TIME Cancer

Pesticides Used in Pet Collars and Home Sprays Connected to Cancer

A World Health Organization group says five pesticides may be cancer-causing

Five pesticides used in pet collars and home insect sprays could cause cancer in humans, health officials said in a new report.

The International Agency for Research on Cancer (IARC), the cancer agency of the World Health Organization (WHO), evaluates studies on chemical compounds and ranks them by the strength of evidence of their cancer-causing effects. The new report, appearing in the journal Lancet Oncology, classifies glyphosate, malathion and diazinon as probable carcinogens. For these, there is only limited evidence that the compounds can cause cancer in animals or people.

Glyphosate is a widely used herbicide around the world, and its use has increased since crops have been genetically modified to resist the spray. It has been detected in low amounts in water, air and food. Malathion is used to control insects in both agriculture and in homes, and people can be exposed via sprayings and through food. Diazinon is used in more limited quantities in agriculture and homes, after regulations restricted spraying in the U.S. and Europe.

The pesticides tetrachlorvinphos and parathion received a slightly stronger designation as possible carcinogens because there is more evidence for their cancer-causing effects in animals, but still little information on their effect on people. Both of these possible carcinogens are already restricted; tetrachlorvinphos is banned in the European Union while still allowed for use in livestock and pet collars in the U.S. Parathion was banned in both the U.S. and Europe in 2003.

The classifications won’t appear on the labels for these products, but serve as the latest review of scientific evidence that governments and international organizations can rely on to create their own regulations.

TIME viral

Watch This Little Boy Adorably Pretend to Be Ed Sheeran

We’ve all done it: Lip-mouthed and mumbled our way through a song. But probably not as adorably as Daniel Breki with his electric blue plastic guitar. Complete with head cocks and hitting all the high notes, he does an irresistible version of Ed Sheeran’s “Thinking Out Loud.”

Who needs the words when you’ve got cuteness?

TIME medicine

A Simple 3-Part Test May Predict Alzheimer’s

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Chris Parsons—Getty Images

Dementia is a part of aging, but how do doctors separate normal brain decline from the first signs of Alzheimer’s? A new test that any physician can perform in their office may help

Diseases like Alzheimer’s start years, even decades, before the first symptoms of memory loss shows up. And with rates of those diseases rising, experts say that more primary care physicians—not neurology experts—will have the task of identifying these patients early so they can take advantage of whatever early interventions might be available.

“If we had a simple blood test, a cholesterol test for Alzheimer’s disease, that would help,” says Dr. Ronald Petersen, director of the Alzheimer’s Disease Research Center at the Mayo Clinic, “but we don’t.” But Petersen has a potential solution, and according to a new paper released Wednesday in the journal Neurology, his Alzheimer’s test has promise.

Petersen and his team wanted to develop a test that any physician can administer to patients, without the need for any new technology or expensive equipment. Petersen believes that the test they came up with could become a useful tool for any physician, even those without special training in the brain. “What we are trying to do is give them some help so they can be as efficient as possible without ignoring these important cognitive issues,” he says.

In the first phase of the test, his researchers simply collected information from 1,500 patients’ medical charts—their age, family history of Alzheimer’s, factors such as diabetes or smoking that have been linked to Alzheimer’s, and whether the patient had ever reported problems with memory.

In the next phase they studied the results of the patient’s basic mental exam as well as of a psychiatric evaluation, because depression and anxiety have been connected to Alzheimer’s.

And another factor that emerged as important in developing the disease—how quickly the participant could walk a short distance. “We were a little surprised,” says Petersen. “But what’s nice about it is that it’s a nice non-cognitive, motor factor so it’s looking at another aspect of brain function.”

MORE: This Alzheimer’s Breakthrough Could Be a Game Changer

Petersen suggests that every physician should get this information on their patients at age 65; that way, they can have a baseline against which to compare any changes as their patients age. Only if they show such changes — a slower walk, for example, or worsening signs of depression or memory issues — should they move on to the third phase of the test, which is a blood analysis. That would look for known genetic factors linked to Alzheimer’s, including the presence of certain versions of the ApoE gene.

