TIME Drugs

FDA Approves New Cholesterol-Lowering Drug

Repatha

It’s the second in a new class of drugs that works in a different way from statins to bring cholesterol levels down

The U. S. Food and Drug Administration approved a new drug for treating high cholesterol levels on Thursday. Evolocumab, called Repatha, is made by Amgen and is the second of a new class of lipid-lowering agents that are hitting the market.

Known as PCSK9 inhibitors, these drugs work by suppressing genes that slow down production of cholesterol receptors on the liver. With these medications, more receptors that are free to emerge and act like sponges can soak up LDL cholesterol and lower their levels in the blood.

MORE: This New FDA-Approved Cholesterol Drug Is a Game Changer

Evolocumab was approved first by the European Medicines Agency in July. In the same month, the U.S. FDA approved another drug in the same class, alirocumab (Praluent), made by Sanofi and Regeneron. In studies, both drugs helped to lower cholesterol levels in the blood by 60% more than the amount achieved by statins. The drugs carry labels that say medications should be used first in people with a strong family history of high cholesterol conditions, or in people who have tried and not responded to statin medications.

PCSK9 inhibitors were discovered among a group of people who happened to have genetic mutations that gave them extremely low cholesterol levels. Researchers studied this rare population, and found they did not have any negative health effects from their mutation other than the beneficial effect on their lipids. So drug makers began investigating ways to replicate the condition with a medication.

MORE: Memory Loss Not Caused By Cholesterol Drugs After All

Having another drug that can lower cholesterol levels will be a boon to treating heart disease, which remains the leading killer of Americans each year. Keeping cholesterol levels down, in addition to eating a healthy diet and exercising to maintain weight are crucial to lowering the risk of heart events.

TIME Research

Only a Third of Psych Studies Are Reliable. Now What?

woman-finger-pointing-books
Getty Images

We must stop treating single studies as unassailable authorities of the truth

The ability to repeat a study and find the same results twice is a prerequisite for building scientific knowledge. Replication allows us to ensure empirical findings are reliable and refines our understanding of when a finding occurs. It may surprise you to learn, then, that scientists do not often conduct – much less publish – attempted replications of existing studies.

Journals prefer to publish novel, cutting-edge research. And professional advancement is determined by making new discoveries, not painstakingly confirming claims that are already on the books. As one of our colleagues recently put it, “Running replications is fine for other people, but I have better ways to spend my precious time.”

Once a paper appears in a peer-reviewed journal, it acquires a kind of magical, unassailable authority. News outlets, and sometimes even scientists themselves, will cite these findings without a trace of skepticism. Such unquestioning confidence in new studies is likely undeserved, or at least premature.

A small but vocal contingent of researchers – addressing fields ranging from physics to medicine to economics – has maintained that many, perhaps most, published studies are wrong. But how bad is this problem, exactly? And what features make a study more or less likely to turn out to be true?

We are two of the 270 researchers who together have just published in the journal Science the first-ever large-scale effort trying to answer these questions by attempting to reproduce 100 previously published psychological science findings.

Attempting to re-find psychology findings

Publishing together as the Open Science Framework and coordinated by social psychologist Brian Nosek from the Center for Open Science, research teams from around the world each ran a replication of a study published in three top psychology journals – Psychological Science; Journal of Personality and Social Psychology; and Journal of Experimental Psychology: Learning, Memory, and Cognition. To ensure the replication was as exact as possible, research teams obtained study materials from the original authors, and worked closely with these authors whenever they could.

Almost all of the original published studies (97%) had statistically significant results. This is as you’d expect – while many experiments fail to uncover meaningful results, scientists tend only to publish the ones that do.

What we found is that when these 100 studies were run by other researchers, however, only 36% reached statistical significance. This number is alarmingly low. Put another way, only around one-third of the rerun studies came out with the same results that were found the first time around. That rate is especially low when you consider that, once published, findings tend to be held as gospel.

The bad news doesn’t end there. Even when the new study found evidence for the existence of the original finding, the magnitude of the effect was much smaller — half the size of the original, on average.

