancer."

Up to 10% of paediatric low-grade gliomas have the BRAF V600 mutation. Today researchers reported the phase I and phase II trial results of dabrafenib, a selective inhibitor of mutant protein. The study included 32 patients aged one to 16 years with BRAF V600-mutant low-grade glioma, of whom 15 participated in the phase I trial and 17 were in the phase II trial.

The phase I trial, which focused on determining the recommended phase II dose, did not find any significant dose-limiting toxicities. The recommended dose was therefore based on the pharmacokinetic activity of the drug and was set at 4.5 mg/kg/day for patients aged 12 years and older and 5.25 mg/kg/day for patients under the age of 12.

The phase II trial assessed toxicities with dabrafenib, and whether it could stop tumours from growing or cause them to shrink. "Paediatric low-grade gliomas are a little bit unique in that patients can survive their entire life with a tumour that stops growing, unlike other cancers which need to be completely removed," said Kieran.

The objective response rate was 72%, with 23 out of 32 patients responding to the drug. In two patients the tumour disappeared and in 11 patients the tumour shrunk by more than half - of these 13 patients eight are still on the therapy. Thirteen patients had stable disease of at least six months' duration, and 11 of them are still on the therapy.

Regarding adverse events, there were no cases of squamous cell carcinoma, which has been observed in previous trials of dabrafenib in adults with BRAF V600E positive tumours, most of whom have melanoma. One patient had an allergic reaction to the drug. Minor side effects were similar to those seen in adults, including transient fever, upset stomach, fatigue and skin rash.

Studies in adults with BRAF V600E mutations have shown that combining a BRAF inhibitor with a MEK inhibitor reduces toxicity and produces more activity for a longer period of time. The encouraging results with dabrafenib in children have provided the impetus for phase I and II trials with a MEK inhibitor to determine the dose and toxicities, and a trial combining the two drugs is now underway.

Kieran said: "We want to make the response rate with dabrafenib even higher by combining it with a MEK inhibitor since that works in adults. Adding two drugs together normally produces twice as much toxicity. But much of the toxicity from the BRAF drug is inhibited by the MEK drug, so the combination is less toxic than either drug alone, which is unusual."

Kieran concluded: "The finding that dabrafenib can shrink tumours or stop them growing is exciting and has led to trials with a MEK inhibitor and now the combination of drugs. This combined therapy may completely change the way we treat low-grade gliomas in children with this mutation. The caveat is that these targeted personalised drugs are relatively new so we need to make sure that they don't have any long-term developmental toxicities in children."

Commenting on the findings, Professor Michael Weller, chairman, Department of Neurology, University Hospital Zurich, Switzerland, said: "The encouraging thing about this study is that this targeted treatment seems to work. At the moment in neuro-oncology we know almost everything about the molecular make-up of gliomas in adults and in children but we have not really been able to translate all this knowledge into an effective therapeutic agent."

"These findings will have implications for clinical practice because many parents are willing to travel all around the world to get access to a promising treatment," he continued. "We have almost no randomised data for brain tumours in children, at least for gliomas, because the tumours are too rare and the trials are difficult for ethical reasons."

Weller concluded: "We need longer follow up to find out how long the responses last and whether we get long-term survival. And then of course in children we want to know if there is any long-term toxicity."

No added benefit proven for pulmonary arterial hypertension drug, IQWiG finds

  

In continuation of my update on Selexipag

Selexipag (trade name: Uptravi) is approved for long-term treatment of pulmonary arterial hypertension (PAH) in adults with moderate to severe symptoms. The drug can be used either as combination therapy with other blood-pressure lowering drugs or as monotherapy in patients who are not candidates for these therapies. Selexipag has been on the market in Germany since May 2016. In an early benefit assessment, the German Institute for Quality and Efficiency in Health Care (IQWiG) has now examined whether this drug has advantages or disadvantages in comparison with the appropriate comparator therapy.

The limitation of the comparator therapy to a specific drug and the subsequent division of the population in the dossier were inadequate. The only study cited by the drug manufacturer for one of its subpopulations compared selexipag with placebo. However, no added benefit can be inferred from such a comparison.