Currently, the only way to truly separate out those on the road to Alzheimer’s is to conduct expensive imaging tests of the brain, or to do a spinal tap, an invasive procedure that extracts spinal fluid for signs of the amyloid protein that builds up in the disease. “We have either expensive techniques or invasive techniques and it’s not practical to do them from a public health screening standpoint,” says Petersen.

MORE: New Test May Predict Alzheimer’s 10 Years Before Diagnosis

While his test is a possible solution to that problem, he acknowledges that the results need be repeated before it’s recommended on a wide scale to physicians across the country. But those who scored higher on the test of risk factors had a seven-fold higher chance of developing mild cognitive impairment than those with lower scores.

For now, even if doctors identify patients around age 65 who might be at higher risk of developing cognitive impairment, there isn’t much they can do to interrupt the process. But they can direct them toward clinical trials of promising new drugs to address Alzheimer’s dementia, which may slow the cognitive decline considerably.

TIME medicine

Here’s How 23andMe Hopes to Make Drugs From Your Spit Samples

The company is making a bold move to enter the drug-making business by using the genetic information donated by its clients

On March 12, 23andMe, the genetic testing company best known for analyzing your DNA from a sample of spit, announced the creation of a new therapeutics group. The group’s mission: to find and develop drugs from the world’s largest database of human genetic material.

That’s a huge shift for the company, which must now build a research and development arm from scratch. Richard Scheller, formerly of the biotechnology corporation Genentech, will lead the group and will also be 23andMe’s chief science officer.

Scheller admits that for now, he’s the therapeutics group’s only member. But soon after he starts on April 1, he anticipates that things will move quickly, as they do in the genetics world. That’s what attracted him to 23andMe after overseeing early drug development at Genentech for 14 years. “I’ve seen over the last couple of years how human genetics has impacted the way Genentech does drug discovery, and I thought it might be fun and interesting to work in an unrestricted way with the world’s largest human genetic database,” he says. “The questions we will ask are research based, but we could identify a drug target extremely quickly. I believe there is the real possibility to do really, really great things for people with unmet medical needs.”

MORE: Genetic Testing Company 23andMe Finds New Revenue With Big Pharma

More than 850,000 people have paid 23andMe to sequence their DNA since the company launched in 2006 until 2013, when the Food and Drug Administration requested that the company stop selling its medical genetic information services over concerns that their marketing claims weren’t supported by strong enough evidence about how the genetic information influenced human health. The company still retains that genetic information and continues to sell kits, but provides only non-medical information now while it continues to work with the FDA on further regulatory issues.

That experience “transformed” the company, as CEO Anne Wojcicki said to TIME earlier this year. Since then, the company has expanded its collaborations with pharmaceutical companies to access its database. The latest addition of drug development is a further evolution in the company’s identity.

Of those who have sent in samples, 80% have agreed to allow their genetic information to be used for research purposes. That’s the database that Scheller is eager to investigate. While at Genentech, he helped broker a collaboration between the biotech firm and 23andMe in which Genentech would have access just to the genetic testing company’s Parkinson’s disease patients, to search for any genetic clues to new therapies. Now, he says, “I plan on asking hundreds or maybe thousands of times more questions of the database than any pharmaceutical partner.”

MORE: 23andMe Finds Genes for Motion Sickness

He will be looking, for example, at whether patients who develop a certain disease tend to have specific hallmark genetic changes in their DNA, which could serve as potential launching points for new drugs. Or he might focus on the extreme outliers: people who have advanced cancer, for example, but somehow survive, or those who seem to succumb early. Mining their genomes might yield valuable information about what makes diseases more or less aggressive, and might become targets for drugs as well.

To do this, Scheller will have to create a drug development team from the ground up. The company is not divulging how much it intends to invest in this effort, but is soliciting another round of financing in the coming months. Initially, Scheller anticipates that even before the company has labs set up, he and his team will take advantage of labs-for-hire, or contract research organizations, to start doing experiments within weeks. Because his drug candidates will be more targeted and designed to address specific mutations or processes in the body, he anticipates that the cost of developing drugs that patients might eventually benefit from may be “substantially reduced” from the average $1 to $2 billion most pharmaceutical companies now spend.

