Seriously, Juice Is Not Healthy

Obesity affects 40 percent of adults and 19 percent of children in the United States and accounts for more than $168 billion in health care spendingeach year. Sugary beverages are thought to be one of the major drivers of the obesity epidemic. These drinks (think soda and sports drinks) are the largest single source of added sugars for Americans and contribute, on average, 145 added calories a day to our diets. For these reasons, reducing sugary beverage consumption has been a significant focus of public health intervention. Most efforts have focused on sodas.

But not juice. Juice, for some reason, gets a pass. It’s not clear why.

Americans drink a lot of juice. The average adult drinks 6.6 gallons per year. More than half of preschool-age children (ages 2 to 5) drink juice regularly, a proportion that, unlike for sodas, has not budged in recent decades. These children consume on average 10 ounces per day, more than twice the amount recommended by the American Academy of Pediatrics.

Parents tend to associate juice with healthfulness, are unaware of its relationship to weight gain and are reluctant to restrict it in their child’s diet. After all, 100 percent fruit juice — sold in handy individual servings — has been marketed as a natural source of vitamins and calcium. Department of Agriculture guidelines state that up to half of fruit servings can be provided in the form of 100 percent juice and recommend drinking fortified orange juice for the vitamin D. Some brands of juice are evenmarketed to infants.

Government programs designed to provide healthy food for children, such as the Special Supplemental Nutrition Program for Women, Infants, and Children, offer juice for kids. Researchers have found that children in the program are more likely to exceed the recommended daily fruit juice limit than those who are similarly poor but not enrolled.

[Here’s a guide to reducing your sugar consumption.]

Despite all the marketing and government support, fruit juices contain limited nutrients and tons of sugar. In fact, one 12-ounce glass of orange juice contains 10 teaspoons of sugar, which is roughly what’s in a can of Coke.

Drinking fruit juice is not the same as eating whole fruit. While eating certain fruits like apples and grapes is associated with a reduced risk of diabetes, drinking fruit juice is associated with the opposite. Juices contain more concentrated sugar and calories. They also have less fiber, which makes you feel full. Because juice can be consumed quickly, it is more likely than whole fruit to contribute to excess carbohydrate intake. For example, research has found that adults who drank apple juice before a meal felt hungrier and ate more calories than those who started with an apple instead. Children who drink juice instead of eating fruit may similarly feel less full and may be more likely to snack throughout the day.

Juice may also be a “gateway beverage” — 1-year-olds who drank more juice also drank more sugary beverages, including more soda, in their school-age years. Children’s excessive consumption of juice has been linked to an increased risk of weight gainshorter stature and cavities. Even in the absence of weight gain, sugar consumption worsens blood pressure and increases cholesterol.

It’s tempting to minimize the negative contributions of juice to our diets because it’s “natural” or because it contains “vitamins.” Studies that support this view exist, but many are biased and have been questioned.

And we doubt you’d take a multivitamin if it contained 10 teaspoons of sugar.

[Children and adults are downing sugary drinks far less often than they used to, a new study finds.]

There is no evidence that juice improves health. It should be treated like other sugary beverages, which are fine to have periodically if you want them, but not because you need them. Parents should instead serve water and focus on trying to increase children’s intake of whole fruit. Juice should no longer be served regularly in day care centers and schools. Public health efforts should challenge government guidelines that equate fruit juice with whole fruit, because these guidelines most likely fuel the false perception that drinking fruit juice is good for health.

It’s much easier to prevent obesity than it is to reverse it. We need to teach kids how to eat healthier when they’re young so that they develop good habits to carry on for the rest of their lives. In the past decade or so, we have succeeded in recognizing the harms of sugary beverages like soda. We can’t keep pretending that juice is different.

Dying Organs Restored to Life in Novel Experiments

When Georgia Bowen was born by emergency cesarean on May 18, she took a breath, threw her arms in the air, cried twice, and went into cardiac arrest.

The baby had had a heart attack, most likely while she was still in the womb. Her heart was profoundly damaged; a large portion of the muscle was dead, or nearly so, leading to the cardiac arrest.

Doctors kept her alive with a cumbersome machine that did the work of her heart and lungs. The physicians moved her from Massachusetts General Hospital, where she was born, to Boston Children’s Hospital and decided to try an experimental procedure that had never before been attempted in a human being following a heart attack.