One caveat: just because something fails to replicate doesn’t mean it isn’t true. Some of these failures could be due to luck, or poor execution, or an incomplete understanding of the circumstances needed to show the effect (scientists call these “moderators” or “boundary conditions”). For example, having someone practice a task repeatedly might improve their memory, but only if they didn’t know the task well to begin with. In a way, what these replications (and failed replications) serve to do is highlight the inherent uncertainty of any single study – original or new.

More robust findings more replicable

Given how low these numbers are, is there anything we can do to predict the studies that will replicate and those that won’t? The results from this Reproducibility Project offer some clues.

There are two major ways that researchers quantify the nature of their results. The first is a p-value, which estimates the probability that the result was arrived at purely by chance and is a false positive. (Technically, the p-value is the chance that the result, or a stronger result, would have occurred even when there was no real effect.) Generally, if a statistical test shows that the p-value is lower than 5%, the study’s results are considered “significant” – most likely due to actual effects.

Another way to quantify a result is with an effect size – not how reliable the difference is, but how big it is. Let’s say you find that people spend more money in a sad mood. Well, how much more money do they spend? This is the effect size.

We found that the smaller the original study’s p-value and the larger its effect size, the more likely it was to replicate. Strong initial statistical evidence was a good marker of whether a finding was reproducible.

Studies that were rated as more challenging to conduct were less likely to replicate, as were findings that were considered surprising. For instance, if a study shows that reading lowers IQs, or if it uses a very obscure and unfamiliar methodology, we would do well to be skeptical of such data. Scientists are often rewarded for delivering results that dazzle and defy expectation, but extraordinary claims require extraordinary evidence.

Although our replication effort is novel in its scope and level of transparency – the methods and data for all replicated studies are available online – they are consistent with previous work from other fields. Cancer biologists, for instance, have reported replication rates as low as 11%25%.

We have a problem. What’s the solution?

Some conclusions seem warranted here.

We must stop treating single studies as unassailable authorities of the truth. Until a discovery has been thoroughly vetted and repeatedly observed, we should treat it with the measure of skepticism that scientific thinking requires. After all, the truly scientific mindset is critical, not credulous. There is a place for breakthrough findings and cutting-edge theories, but there is also merit in the slow, systematic checking and refining of those findings and theories.

Of course, adopting a skeptical attitude will take us only so far. We also need to provide incentives for reproducible science by rewarding those who conduct replications and who conduct replicable work. For instance, at least one top journal has begun to give special “badges” to articles that make their data and materials available, and the Berkeley Initiative for Transparency in the Social Sciences has established a prize for practicing more transparent social science.

Better research practices are also likely to ensure higher replication rates. There is already evidence that taking certain concrete steps – such as making hypotheses clear prior to data analysis, openly sharing materials and data, and following transparent reporting standards – decreases false positive rates in published studies. Some funding organizations are already demanding hypothesis registration and data sharing.

Although perfect replicability in published papers is an unrealistic goal, current replication rates are unacceptably low. The first step, as they say, is admitting you have a problem. What scientists and the public now choose to do with this information remains to be seen, but our collective response will guide the course of future scientific progress.

This article originally appeared on The ConversationThe Conversation

TIME Mental Health/Psychology

A New Theory of Why Neurotics Are Creative

A wandering mind might explain why creative leaders tend to be neurotic.

Adam Perkins is a psychologist and a self-proclaimed neurotic, contemplating things to the point of obsession. He can get anxious about things that might seem mundane to another person. And he’s admittedly quite sensitive.

Perkins also has a new theory, described in a piece published Thursday in the journal Trends in Cognitive Sciences, about why he and many others like him channel their neuroticism into creativity and problem solving. He argues it comes from how certain people daydream.

Neuroticism and creative thinking have long been correlated: some of history’s more exciting minds, from Isaac Asimov to Winston Churchill to Woody Allen, have been famously anxious with a tendency to brood. The trait is also often associated with being risk-averse; neurotic people are often considered “threat sensitive,” a classification that the psychologist Jeffrey Gray first pinpointed while developing a test that predicted a person’s tendency to be neurotic. Gray’s test showed that high scorers on the neuroticism test tended to avoid “dangerous” jobs, preferring occupations that kept them out of harm’s way—hence the association with more analytical jobs, which require creative problem solving, as opposed to physical ones.