MORE: Time Out: Behind the FDA’s Decision to Halt Direct to Consumer Genetic Testing

As for which disorders or medical issues he will tackle first, Scheller is being democratic. “We are going to be opportunistic,” he says. “That’s the nice thing about being part of 23andMe. We don’t really have a say. We can look generally at the database, and try and let it teach us what we should be working on.” In other words, anything is game.

TIME Cancer

A Breakthrough Treatment for Lung Cancer Approved

What you need to know about this promising new drug

On March 5, a novel way to treat lung cancer won approval from the Food and Drug Administration (FDA). The latest drug, Opdivo, has showed promise with other cancers, and is the first to use the immune system to tackle hard-to-treat lung tumors. Here’s what you need to know.

How does the drug work?

Opdivo (nivolumab), made by Bristol-Myers Squibb, works the same way that releasing a parking brake frees a car to move. Normally, the immune system is held back from recognizing tumors as foreign and potentially harmful, since tumors are the body’s own cells that grow abnormally. Without such checks, “the immune system will destroy you,” says Dr. James Allison, chair of immunology at MD Anderson Cancer Center who discovered the first such brake that protected cancer cells from the immune system. But nivolumab releases this check on the immune system’s normally voracious appetite for anything it doesn’t recognize, so the body’s own defenses can preferentially recognize tumor cells as targets.

In the study submitted by the company to the FDA, 15% of patients showed some shrinkage or complete disappearance of their tumors.

MORE On the Horizon at Last, Cancer Drugs that Harness the Body’s Own Immune System

What makes this drug different from other cancer treatments?

Unlike surgery, chemotherapy, radiation or the anti-cancer drugs that interrupt specific signals that tumor cells use to survive, nivolumab doesn’t target the tumor itself. Rather it focuses on the environment in which the tumor lives, unleashing the immune system so it can recognize cancer cells more easily. “This drug doesn’t treat cancer; it doesn’t kill cancer cells so you can’t inject it and expect cancer to melt away immediately because it won’t,” says Allison. But when it’s combined with tumor-targeted treatments, what it could do is lower the risk of recurrent cancers by training the body’s T cells to recognize specific features of tumors, just as they do for viruses and bacteria, so the immune system can be alerted more quickly and efficiently to dispatch any returning or remaining cancer.

MORE A Shot at Cancer

Other drugs that work in different ways to unleash the immune system have also been approved by the FDA and more are in development.

How will this drug change lung cancer treatment?

While this drug was approved in 2011 to treat melanoma, the expanded approval to include non-small-cell lung cancer, the most common type of lung cancer, now means more patients can take advantage of the new, immune-based strategy to fight their disease. It also opens the door for other, next-generation immune therapies for treating the disease, which many experts thought would not be possible, given how aggressively lung cancer progresses. Now lung cancer patients who have failed other therapies and have no other treatment options have another shot at containing their tumors.

MORE Self-Sabotage: Why Cancer Vaccines Don’t Work

Read next: This Is What It’s Like To Be Awake During Brain Surgery

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TIME medicine

One Hour of Sleep Makes a Difference In What You’ll Eat

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Lynn Koenig—Getty Images/Flickr RF

When it comes to teens and sleep, it’s not how much sleep, but how consistently they sleep the same amount that’s important for their health

Plenty of studies have documented that teens don’t get enough sleep. They’re supposed to be in bed for eight to nine hours a night, but most get seven or less. Now the latest sleep research, presented at the American Heart Association EPI/Lifestyle 2015 meeting, shows when it comes to weight gain—which has been tied to sleep deprivation and disturbances—it’s not necessarily the amount of sleep that tips the scales but rather the consistency of that nightly rest.

Fan He, an epidemiologist at Penn State University College of Medicine, and his colleagues found a strong correlation between the variation in sleep patterns among a group of teens and the amount of calories they consumed. And for every hour difference in sleep on a night-to-night basis over a week, for example, they ate 210 more calories—most of it in fat and carbohydrates. Those with uneven sleep patterns were also more likely to snack.

