Weight-loss drug Belviq seems safe for heart, study finds
By MARILYNN MARCHIONE
AP Chief Medical Writer
Sunday, August 26
For the first time, a drug has been shown to help people lose weight and keep it off for several years without raising their risk for heart problems — a safety milestone that may encourage wider use to help curb the obesity epidemic.
The drug, Belviq, has been sold in the United States since 2013 and is the first of several new weight-loss medicines to succeed in a long-term heart safety study now required by federal regulators to stay on the market.
“Patients and their doctors have been nervous about using drugs to treat obesity and for good reason. There’s a history of these drugs having serious complications,” said study leader Dr. Erin Bohula of Brigham and Women’s Hospital in Boston.
With this study, Belviq has been convincingly shown safe for the heart, she said.
Although Belviq did not raise heart risks, it didn’t lower them either, as many had hoped it would. The weight loss it produced was fairly modest — after 40 months, Belviq users had shed 9 pounds (4 kilograms), twice as much as those on dummy pills.
It may be that weight loss alone is not enough to lower heart risks, or that there needs to be more to do that, some doctors said.
Results were discussed Sunday at a European Society of Cardiology meeting in Munich and published by the New England Journal of Medicine. Belviq’s maker, Eisai Inc., sponsored the study and many of the researchers consult or work for the company.
Worldwide, 13 percent of adults are obese and 39 percent are overweight, raising their risk for a host of health problems. Diet and exercise are the first steps doctors recommend, but medicines also can be considered for people with dangerously high weight who cannot drop enough pounds by other means.
Several popular diet medicines were previously withdrawn from sale after they were found to raise the risk for heart valve damage, suicidal thoughts or other problems, prompting the new requirement for heart safety studies.
Belviq is an appetite suppressant that works by stimulating brain chemicals to give a feeling of fullness. It costs roughly $220 to $290 a month in the United States.
Researchers tested it in a study of 12,000 people who were either obese or overweight with heart disease risk factors such as high blood pressure or cholesterol. They were given Belviq or dummy pills to take twice a day and offered lifestyle and diet advice.
At one year, 39 percent on Belviq and 17 percent on dummy pills had lost at least 5 percent of their starting weight. Several previous studies also found the drug effective for weight loss.
After about three years, 6 percent of each group had suffered a heart-related problem or death.
Fewer people on Belviq developed diabetes — 8.5 percent versus 10.3 percent on dummy pills.
Serious side effects were similar, but more on Belviq stopped taking their pills because of them — 7 percent versus 4 percent. Common side effects included dizziness, fatigue, headache and nausea.
Dangerously low blood sugar happened in 13 people on Belviq versus four in the other group; all but one case involved people also taking diabetes medicines, which lower blood sugar.
Tests for heart valve damage were done on 3,270 participants but no big differences in rates were seen. Suicidal thoughts or behavior were reported in 21 people on Belviq versus 11 on dummy pills, but more on the drug had a history of depression and the difference was so small it could have been due to chance, Bohula said.
In a commentary, two of the journal’s editors, Drs. Julie Inglefinger and Clifford Rosen, said there might be alternatives to Belviq. Liraglutide, when used to treat diabetes, also causes weight loss and lowers heart risks, though it hasn’t been tested for cardiac safety at the dose used for weight loss.
For now, Belviq “may be best used on a cautious basis, according to the needs of individual patients,” they write.
Marilynn Marchione can be followed at http://twitter.com/MMarchioneAP
The Associated Press Health & Science Department receives support from the Howard Hughes Medical Institute’s Department of Science Education. The AP is solely responsible for all content.
Don’t lose sleep over it: Even if you don’t get enough shut-eye, most fixes are easy
July 26, 2018
Clinical Affiliate, Stanford University
Brandon Peters-Mathews does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
The serious consequences of sleep deprivation perennially capture society’s attention. And, as kids head back to school, sleep and a lack of it are of particular concern.
Compared to historical norms, how have our contemporary expectations of sleep changed? What are the effects of inadequate sleep? What can be done to optimize the experience of sleep, especially in the context of insomnia?
I am a clinician and sleep researcher who treats people with sleep problems. I think there is little reason to suspect that our collective sleep needs have dramatically changed in the recent past, rooted as they are in immutable physiological processes. We should, however, be paying attention to our sleep needs, and that isn’t as hard as it sounds.
What is sleep anyway?
From a clinical perspective, sleep is defined as a reversible behavioral state of unresponsiveness and perceptual disengagement from the environment. It is dependent on the balance between sleep drive – the desire for sleep that builds during wakefulness and is linked to the accumulation and clearance of chemicals within the brain like adenosine – and the circadian alerting signal. The circadian rhythm coordinates processes of the body to the environmental patterns of light and darkness. Adequate sleep is and always has been restorative to the body. Giving sleep respect, and preserving it to the benefit of health, has not been so permanent.