They would take a billion mitochondria — the energy factories found in every cell in the body — from a small plug of Georgia’s healthy muscle and infuse them into the injured muscle of her heart.

Mitochondria are tiny organelles that fuel the operation of the cell, and they are among the first parts of the cell to die when it is deprived of oxygen-rich blood. Once they are lost, the cell itself dies.

But a series of experiments has found that fresh mitochondria can revive flagging cells and enable them to quickly recover.

In animal studies at Boston Children’s Hospital and elsewhere, mitochondrial transplants revived heart muscle that was stunned from a heart attack but not yet dead, and revived injured lungs and kidneys.

Infusions of mitochondria also prolonged the time organs could be stored before they were used for transplants, and even ameliorated brain damage that occurred soon after a stroke.

In the only human tests, mitochondrial transplants appear to revive and restore heart muscle in infants that was injured in operations to repair congenital heart defects.

For Georgia, though, the transplant was a long shot — a heart attack is different from a temporary loss of blood during an operation, and the prognosis is stark. There is only a short time between the onset of a heart attack and the development of scar tissue where once there were living muscle cells.

The problem was that no one knew when the baby’s heart attack had occurred. Still, said Dr. Sitaram Emani, a pediatric heart surgeon who administered the transplant, there was little risk to the infant and a chance, though slim, that some cells affected by her heart attack might still be salvageable.

“They gave her a fighting chance,” said the infant’s mother, Kate Bowen, 36, of Duxbury, Mass.


Dr. Jesse Esch, right, with Brian Quinn, a cardiology fellow, performing a mitochondrial transplant on Georgia Bowen. Angiograms showing the infant’s coronary arteries and the catheter can be seen on the monitor.CreditKatherine Taylor for The New York Times

Dr. James McCully prepared to inject mitochondria for Georgia Bowen during her operation. Animal experiments have suggested that the procedure may repair damaged tissue.CreditKatherine Taylor for The New York Times

The idea for mitochondrial transplants was born of serendipity, desperation and the lucky meeting of two researchers at two Harvard teaching hospitals — Dr. Emani at Boston Children’s and James McCully at Beth Israel Deaconess Medical Center.

Dr. Emani is a pediatric surgeon. Dr. McCully is a scientist who studies adult hearts. Both were wrestling with the same problem: how to fix hearts that had been deprived of oxygen during surgery or a heart attack.

“If you cut off oxygen for a long time, the heart barely beats,” Dr. McCully said. The cells may survive, but they may never fully recover.

While preparing to give a talk to surgeons, Dr. McCully created electron micrographs of damaged cells. The images turned out to be revelatory: The mitochondria in the damaged heart cells were abnormally small and translucent, instead of a healthy black.

The mitochondria were damaged — and nothing Dr. McCully tried revived them. One day, he decided simply to pull some mitochondria from healthy cells and inject them into the injured cells.

Working with pigs, he took a plug of abdominal muscle the size of a pencil eraser, whirled it in a blender to break the cells apart, added some enzymes to dissolve cell proteins, and spun the mix in a centrifuge to isolate the mitochondria.

He recovered between 10 billion and 30 billion mitochondria, and injected one billion directly into the injured heart cells. To his surprise, the mitochondria moved like magnets to the proper places in the cells and began supplying energy. The pig hearts recovered.

Dr. Sitaram Emani of Boston Children’s Hospital and his colleagues have treated 11 babies with mitochondrial transplants, most of them successfully.CreditKatherine Taylor for The New York Times

Meanwhile, Dr. Emani was struggling with the same heart injuries in his work with babies.

Many of his patients are newborns who need surgery to fix life-threatening heart defects. Sometimes during or after such an operation, a tiny blood vessel gets kinked or blocked.

The heart still functions, but the cells that were deprived of oxygen beat slowly and feebly.

He can hook the baby up to a machine like the one that kept Georgia Bowen alive, an extracorporeal membrane oxygenator, or Ecmo. But that is a stopgap measure that can work for only two weeks. Half of the babies with coronary artery problems who end up on an Ecmo machine die because their hearts cannot recover.

But one day Dr. Emani was told of Dr. McCully’s work, and the two researchers met. “It was almost an ‘aha’ moment,” Dr. Emani said.