Previous studies have linked poor or disrupted sleep to obesity; people not getting enough shut-eye, for example, may experience changes in the hormones that regulate appetite and how well they break down glucose in their diet. Levels of the hormone leptin, for instance, drop in those who are sleep deprived, and less leptin prompts the body to feel hungry.

MORE: The Power of Sleep

In the current study, however, all the teens got an average of seven hours a night, so it wasn’t as if some of the teens were sleeping for extremely long or short periods of time. Any metabolic changes they would have experienced due to their sleeping less than the recommended eight to nine hours would have been similar among the consistent and inconsistent sleepers.

Dr. Nathaniel Watson, president-elect of the American Academy of Sleep Medicine and co-director of the University of Washington Medicine Sleep Center, stresses that good quality sleep involves three things — getting enough sleep, making sure the timing of the sleep if appropriate, and avoiding sleep disorders. While the amount of sleep has gotten the lion’s share of attention in recent years, a new phenomenon called social jet lag, which the current study investigates, may deserve equal consideration. “We live in a society of yo-yo sleep in which people sleep less because of social or work demands, then try to catch up,” says Watson. “There haven’t been a lot of studies that looked at what kind of impact this has on our health, but teenagers may be particularly susceptible to social jet lag than older adults, and this study assessed that.”

MORE: This Is What’s Keeping Teens From Getting Enough Sleep

These results show that it was the variability in their sleep that was most strongly linked to their eating habits.

Why? The researchers guess that teens who aren’t sleeping consistently are more likely to get too little sleep on one night, for example, and therefore be more tired or sedentary the following day, which leads them to sit around and eat more. It may also be possible that teens with irregular sleep habits are more likely to stay up later on weekends; He found that these adolescents had a 100% higher chance of snacking on weekends compared to those who slept more regularly.

MORE: School Should Start Later So Teens Can Sleep, Urge Doctors

That suggests that health experts should focus not just on the amount of sleep teens are getting, but on their sleep patterns. “Instead of focusing on how much we sleep, we also need to pay attention to maintaining a regular sleep pattern,” says He. Such consistency, however, may not be so easy for teens to master.

 

TIME Heart Disease

Statins May Seriously Increase Diabetes Risk

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Getty Images

Statins can lower cholesterol and even tamp down inflammation to keep the risk of heart disease down. But these commonly prescribed drugs may increase the risk of diabetes, and by a considerable amount

Doctors may have to weigh a serious potential risk before prescribing statins, the cholesterol-lowering drugs that are among most prescribed drugs in America. In a study published in Diabetologia, scientists from Finland found that men prescribed statins to lower their cholesterol had a 46% greater chance of developing diabetes after six years compared to those who weren’t taking the drug. What’s more, the statins seemed to make people more resistant to the effects of insulin—which breaks down sugar—and to secrete less insulin. The impact on insulin seemed to be greatest among those who started out with the lowest, and closest to normal, levels of blood glucose. And the higher the dose of the statin, and the longer the patients took them, the greater their risk of diabetes.

Previous studies have suggested that statins can raise blood sugar levels, and increase the risk of diabetes by anywhere from 10% to 20%, but none have documented an effect this large. Doctors often consider statins for patients who are at higher risk of heart disease, and one of the risk factors for future heart trouble is diabetes. So how do these results affect that decision?

“It’s a good news-bad news scenario,” says Dr. Robert Eckel, past president of the American Heart Association and professor of medicine at University of Colorado School of Medicine. “Although there is convincing evidence that patients on statins are at increased risk of new-onset diabetes, the benefit accrued [from statins] in reducing risks of heart attack, stroke and fatal heart disease trumps the effects of being new onset diabetics.”

In other words, the good that statins can do for people who are not yet diabetic but at higher risk of heart problems outweighs the increased risk of diabetes.

MORE New Guidelines for Cholesterol Treatments Represent “Huge Change”

And while the increased risk that the Finnish scientists found — 46% — is noteworthy, Eckel points out that the study involved only white men, and therefore may not be generalizable to a broader population. It’s not clear what the men’s family history or personal history of diabetes was; some may have had other risk factors for the disease that put them at higher risk of developing diabetes anyway, even if they didn’t take a statin.