Researchers have learned more about sleep in the past 100 years than in all the preceding millennia combined.
The advent of, and inexpensive access to, artificial light no doubt marked a significant shift in this history. Scientific understanding of sleep continues to evolve and remains incomplete.
Nevertheless, it does seem that people are sleeping less now than they have in the past several decades. Recent self-reported national polling among American adults consistently suggests that Americans are not getting adequate sleep. This begs the question: How much sleep do people really need?
Sleep needs change over the lifespan
Sleep needs change over one’s lifetime. Toddlers may require 11 to 14 hours of sleep to feel rested and typically take naps.
Through adolescence, the need for sleep diminishes until it approaches the adult average. A typical adult requires from seven to nine hours of sleep nightly to avoid the effects of sleep deprivation. Adults older than 65 years may require just seven to eight hours of sleep.
Surveys suggest that 35 to 40 percent of the adult population sleeps less than seven to eight hours on weekdays. This self-reported sleep data may overestimate the objectively measured sleep obtained by up to one hour, due to time spent falling or getting back to sleep. We are in trouble.
If someone eats too many calories, or too few, the effects on the body become apparent. Unfortunately, there is no “sleep scale” to step onto to gauge the physical tolls of sleep deprivation. Sleep deprivation, either from not allotting enough time to get sufficient sleep or due to sleep disorders like insomnia, may have important consequences.
Bad for the brain?
Beyond sleepiness, sleep deprivation wreaks havoc on the brain, affecting mood and worsening depression, exacerbating pain and undermining executive functions that affect judgment, planning, organization, concentration, memory and performance. Hormones influencing weight and growth become imbalanced. Immune dysfunction, leading to an increased susceptibility to illness, and a pro-inflammatory state develop.
Sleep deprivation can become deadly, too. The increased risk of fatal traffic accidents associated with lost sleep parallels that linked to alcohol consumption. Those who sleep fewer than five hours per night have two to three times the risk of a heart attack. Chronic sleep loss may slowly undermine the central pillars of health.
Ditch the digital devices, keep a routine
How can we avoid the perils of inadequate sleep?
First, prioritize sleep and ensure that you are obtaining sufficient hours to feel rested. Ensure an easy transition to sleep by maintaining an hour to unwind with relaxing activities before going to bed.
Using a laptop and other digital devices before going to bed can be harmful to your sleep. GaudiLab/Shutterstock.com
Reserve the bedroom as a space for sleep: leave electronic devices elsewhere.
Keep a regular sleep-wake schedule, especially fixing the wake time, including on weekends.
Get 15 to 30 minutes of sunlight upon awakening, or at sunrise.
Always go to bed feeling sleepy, even if that means delaying bedtime a little.
As needed, consider reducing the time in bed if more than 30 minutes is consistently spent awake.
Be physically active.
Moderate the use of alcohol and caffeine.
When sleep problems persist, get help.
If these do not work, consider evaluation by a board-certified sleep physician. Chronic insomnia may respond well to cognitive behavioral therapy for insomnia. This treatment is increasingly accessible via trained therapists, workshops, online courses and books.
Symptoms such as frequent or early awakenings, excessive daytime sleepiness, snoring, witnessed pauses in breathing, frequent peeing at night, night sweats, teeth grinding, and morning headaches may suggest the presence of sleep apnea. A comprehensive evaluation and appropriate testing may lead to an effective treatment.
Sleep should come naturally. It should never become an additional source of stress. Simple adjustments can yield benefits quickly.
Fortunately, the first step to better sleep is recognizing its importance – an objective that has hopefully been achieved. Now, consider making a few changes and, as necessary, access further resources to yield the long-term benefits to health and well-being that only sleep may provide.
Why you can smell rain
August 27, 2018
Your nose knows what’s on the way. Lucy Chian/Unsplash, CC BY
Instructional Assistant Professor of Atmospheric Sciences, Texas A&M University
Tim Logan does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
Texas A&M University provides funding as a founding partner of The Conversation US.
When those first fat drops of summer rain fall to the hot, dry ground, have you ever noticed a distinctive odor? I have childhood memories of family members who were farmers describing how they could always “smell rain” right before a storm.
Of course rain itself has no scent. But moments before a rain event, an “earthy” smell known as petrichor does permeate the air. People call it musky, fresh – generally pleasant.
This smell actually comes from the moistening of the ground. Australian scientists first documented the process of petrichor formation in 1964 and scientists from the Massachusetts Institute of Technology further studied the mechanics of the process in the 2010s.