Dr. McCully moved to Boston Children’s, and he and Dr. Emani prepared to see if the new technique might help tiny babies who were the sickest of the sick — those surviving on Ecmo.

It was not long before they had their first patient.

Early one Saturday morning in March 2015, the hospital got a call from a hospital in Maine. Doctors there wanted to transfer to Boston Children’s a newborn baby boy whose heart had been deprived of oxygen during surgery to fix a congenital defect.

The baby was on an Ecmo but his heart had not recovered.

“We turned the intensive care unit into an operating room,” Dr. Emani said.

He snipped a tiny piece of muscle from the baby’s abdomen. Dr. McCully grabbed it and raced down the hall.

Twenty minutes later, he was back with a test tube of the precious mitochondria. Dr. Emani used an echocardiogram to determine where to inject them.

“The spot that is weakest is where we want to go,” he said. “It is important to give as much of a boost as you can.”


Dr. McCully placed mitochondria from Georgia Bowen’s neck muscle into a centrifuge before infusing them into her heart muscle.CreditKatherine Taylor for The New York Times

Dr. Emani taking tissue samples from Georgia’s neck.CreditKatherine Taylor for The New York Times

He injected a billion mitochondria, in about a quarter of a teaspoon of fluid.

Within two days, the baby had a normal heart, strong and beating quickly. “It was amazing,” Dr. Emani said.

The scientists have now treated 11 babies with mitochondria, and all but one were able to come off Ecmo, Dr. Emani said. Still, three of them ultimately died, which Dr. Emani attributes to a delay in treatment and other causes.


Dr. Esch prepared the mitochondria to be infused into Georgia’s heart. The fluid amounts to a quarter of a teaspoon.CreditKatherine Taylor for The New York Times

Two died because their hearts were still so damaged, and one died of an infection. All of the more recent patients survived and are doing well.

In comparison, the death rate among a similar group of babies that did not get mitochondrial transplants was 65 percent. And none of the untreated babies recovered any of their heart function — more than a third of the survivors ended up on heart transplant lists.

More recently, Dr. Emani and his colleagues have discovered that they can infuse mitochondria into a blood vessel feeding the heart, instead of directly into the damaged muscle. Somehow the organelles will gravitate almost magically to the injured cells that need them and take up residence.

He and his colleagues are persuaded that these transplants work, but acknowledge that it would take a randomized trial to prove it.


Photos and get-well wishes in the hospital room where Georgia is recovering.CreditKatherine Taylor for The New York Times

From left, Kendal, Scarlett, Kate, Ryan and Jack Bowen on a recent visit to Georgia in the I.C.U. She was put on a list for a heart transplant.CreditKatherine Taylor for The New York Times

The main problem is a scarcity of patients. Even if every pediatric center in the United States participated, along with every infant with injured heart muscle, it still would be hard to enroll enough participants in the trial.

But what about adult heart patients? Researchers are hoping that mitochondrial transplants also can repair heart muscle damaged during heart attacks in adults. And finding enough of those patients should not be an issue, said Dr. Peter Smith, chief of cardiothoracic surgery at Duke University.

Already researchers are planning such a trial. The plan is to infuse mitochondria or a placebo solution into the coronary arteries of people having bypass surgery or — an even more dire situation for the heart — having both bypass and valve surgery.

The patients would be those whose hearts are so damaged that it would be difficult to wean them from heart-lung machines after surgery. For these desperate patients, mitochondrial transplants “are a really intriguing option,” Dr. Smith said.

“The likelihood is very high” that the study will begin next year, said Annetine Gelijns, a biostatistician at Mount Sinai Medical Center in New York.

For Georgia Bowen, the procedure came too late: The portion of her heart muscle affected by the heart attack had died. Her doctors implanted a device that takes over the heart’s pumping, and hope her heart will recover enough for them to remove the device.

But, to be safe, they put her on a list for a heart transplant. She seems to be improving, though — she is breathing on her own and can drink breast milk through a tube. Her heart is showing signs of healing.

“Georgia is a miracle who continues to fight daily and persevere through the obstacles she is dealt,” Ms. Bowen said.

“In our hearts, we know she will pull through this and come home.”


This article was originally published in The New York Times.  Read the original article.