Those who developed diabetes while taking statins were similar on many metabolic measures to those who developed diabetes but weren’t taking statins, suggesting that “that statin treatment increased the risk of diabetes independently of the risk profile of the background population,” the authors write. In a separate, U.S.-based study on statins, researchers found that those who went on to develop diabetes while taking statins also had risk factors for the disease before they started taking the medications.

MORE Should You Take Statins? Study Says Heart Benefits Outweigh Diabetes Risk

Which means that for confused patients, and their doctors, the current advice about who should take statins doesn’t change. The results, in fact, highlight the need for a discussion rather than just working through a checklist before prescribing statins. For patients who may not yet be diabetic, but are vulnerable to developing the disease and also may need a statin, Dr. Neil Stone, lead author of the 2013 American College of Cardiology and American Heart Association cholesterol guidelines, says he stresses the importance of lifestyle changes in diet and exercise.

“If you have a patient who is prone to developing diabetes, you’re getting into a higher risk group, because they also have risk factors associated with heart disease. So they have the potential to benefit from statins. If they are going to take a statin, I tell them we are going to help you get more fit, and work with your lifestyle. It’s even more important because if you don’t do that, and the patient decides to take the statin and go on with their unhealthy habits, then they are going to be even more prone to developing diabetes,” says Stone.

The patient’s family history of diabetes is another important part of the decision to start someone on a statin. It’s all about making sure that each patient’s risks and benefits are weighed carefully. And the potentially greater risk of diabetes created by statins should be part of that consideration. “Communication here is everything,” says Eckel.

Read next: New Hormone Discovered That Curbs Weight Gain, Diabetes Just Like Exercise

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TIME Diet/Nutrition

The Weird Benefit of Eating Salty Food

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Andrew Unangst—Getty Images

Too much salt can lead to heart disease, but there may be a healthy side to salt that hasn’t been appreciated — until now

If you’re an average American, chances are that you’re eating too much salt. But the latest research — which, the scientists stress, is still in its early stages — hints that there may be some benefits to salt that have gone unnoticed. Salt, it seems, may be an ancient way for the body to protect itself against bacteria.

Reporting in the journal Cell Metabolism, Jonathan Jantsch, from the University of Regensburg in Germany, says that salt may be an effective way to ward off microbes. In a series of studies using both mice and human cells, he and his colleagues found that levels of sodium go up around an infection site, and that without salt, bacteria tend to flourish and grow better.

MORE Older Adults May Be OK to Eat More Salt Than Previously Thought

The discovery came about by accident, after Jens Titze, the study’s senior author, noticed that mice who had been bitten by their cage mates showed higher levels of sodium in their skin than those who were wound-free. Jantsch decided to find out whether the salt had something to do with the infection-fighting functions of the immune system.

He and his team conducted a series of experiments in which they subjected mouse and human cells to high levels of sodium chloride, and watched the immune cells activate. They also fed mice diets that were low and high in sodium, and then infected them with Leishmania major. The mice fed the higher amounts of sodium showed stronger immune responses to the wounds, and cleared their infections faster than the mice eating less salt. In fact, Jantsch speculates that certain skin cells may transport sodium preferentially to sites where bacterial populations are high in order to create another barrier preventing the microbes from entering deeper into the body.

That opens the possibility that salt may be an unrecognized contributor to the immune system, and possibly a remnant from the days before antibiotics, when mammals, including humans, needed some allies in the fight against microbes. After all, salt has been used for centuries to preserve food from spoiling in bacteria’s presence, so it makes sense that evolutionarily, sodium might have also been co-opted by the body in a similar way. “I really think salt is an unappreciated factor of immunity,” says Jantsch.