Hence the manufacturer presented no suitable data for the assessment of the added benefit of selexipag, and IQWiG concluded: An added benefit of selexipag in comparison with the appropriate comparator therapy is not proven.

Selective widening of vessels and inhibition of tissue growth

In PAH, the pulmonary artery is narrowed, and the heart has to work harder to pump oxygen-poor blood through the pulmonary artery into the lungs. The permanently increased workload of the right heart chamber decreases the body's oxygen supply. The high blood pressure (hypertension) is often caused by another heart or lung disease, e.g. by chronic obstructive pulmonary disease (COPD) or a congenital heart defect.

Selexipag aims to widen the pulmonary artery and slow down the overload of the heart. The drug is approved for long-term treatment of PAH patients who have no symptoms at rest but who have slight (WHO functional class II) or marked (WHO functional class III) limitation of physical activity. These restrictions cause symptoms such as dyspnoea, tiredness, chest pain, or dizziness. Selexipag is an option as combination therapy in patients insufficiently controlled with an endothelin receptor antagonist (ERA) and/or a phosphodiesterase-5 (PDE-5) inhibitor, or as monotherapy in patients who are not candidates for these therapies.

PARP inhibitor prolongs progression-free survival in patients with recurrent ovarian cancer

 

The PARP inhibitor niraparib significantly improves the outcome of platinum-sensitive recurrent ovarian cancer, according to full data from the ENGOT-OV16/NOVA trial presented for the first time at the ESMO 2016 Congress in Copenhagen and published in the New England Journal of Medicine (NEJM). The trial met its primary endpoint, with niraparib considerably prolonging progression-free survival compared to placebo.

"There are limited treatment options in recurrent ovarian cancer," said lead author Dr Mansoor Raza Mirza, chief oncologist, Rigshospitalet, Copenhagen University Hospital, Denmark and medical director of the Nordic Society of Gynaecological Oncology (NSGO). "Cumulative toxicity with platinum-based chemotherapy and lack of additional benefit limits its use. We then pause treatment until the next relapse and start combination chemotherapy."

"The current options for maintenance therapy in the EU are bevacizumab, which can only be given once and improves progression-free survival by just a few months, and the PARP inhibitor olaparib, which is only approved in patients with a germline BRCA mutation (about 10-15% of ovarian cancer patients). No maintenance therapy is approved outside the EU," he continued.

This phase III trial was performed in collaboration with European Network of Gynaecological Oncology Trial groups (ENGOT). The ENGOT-OV16/NOVA trial evaluated the efficacy and safety of the PARP inhibitor niraparib as maintenance therapy in patients with recurrent ovarian cancer who respond to platinum-based chemotherapy. Patients were assigned to cohorts by BRCA mutation status and randomised 2:1 to receive niraparib 300 mg or placebo once daily.

The trial included 553 patients, of whom 203 had the germline BRCA mutation and 350 did not. Niraparib significantly improved the primary endpoint of progression-free survival compared to placebo in both cohorts, as well as in all subgroups.

Median progression-free survival with niraparib compared to placebo was 21.0 vs 5.5 months in the germline BRCA mutation group (hazard ratio [HR] 0.27, 95% confidence interval [CI] 0.173 to 0.410, p<0.0001), 9.3 months vs 3.9 months in the non-germline BRCA mutation group (HR 0.45, 95% CI 0.338 to 0.607, p<0.0001), and 12.9 vs 3.8 months in a subgroup of the non-mutation cohort who had homologous recombination DNA repair deficiencies (HRD) (HR 0.38, 95% CI 0.243 to 0.586, p<0.0001).

More than 10% of patients had grade 3/4 adverse events following treatment with niraparib, of whom 28% had thrombocytopaenia, 25% had anaemia, and 11% had neutropaenia. These were resolved with dose adjustments and patients could continue their treatment. Patient-reported outcomes were similar with niraparib and placebo. Patients on niraparib maintained symptom control and had a quality of life comparable to those on placebo.