Petrichor’s main ingredients are made by plants and bacteria that live in the ground. vovan/Shutterstock.com
Petrichor is a combination of fragrant chemical compounds. Some are from oils made by plants. The main contributor to petrichor are actinobacteria. These tiny microorganisms can be found in rural and urban areas as well as in marine environments. They decompose dead or decaying organic matter into simple chemical compounds which can then become nutrients for developing plants and other organisms.
A byproduct of their activity is an organic compound called geosmin which contributes to the petrichor scent. Geosmin is a type of alcohol, like rubbing alcohol. Alcohol molecules tend to have a strong scent, but the complex chemical structure of geosmin makes it especially noticeable to people even at extremely low levels. Our noses can detect just a few parts of geosmin per trillion of air molecules.
During a prolonged period of dryness when it has not rained for several days, the decomposition activity rate of the actinobacteria slows down. Just before a rain event, the air becomes more humid and the ground begins to moisten. This process helps to speed up the activity of the actinobacteria and more geosmin is formed.
Before you see it, do you smell it?
When raindrops fall on the ground, especially porous surfaces such as loose soil or rough concrete, they will splatter and eject tiny particles called aerosols. The geosmin and other petrichor compounds that may be present on the ground or dissolved within the raindrop are released in aerosol form and carried by the wind to surrounding areas. If the rainfall is heavy enough, the petrichor scent can travel rapidly downwind and alert people that rain is soon on the way.
The scent eventually goes away after the storm has passed and the ground begins to dry. This leaves the actinobacteria lying in wait – ready to help us know when it might rain again.
Glioblastoma topples an American hero, but researchers will continue the fight
August 27, 2018
Professor of Neurosurgery, University of Florida
Duane Mitchell holds patents related to brain tumor immunotherapy that have been licensed by Celldex Therapeutics, Inc., Annias Immunotherapeutics, Inc., and Immunomic Therapeutics, Inc. He is the co-founder of, iOncologi, Inc., a biotechnology company focused on cancer immunotherapy treatment. . He serves as an advisor for Bristol-Myers Squibb, Inc., Tocagen, Inc., and Oncorus, Inc. He receives funding from the National Cancer Institute, Department of Defense, and several private foundations focused on brain tumor research and treatment.
University of Florida provides funding as a founding partner of The Conversation US.
Sen. John McCain withstood beatings and torture as a prisoner of war, but he was confronted with an enemy in July 2017 that he was ultimately unable to overcome. An aggressive and deadly brain cancer known as glioblastoma, or GBM, took McCain’s life on Aug. 25, 2018.
The man noted for his unstoppable resilience, pervasive optimism and uncompromising personal ethos was not able to conjoin forces with the marvels of modern medicine and defeat the insidious enemy of brain cancer.
Why is GBM so deadly? Why have so many individuals, with presumably all the physical and financial resources that can be amassed readily available to them, been unable to conquer this dreadful enemy? Sen. Edward M. Kennedy died from the disease exactly nine years earlier. In 2015, GBM also claimed the life of Joseph “Beau” Biden III, son of Joe Biden, the former vice president. It kills about 15,000 people in the U.S. each year. Most people diagnosed with the disease survive less than two years.
Has GBM been cured in any individuals, and if so, why not in most who are affected by this disease?
I am a physician and scientist who studies ways to stop GBM. Despite the sadness and great loss we feel at Senator McCain’s passing, we are making progress in the treatment of this disease.
An ongoing battle
By 1970, cancer had become the second-leading cause of death in the United States. It still is today, claiming about 600,000 lives a year.
In 1971, President Richard Nixon signed the National Cancer Act. While the legislation did not contain the phrase “War on Cancer,” those words quickly caught on. A concerted quest to find a cure for malignant diseases had begun.
The landmark legislation broadened the authority of the director of the National Cancer Institute (NCI) to implement research programs and cooperate with other agencies to direct educational efforts focused on reducing cancer mortality in the U. S. The act created a “bypass budget” for the NCI that is submitted directly from the NCI director to the president of the United States and to Congress, highlighting the priority put on reducing cancer mortality by the U.S. government.
The NCI investment in cancer research, along with billions of dollars from the pharmaceutical industry, have undoubtedly had a profound positive impact on the prevention, diagnosis and treatment of cancer. However, unlike the decade of success embodied by our nation’s quest to put a man on the moon, winning the war on cancer has proven to be a much more elusive goal – and much longer than 10 years.
While decades of research have led to many new, effective treatments, research also has revealed a marked complexity in many cancers, particularly those that have spread beyond the site where the tumor originated.