MORE New Dietary Guidelines: Cut Salt and Sugar, Eat More Fish

If that’s the case, then it may be possible to take advantage of salt-based dressings, for instance, to improve wound healing. Burn patients may benefit the most, since their skin, the first line of defense against microbes, is compromised. And for those with hyperactive immune responses, dialing down the concentration of sodium at specific areas might also be helpful. “We are interested in how this works, because it can have broad applications,” says Jantsch. “We can possibly target and boost sodium in situations where we need more salt if it’s deficient, and lower it in situations where there is salt overload and hypertension.” Already, some companies have produced wound dressings with enhanced sodium concentration as a way to help infections heal faster.

MORE Salt Doesn’t Cause High Blood Pressure? Here’s What a New Study Says

He stresses, however, that the results don’t mean high salt diets are now healthy — or advisable. His studies, even in mice, haven’t worked out exactly how salt in the diet affects the body’s ability to recruit the nutrient to fight infections. And to get the bacteria-fighting effect, the mice were fed a diet that was extremely high in sodium — 4%, compared to the average mouse chow which is only 0.2% to 0.3% sodium. “There is overwhelming data that tells you a high salt diet is detrimental to the heart,” he says. “We used one animal approach to look at the beneficial role of salt. So I would be hesitant to draw any conclusions for humans at this stage.” He and others are already setting up more experiments, however, to study how salt might become the next weapon in fighting infections.

MORE FDA Wants to Limit Your Salt Intake. Is That a Good Thing?

Read next: 11 Bad Habits That Bloat You

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TIME neuroscience

Alzheimer’s Protein Found in Young Brains for the First Time

The brain-damaging protein in Alzheimer’s disease may start accumulating as early as in our 20s

For the first time, scientists have found evidence of a protein found in Alzheimer’s disease, called amyloid, in the brains of people as young as 20.

In a report published in the journal Brain, Changiz Geula, a professor at the Cognitive Neurology and Alzheimer’s Disease Center at Northwestern University Feinberg School of Medicine, reveals that the protein—which gradually builds up and forms sticky plaques in the brain in Alzheimer’s disease—starts appearing early in life. Amyloid is normally made by the brain and has important functions; it’s an antioxidant and promotes the brain’s ability to remain adaptable by forming new connections and reinforcing old ones, especially those involving memory. But in some people, the proteins start to clump together with age, forming sticky masses that interfere with normal nerve function. Eventually, these masses kill neurons by starving them of their critical nutrients and their ability to communicate with other cells.

MORE: New Research on Understanding Alzheimer’s

When Geula compared the autopsy brains from normal people between ages 20-66 years, older people without dementia between 70-99 years, and people with Alzheimer’s between 60-95 years, they found evidence of amyloid in a particular part of the brain in all of them. That region isn’t normally studied in Alzheimer’s, but it plays roles in memory and attention.

The results show that the process responsible for causing Alzheimer’s begins as early as in the 20s, and it also pointed to a population of cells that are especially vulnerable to accumulating amyloid—essentially serving as a harbinger of future disease. “There is some characteristic of these neurons that allows amyloid to accumulate there more than in other neurons,” says Geula. “At least in this cell population, the machinery to form aggregates is there.” Reducing the amount of amyloid in the brains of young people might help halt the formation of Alzheimer’s, he says.

MORE: This Alzheimer’s Breakthrough Could Be a Game Changer

Because the study involved autopsy specimens, there’s no way to tell whether those younger individuals would have gone on to develop Alzheimer’s. But they provide a clue about the early steps behind the disease.

They may also shed light on one way to prevent, or at least minimize, the effects of Alzheimer’s. Experts currently believe that the memory-robbing condition occurs when the balance between the production of amyloid and processes that clear the protein from the brain veer out of balance with age. As more amyloid is left in the brain, it tends to become stickier and adhere to other amyloid fragments, eventually forming damaging plaques. Geula believes that even in people with a genetic predisposition to forming these sticky plaques, removing amyloid as early as possible can slow down the progression of the disease. While there aren’t any effective ways to do this yet, there are promising compounds currently being tested in clinical trials. And given Geula’s findings, those studies become even more critical as a way to help more people to treat and even prevent the disease.

MORE: New Test May Predict Alzheimer’s 10 Years Before Diagnosis

The key, as the findings show, is to start early. “If you can get rid of the background [amyloid], then it can’t do anything,” says Geula.

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