Significant improvements were also observed in all secondary endpoints. Compared to placebo, niraparib significantly prolonged the second progression-free survival, time to first subsequent treatment, and chemotherapy-free interval in the mutation and mutation-free groups, and in the HRD subgroup.

"This is a breakthrough for patients with ovarian cancer," said Mirza. "We have never seen such large benefits in progression-free survival in recurrent ovarian cancer. Niraparib significantly improved all endpoints across a broad patient population representing 70% of all ovarian cancer patients. These landmark results could change the way we treat this disease."

He concluded: "Once it is approved by the regulatory authorities, I'll consider niraparib for all my patients with recurrent ovarian cancer who respond to platinum regardless of BRCA status."

Commenting on the results, Dr Andrés Poveda, head of the Gynaecological Cancer Clinic, Oncology Foundation Institute Valencia, Spain, said: "This study more than doubles the population of patients who benefit from a PARP inhibitor."

"Personalised medicine has arrived in high grade serous ovarian cancer," he continued. "This was the first trial to use HRD to select patients for treatment and showed that it is a useful strategy. We also know that PARP inhibitors benefit patients with BRCA mutations."

Poveda concluded: "Future studies are needed to unravel which patients with HRD are not responders to PARP inhibitors and why, and which patients are long responders and why. We also need to know if there are other non-HRD factors, such as cyclin E positivity, that predict which patients will respond to treatment.

Combination treatment for myocardial infarction shows no added benefit compared to ASA monotherapy

The drug ticagrelor has been approved since February 2016 for adults who had a myocardial infarction a year or more ago and are at a high risk of a new myocardial infarction or stroke. Ticagrelor is used together with low-dose acetylsalicylic acid (ASA). In its dossier assessment published in early July 2016, the German Institute for Quality and Efficiency in Health Care (IQWiG) determined an indication of a minor added benefit of ticagrelor in comparison with the administration of ASA alone.

 acetylsalicylic acid(ASA)   Ticagrelor

On the inclusion of additional analyses that the drug manufacturer provided in the commenting procedure conducted by the Federal Joint Committee (G-BA), the Institute now came to a different conclusion, however: An added benefit is not proven because positive effects are called into question by negative effects.

Non-severe bleeding notably more common

The dossier had only contained data on severe bleeding. There were no data on non-severe bleeding that are clinically relevant. The results of the analyses subsequently submitted by the manufacturer were to the disadvantage of ticagrelor: Since these bleeding events were notably more common than under ASA monotherapy, IQWiG determined proof of greater harm with the extent "considerable".

No data on quality of life

In addition, there were no data on quality of life. Particularly in coronary heart disease (CHD), this is a very important outcome criterion however, which is even more important in view of side effects such as dyspnoea. "Disease-related quality of life" is the first treatment goal listed in the recently published revised version of the National Care Guideline for Coronary Heart Disease.

Since, on the one hand, greater harm was proven for an additional outcome, and, on the other, no data on quality of life were available, the positive effects, including the ones regarding mortality and late complications, were called into question by the negative effects. In the overall consideration, no added benefit of ticagrelor plus ASA in comparison with ASA monotherapy could be derived from the data.

Dandelion tea touted as possible cancer killer

Researchers hope to test dandelion tea on patients at a Windsor, Ont., clinic after it was found the roots of the weed killed cancer cells in the laboratory.

The promising research is being led by a University of Windsor oncologist, in association with the Windsor Regional Cancer Centre.

Dr. Caroline Hamm said dandelion root extract is unique, and is one of the only things found to help with chronic myelomonocytic leukemia.

"It was really unusual to find a product that had efficacy in that area," said Hamm.

Some patients swear by it

John DiCarlo, 72, was admitted to hospital three years ago with leukemia. Even after aggressive treatment, he was sent home to put his affairs in order with his wife and four children.

The cancer clinic suggested he try the tea. Four months later, he returned to the clinic in remission. He has been cancer free for three years.

He said his doctor credits the dandelions.