A first in the fight
GBM was the first cancer to undergo comprehensive genetic analysis as part of the multibillion-dollar NCI-led project called “The Cancer Genome Atlas.” This ambitious quest sought to completely analyze the gene expression patterns and DNA sequence of several human cancers and make the data publicly available for scientists to study. It has been a game changer in the assault against cancer.
Scientists have learned, for instance, that GBM, like many cancers, is not a single disease. Even though two patients may receive the same diagnosis of GBM and may have tumors that look almost identical under a microscope, at the cellular level these tumors can be quite different, with different mutations in the DNA code and different pathways driving tumor growth. This understanding means that a single therapeutic approach is very unlikely to work the same in all individuals with the same diagnosis of GBM.
Essentially, these patients really don’t have the same disease. This new understanding, while tremendously important in shaping our strategies for treating GBM going forward, also raises the realization that the enemy we face in GBM is even more insidious than thought.
To add to this complexity, we understand now that even within a given patient’s tumor, the individual cancer cells can even differ significantly from one another, having diverged over time through rapid growth and through the accumulation of different mutations within different tumor cells. This means that the same treatment hitting the tumor cells within a single patient will likely not kill all cancer cells with the same effectiveness. This allows resistant tumor cells within the population to grow back in the face of treatment that may have been initially effective.
Tackling this complexity at the cellular level to develop treatments that are effective against all tumor cells within a patient is a major challenge for tumors such as GBM. It likely accounts for much of the resistant nature of the disease.
An additional characteristic of GBM is the invasive nature of the disease. GBM tumor cells essentially crawl away from the main tumor mass and embed themselves deep within the normal brain, often hidden behind a protective barrier known at the blood-brain barrier. This invasive feature means that while neurosurgeons can often remove the main central tumor mass of a GBM, the invasive finger-like projections protrude into other areas of the brain. The distant islands of tumor cells that have migrated away cannot be effectively removed by surgery.
Radiation treatment is effective in controlling tumor growth, but there are limits to the doses of radiation that can be delivered to normal brain. Chemotherapy treatment with temozolomide currently can extend survival on average by several months. But the blood-brain barrier, or specialized cells that keep threats away from the brain, restricts many drug treatments from getting into the brain, and the mixed populations of tumor cells are already poised to grow out of the cancer cells that are resistant to the agents that do get through.
When one takes an inventory of what we’ve learned about GBM, it is easy to become discouraged and perhaps to conclude that we are facing an insurmountable foe. Such a conclusion might be warranted, were it not for the fact that despite the incredible complexity and challenges faced in successfully treating GBM, long-term survivors of this disease do exist.
Long-term survival, or five years or longer from time of diagnosis, with standard treatment regimens is reported at 9.8 percent from a systematic study of 573 patients with GBM. While 9.8 percent is an unacceptably low rate, it is demonstrable evidence that long-term survival is feasible.
We have learned that survivors tend to be younger than 50, have tumors that were able to undergo more extensive surgical removal at diagnosis, and have molecular features that predict a better response to the chemotherapy.
Recent advances in the treatment of GBM have also brought the advent of a new device technology that delivers alternating low-intensity electric fields called tumor-treating fields. Long-term survival data has not yet been reported for the addition of tumor-treating fields to standard treatment, but a median survival improvement of 4.9 months from 16.0 months to 20.9 months was reported in a recently completed phase III clinical trial involving 695 patients. It is possible that an improvement in long-term survival rates will also be observed in patients receiving this combined treatment.
Perhaps our greatest hope comes from emerging therapeutic strategies such as immunotherapy and personalized medicine approaches. Our immune systems are hard-wired to deal with complexity and variety, needing to respond rapidly and effectively to a myriad of unknown and changing infectious threats from the environment. The field is just beginning to understand how to harness this potent and adaptable killing power to hone in on cancer cells in a comprehensive way. We have observed encouraging long-term survival outcomes in patients with GBM during our early phase clinical trials of immunotherapy and are currently evaluating the effectiveness of these treatments in large-scale clinical trials at our medical center.
The war on cancer has certainly proven to be harder, longer and more complex than many envisioned in 1971. While tremendous gains have been made in cure rates for some malignant diseases like childhood leukemia, GBM has perhaps stood stalwart in resistance over the decades to transformative progress. However, through diligence and persistence, we have begun to better understand the enemy we face at the root of this invasive brain cancer. This understanding has transformed our plans of attack and has begun to bear evidence that breakthroughs are possible and forthcoming.
Sen. McCain will be remembered for his many contributions, accomplishments and sacrifices in service of his country. He is also but one of the 600,000 Americans and 8.2 million people worldwide whose life will be claimed by cancer this year. Among the many things to be remembered, honored and cherished about his life, let the fighting legacy of this warrior remind us that war on cancer goes forward in his memory, and in honor of all that have been and will be impacted by this disease.