Swift Gene-Editing Method May Revolutionize Treatments for Cancer and Infectious Diseases

For the first time, scientists have found a way to efficiently and precisely remove genes from white blood cells of the immune system and to insert beneficial replacements, all in far less time than it normally takes to edit genes.

If the technique can be replicated in other labs, experts said, it may open up profound new possibilities for treating an array of diseases, including cancer, infections like H.I.V. and autoimmune conditions like lupus and rheumatoid arthritis.

The new work, published on Wednesday in the journal Nature, “is a major advance,” said Dr. John Wherry, director of the Institute of Immunology at the University of Pennsylvania, who was not involved in the study.

But because the technique is so new, no patients have yet been treated with white blood cells engineered with it.

“The proof will be when this technology is used to develop a new therapeutic product,” cautioned Dr. Marcela Maus, director of cellular immunotherapy at Massachusetts General Hospital.

That test may not be far away. The researchers have already used the method in the laboratory to alter the abnormal immune cells of children with a rare genetic condition. They plan to return the altered cells to the children in an effort to cure them.

Currently, scientists attempting to edit the genome often must rely on modified viruses to slice open DNA in a cell and to deliver new genes into the cell. The method is time-consuming and difficult, limiting its use.

Despite the drawbacks, the virus method has had some success. Patients with a few rare blood cancers can be treated with engineered white blood cells — the immune system’s T-cells — that go directly to the tumors and kill them.

This type of treatment with engineered white cells, called immunotherapy, has been limited because of the difficulty of making viruses to carry the genetic material and the time needed to create them.

But researchers now say they have a found a way to use electrical fields, not viruses, to deliver both gene-editing tools and new genetic material into the cell. By speeding the process, in theory a treatment could be available to patients with almost any type of cancer.

“What takes months or even a year may now take a couple weeks using this new technology,” said Fred Ramsdell, vice president of research at the Parker Institute for Cancer Immunotherapy in San Francisco. “If you are a cancer patient, weeks versus months could make a huge difference.”

“I think it’s going to be a huge breakthrough,” he added.

The Parker Institute already is working with the authors of the new paper, led by Dr. Alexander Marson, scientific director of biomedicine at the Innovative Genomics Institute — a partnership between University of California, San Francisco and the University of California, Berkeley — to make engineered cells to treat a variety of cancers.

In the new study, Dr. Marson and his colleagues engineered T-cells to recognize human melanoma cells. In mice carrying the human cancer cells, the modified T-cells went right to the cancer, attacking it.

The researchers also corrected — in the lab — the T-cells of three children with a rare mutation that caused autoimmune diseases. The plan now is to return these corrected cells to the children, where they should function normally and suppress the defective immune cells, curing the children.

The technique may also hold great promise for treating H.I.V., Dr. Wherry said.

The H.I.V. virus infects T-cells. If they can be engineered so that the virus cannot enter the T-cells, a person infected with H.I.V. should not progress to AIDS. Those T-cells already infected would die, and the engineered cells would replace them.

Previous research has shown it might be possible to treat H.I.V. in this way. “But now there is a really efficient strategy to do this,” Dr. Wherry said.

The idea of engineering T-cells without using a virus is not new, but the immune cells are fragile and hard to keep alive in the lab, and it has always been difficult to get genes into them.

Scientists usually introduced replacement genes into T-cells with a type of virus that was disarmed so that it would not cause disease and that can insert new genes into cells. But when these viruses insert the genes into a cell’s DNA, they do so haphazardly, sometimes destroying other genes.

“We needed something targeted, something fast and something efficient,” Dr. Marson said. “What if we could just paste in a piece of DNA and avoid the viruses altogether?”

The idea would be to slip a type of molecular scissors, known as Crispr, into cells that would slice open DNA wherever scientists wanted a new gene to go. That would avoid the problem of using a virus that inserts genes pretty much at random.

And along with the scissors, they would add a piece of DNA containing the new gene to be added to the cells.

One way to do that would be to use an electrical field to make the cells permeable. It required a herculean effort by a graduate student, Theo Roth, to finally figure out the right molecular mixture of genes, gene-editing tools and electrical fields to modify T-cells without a virus.

“He tested thousands of conditions,” Dr. Marson said.

Already the scientists are talking to the Food and Drug Administration about using the new method to precisely attack solid tumors, as well as blood cancers.

“Our intent is to try to apply this as quickly as possible,” Dr. Ramsdell said.