"He said, 'You are doing pretty good, you aren't a sick man anymore'," DiCarlo told CBC News.

The roots of the common dandelion were ground up and made into tea. According to researchers, early results show that the tea kills cancer cells in the lab.

Using dandelion tea extract to treat leukemia is not a new idea. The Memorial Sloan-Kettering Cancer Center in the U.S., among other research sites, has been looking at the plant since at least 2010.

John DiCarlo, 72, says dandelion tea saved his life, after other medical treatments for his leukemia failed. (Steven Bull/CBC)

Hamm said the tea doesn't work for everyone and they need to find out why. The first phase of the trials will attempt to determine the right dose to administer.

Hamm was convinced that the weed contains an active ingredient, but warned "it can harm as well as benefit." She said taking dandelion extract tea could interfere with regular chemotherapy, and she urged patients not to mix the natural remedy with other cancer drugs without speaking to a doctor first.

The researchers have filed an application with Health Canada. If it's approved, Hamm expected to start the first phase of the trials in about two to three months.

Phase 1 involves 21 cancer patients where the standard of care is not working. Hamm said it would include patients with a wide variety of cancer types. The first phase should last six to eight months, she said.

Phase 2 will look at which types of cancer dandelion extract works best on, based on the results of Phase 1.

Fruits, Veggies Powerful Rx for Kidney Disease: Study

Kidney disease patients who eat three to four more servings of fruits and vegetables every day could lower their blood pressure and nearly halve their medication costs, new research suggests.

The findings stem from the multi-year tracking of a small group of patients, in which standard medical treatment was compared with the simple nutritional intervention.

The goal: to see which approach did a better job at driving down both blood pressure and drug expenses.

The result on both fronts showed a clear win for healthy food.

Study author Dr. Nimrit Goraya described the links seen between increased fruit and vegetable intake, kidney disease control and lower medication expenses as "huge." And "the impact was visible from the very first year," she said.

"This study has been done over five years, but every year since the therapy with fruits and vegetables began, we were able to lower medications," she noted.

Goraya is program director for nephrology with Baylor Scott & White Healthcare in Temple, Texas.

She and her colleagues are scheduled to present their findings this week at an American Heart Association meeting on blood pressure, in Orlando, Fla.

High blood pressure is the second leading cause of kidney failure. The kidneys and the circulatory system depend on each other for good health, according to the heart association.

In all, 108 kidney disease patients were enlisted in the study, all of whom were taking similar doses of blood pressure drugs.

Patients were divided into three groups. One group was treated with sodium bicarbonate (baking soda), the standard treatment designed to neutralize the lingering acid that kidney patients typically struggle to excrete. Failure to excrete can lead to abnormally high acid levels, a condition known as "metabolic acidosis."

A second group was not prescribed sodium bicarbonate, but instead was provided three to four servings of fruits and vegetables a day. These patients were not instructed to alter their usual diet beyond consuming their new fruit and vegetable allotment.

A third group was not treated in any way.

The result: After five years, systolic blood pressure (the top number in a reading) was pegged at 125 mm Hg among the fruit and vegetable group, compared with 135 mm Hg and 134 mm Hg, respectively, among the medication and no treatment groups.

What's more, those in the food group were taking considerably lower doses of daily blood pressure medication than those in the other groups, the study authors said.

This translated into a near halving of the food group's total expenditure on such drugs, down to roughly $80,000 over five years compared with an average total of more than $153,000 among each of the other two groups.

As to the exact mechanisms by which an increased intake of fruits and vegetables appears to promote kidney disease control, Goraya pointed to a variety of things that are set in motion whenever nutrition improves.

"I think that the benefit is not singular," she said. Goraya suggested that kidney disease control is likely triggered not only by the protective benefits of healthier foods but also by a corresponding reduction in fast-food consumption, a lowering of salt intake, and perhaps even weight loss.

Those looking for more ways to achieve some measure of kidney disease control without medication might look to the findings of a new Brazilian study also presented at the Orlando meeting that highlighted the potential benefits of exercise.

After reviewing 28 studies involving more than 1,000 patients on dialysis, researchers at the University of Sao Paulo Medical School found that those who routinely engaged in both aerobic exercise and resistance (strength) training significantly lowered their blood pressure.

Lona Sandon is program director in the department of clinical nutrition at the School of Health Professions at UT Southwestern, in Dallas. "It is remarkable what fruits and vegetables can do, along with a little exercise," she said.

"Blood pressure meds come with many side effects that may leave people feeling sluggish, or other problems," Sandon explained. "The side effects of fruits and vegetables and exercise is better health."

The bottom line: "When people have access to healthy foods, they can change their health," said Sandon. "And especially when they eat the recommended amounts that were provided to them in the study."

The findings of studies presented at medical meetings should be viewed as preliminary until published in a peer-reviewed journal.

New study to examine effectiveness of orally administered drug in treating stuttering

Stuttering, an interruption in the flow of speech, affects about three million Americans. It begins most often in childhood, affecting four men for every woman. A precise cause of this complex communicative disorder is not known.

A genetically influenced condition, stuttering appears to originate when various aspects of a young child's development interact, and is best addressed with early intervention. No cure for it has been found, but behavioral treatment options are available. Currently, no Food and Drug Administration (FDA)-approved drug treatments are available.

In an attempt to find a new medicine, a research team at the School of Medicine at the University of California, Riverside, in partnership with the speech pathology laboratory at the University of Redlands, will conduct a study at CITrials in Riverside, Calif., to determine how effective ecopipam, an orally administered medication, is as treatment against stuttering.

Ten volunteers will be selected to participate in the FDA-approved clinical trial. The study, scheduled to begin next month, is seeking volunteers, although space is limited. People interested in participating in the study may contact Gerald Maguire, M.D., the chair of psychiatry and neuroscience at UC Riverside and the associate dean for graduate medical education, who is leading the study: gerald.maguire@medsch.ucr.edu.

"The study is exploratory," Maguire said. "We are the only site in the world conducting this trial; ecopipam has never been tested for stuttering. It has been tested for treatment of tics in Tourette syndrome, a neurological disease, with some encouraging results. Stuttering shares some similarities to the vocal changes seen in subjects with Tourette syndrome. We are hopeful ecopipam will yield beneficial effects in stuttering."

Ecopipam is a first-in-class drug that selectively blocks the actions of the neurotransmitter dopamine at its receptor. Dopamine receptors can be broadly classified into two families based on their structures: D1 receptors and D2 receptors. Ecopipam blocks dopamine only at D1 receptors, and thus acts differently than other commercially available medications. This mechanism explains why ecopipam is being tested as a potential treatment for stuttering.

The 10 patients selected for the clinical trial next month will undergo a physical examination and their medical history will be recorded. To ensure that their stuttering symptoms are sufficiently severe, their speech patterns will be analyzed by Professor Lisa LaSalle, a speech pathologist at the University of Redlands, and co-investigator on the study. Each patient will receive ecopipam for a limited time.

"We believe we could have results from our analysis in as soon as nine months," Maguire said. "A placebo-controlled clinical trial may then follow, pending approval. If ecopipam is found to be effective in controlling stuttering, we may have a viable solution for a disorder that can be traced back centuries."

TSRI scientists shed light on molecular workings of MS drug

In continuation of my update on Tecfidera

A study by scientists at The Scripps Research Institute (TSRI) has helped to de-mystify the molecular workings of the multiple sclerosis (MS) drug Tecfidera®. The drug is the most widely prescribed pill-based therapy for MS, but its biological mechanism remains mysterious.

Using a new TSRI technology that can quickly reveal a drug's protein targets, the scientists showed that Tecfidera® interacts with multiple T cell proteins, in some cases inhibiting their activity, and helping to suppress the T cell activation that is a key feature of MS flare-ups.

"This new technology has given us insights into the therapeutic modulation of the immune system that we could not have obtained with standard approaches," said co-senior author John R. Teijaro, an assistant professor at TSRI.

The study was reported recently in Science Signaling.