So when they knew they had a system that worked, did they break out the champagne? Have a party?

Well, no, Mr. Roth said in an interview. He just took the data to Dr. Marson.

“We certainly had an exuberant walk to Alex’s office,” he recalled.


This article was originally published in The New York Times.  Read the original article.

Some Birds Are Better Off With Weak Immune Systems

Twice a year in southern Sweden, the skies fill with migrating birds. Streams of them funnel through the country’s southern tip, traveling to and from wintering grounds in Africa and nesting grounds in Europe.

It’s a tough and strenuous journey in the best of times. So ornithologist Emily O’Connor wondered: How do these compulsive wanderers deal with infections?

“One of the big biological questions regarding migration is how these birds cope with diseases in two entirely different geographical regions,” said Dr. O’Connor, a researcher at Lund University in Sweden.

“If I was to travel from my home in Europe to Africa for a holiday, then I would need all sorts of vaccinations to protect me from diseases. But migratory birds move regularly between Europe and Africa with no help from medicine.”

The evolutionary origins of bird migration are a longstanding puzzle for ornithologists, and the role of disease in influencing the behavior has never been entirely clear. A recent study by Dr. O’Connor and her colleagues examined the genealogy and immune responses of about 1,300 species of songbirds from both continents.

The surprising result: Migratory birds have weaker immune systems than tropical species that stay put.

Dr. O’Connor began by looking at the evolutionary history and relationships between European and African songbirds, including data on their current ranges and relationships.

Most songbirds in Europe, including those that breed there, descended from African ancestors, the researchers found. Because areas closer to the Equator tend to have a greater incidence of disease, both European migrants and permanent residents had in effect spread from a deeply infectious environment to a relatively benign one.

For European birds, this lends support to the idea of “pathogen escape,” which suggests that species tend to move away from more disease-heavy environments. But migratory species still spend a lot of time in Africa and therefore around African pathogens.

The obvious implication, Dr. O’Connor said, is that they have particularly tough immune systems.

To check, the team examined the pathogen-recognition genes in 32 sedentary and migratory species. These genes govern cellular proteins that help the immune system recognize foreign molecules.

The greater the diversity of these genes, the theory goes, the greater the exposure to infectious diseases during evolution.

To their surprise, the team found that African species that stayed put had significantly tougher immune systems than their European or migratory cousins. That suggested something different: that migration might also be part of an evolutionary trade-off to get away from diseases.

According to prior research, Dr. O’Connor said, birds are most vulnerable to infection after hatching. Birds like the African plain-backed pipit combat this with a powerful immune response.

But maintaining a complex immune response comes with significant costs. Animals that have them are more likely to suffer autoimmune disorders, chronic inflammation and other related ailments.

European redstarts and other birds that shifted their nesting grounds to Europe no longer bring up chicks in a disease-rich environment, and thus don’t need to bear the costs of a powerful immune response, whether they visit Africa or not.


The plain-backed pipit, native to Africa, has a stronger immune system than its European cousin, raising the likelihood of autoimmune disorders, chronic inflammation or other ailments.CreditPeter Steward

“Ours is the first study, to my knowledge, to show that migration and changes in the immune system are linked on a broad evolutionary level,” Dr. O’Connor said.

“I am not saying that escaping pathogens was necessarily one of the factors driving the evolution of migration, just that the two processes are linked.”

The paper makes a compelling case, said Joel Slade, an evolutionary ecologist at Michigan State University, but the precise relationship between migration and pathogen escape still needs untangling.

Traveling between continents is taxing, and birds that haven’t managed to stock up their energy reserves often die along the route. The strain of such journeys can leave birds more susceptible to disease, and the metabolic cost of fighting off infections can leave birds unable to complete their journey or successfully breed at the end of it.

In addition, he said, temperate regions have plenty of diseases of their own.

“Equatorial diseases can travel to more temperate zones, and it is a concern that climate change is shifting the range of these diseases,” Dr. Slade said. “What’s also notable is avian malaria seems to be a generalist, by which one type can infect multiple species, and these species can be found in what this paper considers ‘pathogen-light’ zones.”

While ornithologist Frank La Sorte, of Cornell University, also finds the study convincing, he’s cautious about applying the findings to other regions. Migration is a local phenomenon that has evolved, disappeared and re-evolved in different areas, he said.