Treatment for an Autoimmune Disease

MS is an autoimmune disease of the brain featuring damage to nerve fibers and producing a range of symptoms, including tingling in the extremities, muscle weakness, muscle spasms, visual problems and mood instability. About 400,000 people in the United States and about 2.5 million worldwide have MS, mostly in a form with intermittent flare-ups of symptoms—which can start to worsen inexorably.

Two large clinical trials published in 2012 found that Tecfidera® is almost twice as effective as an older standard MS drug at reducing the rate of flare-ups. It also appears to slow the disease's progression. But how the drug works has never been clear.

Despite its recent (2013) US Food and Drug Administration approval for MS, the drug is neither new nor high-tech. It is a relatively simple organic compound, dimethyl fumarate (DMF), that has been in the biomedical literature for decades. It was once used in Europe to prevent mold growth in sofas during storage and shipping, although the European Union banned it from consumer products in 2009 after it was linked to severe allergic skin reactions. It has proved more useful as a pharmaceutical: since the 1990s it has been an effective treatment—as the main ingredient in the drug Fumaderm®—for the autoimmune skin disease psoriasis. Success against psoriasis led to its investigation as a potential MS drug.

Until recently, the leading theory was that DMF works against MS primarily by unleashing the activity of a protein called Nrf2, which helps protect the brain from autoimmune damage by marshaling a powerful anti-oxidant response and which may also reduce immune system activation. Studies published in the past year have suggested, however, that DMF works principally by reducing immune system activity and does so independently of Nrf2. In recent years, there have also have been several reports among patients taking Fumaderm® or Tecfidera® of a potentially fatal viral brain infection called progressive multifocal leukoencephalopathy, which normally occurs only in people whose immune systems have been seriously weakened.

Study shows maritime pine bark extract may be effective in limiting muscle loss due to aging

In continuation of my update on Pycnogenol....

A new peer-reviewed, published study shows French maritime pine bark extract, Pycnogenol®, may be effective in curbing muscle loss that occurs with aging – a natural process that leads to sarcopenia, a common condition affecting adults as early as age 65. The study, published in the September 2016 Journal on Orthopedics and Traumatology, revealed that daily supplementation with Pycnogenol® helps to stabilize muscles through this natural process and supports muscular function and endurance.

 

According to the National Library of Medicine, physically inactive individuals can lose as much as eight percent of muscle mass each decade after 30. Those who are physically active can maintain more muscle mass yet are still affected by muscle loss due to aging.

"Muscle loss due to aging can affect even the most active individuals and can result in feelings of weakness and frustrating fatigue which can interfere with our daily activities. This natural process is why opening a jar of pickles gets harder as we get older. We have less muscle to work with, so our muscles must work harder and, thus, we get tired faster," said nationally-known natural nutrition expert Dr. Fred Pescatore.

"This new study builds on a body of research connecting Pycnogenol® to healthy aging," said Dr. Pescatore. "As we age, muscle loss starts to impact the daily activities we tend to take for granted like climbing stairs, lifting groceries or enjoying walks without getting tired. This research shows that Pycnogenol can help alleviate the symptoms of sarcopenia and can support muscle function as we age."

In the study, participants between ages 70 - 78 and exhibiting symptoms of muscle loss, sarcopenia and fatigue but otherwise healthy, reported feeling increased muscle endurance in completing daily tasks such as walking and stair climbing, and improved overall muscular function by more than 40 percent. After just 8 weeks of taking 150 mg of Pycnogenol® the study results showed:

"What I found really compelling is the measurable effect Pycnogenol® had on the participants in relation to completing daily tasks -- the research shows that Pycnogenol® can play a role in helping you stay active with greater muscular stability and maintain muscle function as you age," Dr. Pescatore noted.

While experts recommend adequate amounts of sleep, in addition to diet and daily exercise to maintain physical fitness in later years, the study results are encouraging for those looking for an added boost in muscle function overall.

Ref : http://www.webmd.com/vitamins-supplements/ingredientmono-1019-pycnogenol.aspx?activeingredientid=1019