For example, songbirds that migrate between North America and South America seem to have done the opposite of African species, with northern ancestors colonizing the equatorial south. That means the evolution of their immune systems may have been quite different.

Still, Dr. La Sorte said, the study strongly supports the idea that diseases are an important selection pressure in shaping bird migration strategies — at least, between the African and European flyways.

It’s also handy at highlighting the many remaining mysteries in how bird migration originated in the first place. “Each region might have a unique combination of factors that promotes the development of migratory behavior in bird populations,” he said.

For Dr. O’Connor, the research also offered an opportunity to consider how living in different environments can shape the evolution of immune responses.

All vertebrates — including humans — share similar immune systems, she pointed out. In a world where diseases and species are shifting their ranges because of climate change, among other factors, it’s more important to than ever to understand how animals evolve to deal with illness.

“There are lots of factors that we believe play a role in the evolution of migration, and probably the traditional answers of food and competition are the main players. But I do think we’ve potentially overlooked the role that pathogen avoidance may have played.”

“After all, disease is a strong selective force,” she said.


This article was originally published in The New York Times.  Read the original article.

FDA Approves First Drug Derived From Marijuana Plant

The U.S. Food and Drug Administration approved the first prescription drug derived from the marijuana plant, as a treatment for rare forms of epilepsy that primarily afflict children.

The FDA said Monday that it cleared GW Pharmaceuticals PLC’s  Epidiolex, also known as cannabidiol, to reduce seizures associated with forms of epilepsy known as Lennox-Gastaut syndrome and Dravet syndrome, in patients 2 years of age and older.

Cannabidiol is derived from the cannabis plant, also known as marijuana. U.K.-based GW Pharmaceuticals says the solution, taken by mouth, is made from a proprietary strain of cannabis designed to maximize a therapeutic component while minimizing components that produce euphoria. GW Pharmaceuticals grows the plants in the U.K.

The FDA said Monday that the drug doesn’t cause the high that comes from the chemical tetrahydrocannabinol, or THC, which is the main psychoactive component of marijuana. FDA officials also said the drug doesn’t appear to have abuse potential, citing minimal reports of euphoria in patients who took the drug in clinical studies.

The FDA action follows rising interest in medical uses for marijuana. Since the 1990s, some 30 states and the District of Columbia have legalized medical use of marijuana, according to the National Conference of State Legislatures. In addition, some states have specifically legalized the medical use or clinical testing of cannabidiol. But the products sold under these laws haven’t previously received FDA approval.

“This approval serves as a reminder that advancing sound development programs that properly evaluate active ingredients contained in marijuana can lead to important medical therapies,” FDA Commissioner Scott Gottlieb said.

Dr. Gottlieb also warned in a conference call that the agency would take action against any illegal marketing of cannabidiol-containing products with serious, unproven medical claims. He said some firms have marketed cannabidiol, or CBD oil, for diseases including cancer, which he said could cause patients to forgo proven effective treatments for those diseases.

In company-sponsored clinical studies, cannabidiol reduced the frequency of patients’ seizures. In one study of 120 children and young adults with Dravet syndrome, cannabidiol reduced the median frequency of convulsive seizures to 5.9 a month from 12.4 before treatment, while patients getting a placebo saw minimal reductions, according to results published last year in the New England Journal of Medicine.

The drug is associated with some adverse events, including gastrointestinal problems and abnormal liver-function test results. But FDA officials have said they believed the risks were manageable if cautionary language was placed in the drug’s prescribing label, and if the agency monitored liver risk after the drug was on the market.

In April, an advisory committee to the FDA voted unanimously that the risk-benefit profile for Epidiolex was favorable.

Several parents of children with epilepsy testified before the panel, saying cannabidiol helped reduce seizures and improve quality of life.

The LGS Foundation estimates there are between 30,000 and 50,000 Americans with Lennox-Gastaut Syndrome. GW Pharma says about 6,000 to 10,000 have Dravet Syndrome.​

GW Pharmaceuticals said it expected to make the product available by the fall, pending expected action by the Drug Enforcement Administration to reclassify the drug. It is currently a Schedule 1 drug, along with heroin, because of abuse potential, but GW expects Epidiolex to have a less restrictive DEA scheduling because of studies showing minimal abuse potential and now an approved medical use.

GW Pharmaceuticals Chief Executive Officer Justin Gover said in an interview the company hasn’t set a price yet. He said the company would deploy about 70 sales representatives to promote the drug to doctors specializing in severe epilepsy.

“Now that the FDA has approved this medication, it allows us to talk about Epidiolex in the context of a novel and first-in-class approach to the treatment of epilepsy,” he said. “In that respect we now turn to what this product does as opposed to what this product is.”

Mr. Gover said he expected other cannabidiol preparations to remain available in states where they are legal. It’s “a matter for relevant health authorities and agencies” to monitor the marketing of competing versions of cannabidiol that aren’t approved by the FDA. He noted that the FDA-approved prescribing label for Epidiolex describes the safety and efficacy of that drug and not other forms of cannabidiol.

“It’s not in our interest to impact those laws and businesses,” he said. “The only question for us which was relevant is that medical claims should be made only for those products which have received FDA approval.”



This article was originally published in The Wall Street Journal. Read the original article.

The first clear evidence of a sense of magnetism in insects

BOGONG moths are not as glamorous as monarch butterflies. Their name means “brown” in Dhudhuroa, a now-extinct language once spoken in eastern Australia, where they live. And that is what they are—in contradistinction to a monarch’s glorious orange and black. But drab though they may be, bogongs surely match monarchs in migratory tenacity.

Monarchs, famously, fly across much of North America, starting or ending their journeys in one of a few groves of trees in central Mexico. An adult monarch, though, migrates only once. During their lifetimes, bogong moths that survive to do so will make a pair of 1,000km journeys. One is from their winter birthing grounds in sun-scorched Queensland and New South Wales to a small number of cool caves in the mountains of Victoria where they will spend the summer months resting. The other is back again.

How they find their way to and from these caves is a mystery. But it is less mysterious in light of work by David Dreyer and Eric Warrant at the University of Lund, in Sweden, published this week in Current Biology. Dr Dreyer and Dr Warrant suggest that bogongs use a combination of magnetic compasses and topography.

Several types of animals, including birds, turtles and fish, are known to sense and navigate by Earth’s magnetic field, but evidence for such powers in migratory insects has been tenuous. A lone experiment has suggested monarchs may be able to detect magnetism—but, if so, that is probably just a back-up mechanism. Abundant other evidence suggests monarchs navigate mainly by the sun. For a night-flying moth, though, that is not an option.

To explore any magnetic sense bogongs might possess Dr Dreyer and Dr Warrant used light traps to capture hundreds of the moths during their migrations over the course of two seasons. They and their colleagues then glued stalks to the moths’ backs and, using those stalks, tethered the insects inside a flight simulator in which they were free to “fly” in any direction they wished—though, of course, they could not actually move. The simulator was surrounded by a pair of magnetic coils that cancelled out Earth’s field and replaced it with one of similar strength that could be turned through 120°. Because experiments like these, conducted on birds such as pigeons, have revealed that those animals do use Earth’s magnetic field for navigation, the researchers hoped their set up would to do the same with the moths.

It did not. Unlike birds, the moths either failed to react to the movement of the field or reacted in an unpredictable manner. Unwilling to give up their hypothesis, though, Dr Dreyer and Dr Warrant wondered if they had simplified their apparatus too much. Many nocturnal insects have exquisite night vision so the two researchers thought that perhaps the absence of visual cues within their flight simulator, which had been intentional, might actually have confounded their experiment.

To test this, they lined the simulator’s interior with white felt and introduced a triangular black “mountain” above a black horizon as a landmark. During the experiment they started by keeping their magnetic field in alignment with Earth’s and then, after five minutes, began moving it. The moths continued to travel in the same direction with respect to the field for about three minutes after the field began moving but then, presumably as they realised that their visual cue and their magnetic cue were now in conflict with one another, they became disoriented.

This finding suggests that the moths do indeed depend on a magnetic sense to navigate during their long journey, but that they cannot, as it were, fly on instruments alone. They have rather to have sight of visual markers as well.

The test of this will be in the next series of experiments Dr Dreyer and Dr Warrant are planning, which will move the “mountain” and the magnetic field simultaneously. That, they hope will fool the insects into thinking they are flying home.




This article was originally published in The Economist. Read the original article.