But Gray’s analysis seemed simplistic, Perkins says. “Why should having a magnified view of threat make you good at coming up with solutions to difficult problems?” he tells TIME. “It doesn’t add up. On one hand, it’s a clever theory—it shows the difficulty of holding down a dangerous job, for example—but on the other hand, it doesn’t explain why [neurotic people] tend to feel unhappy or why they’re more creative.”

Perkins had an epiphany when he attended co-author Jonathan Smallwood’s lecture on mind wandering. Smallwood, an expert who studies the neuroscience of daydreaming, was describing self-generated thought and its origins in the brain’s medial prefrontal cortex, a part of the brain that has been linked with memories and recall.

“He started describing how people whose minds wander are better at things like creativity, delaying gratification and planning. He also talked about the way that daydreamers’ minds wander when they’re feeling kind of blue,” Perkins says. “And my ears perked up.”

Smallwood had run a series of tests on volunteers, where he’d put them through an MRI scanner with no instructions. Naturally, the volunteers began daydreaming. Those with negative thoughts would display greater activity in the medial prefrontal cortex. “If you have a high level of activity in this particular brain area, then your mind wandering tends to be threat-related,” he says.

That’s what happens in the brains of neurotic people when their minds wander.

And of course, no surprise, the longer one dwells on a problem, unwilling to let it go, the more likely they are to come up with a solution—making that a potential upside to neurotic daydreaming.

“There’s costs and benefits to being a neurotic,” Perkins says. “What’s interesting is that you can be neurotic and have a creative benefit, but we still don’t understand it.”

TIME Infectious Disease

The Vast Majority of U.S. Kids Are Vaccinated

TIME.com stock photos Health Syringe Needle
Elizabeth Renstrom for TIME

Less than 1% of children received no vaccinations in 2014, but pockets of low vaccination rates put kids at risk

Vaccines are one of the most effective tools for preventing serious diseases in childhood and later in life, and new data from the U.S. Centers for Disease Control and Prevention (CDC) shows most children in the U.S. are vaccinated.

CDC researchers looked at national, regional, state and local vaccine coverage rates and found that overall coverage remains high, and hasn’t changed much between 2013 and 2014. The data shows that the national target of 90% coverage was reached for poliovirus (three or more doses of the vaccine), measles, mumps and rubella (one or more doses of the vaccine), hepatitis B (three or more doses of the vaccine) and varicella (one or more dose of the vaccine).

Overall, children below the federal poverty level had the lowest coverage for nearly all types of vaccinations.

A second report published Thursday from CDC researchers found that most kindergarteners entering the 2014-15 school year were vaccinated, and the exemption rate for vaccines nationwide was about 1.7%.

That’s the national picture at least. The data also shows that state-exemption rates range pretty significantly, with Mississippi at less than 0.1% and Idaho at a high of 6.5%. There were five states that did not meet the CDC’s reporting standards for providing vaccine exemption data. Pockets of children who miss vaccinations exist in our communities and they leave these communities vulnerable to outbreaks of vaccine-preventable diseases,” said Dr. Anne Schuchat, director of the National Center for Immunization and Respiratory Diseases in a press conference.

Pockets of low vaccination rates have proven problematic this year. In the new report, the researchers write that in 2015, measles outbreak cases included 68 unvaccinated Americans, and among those people, 29 cited philosophic or religious objections to vaccines. The CDC says the U.S. experienced a record number of measles cases in 2014 at 668 cases. That’s the highest number of measles cases since the disease was eliminated in the U.S. in 2000. Between January to August 21, 2015, there have been 188 cases of measles so far.

“We always worry about children and others with leukemia and other similar medical problems who can’t actually receive the [measles, mumps, and rubella] vaccine themselves,” said Schuchat.

The CDC reports in its latest study, that among the 49 reporting states and the District of Columbia (DC), the median vaccination coverage rate was 94% for the measles, mumps, and rubella (MMR) vaccine, and approximately 94% for local requirements for the diphtheria, tetanus, and acellular pertussis vaccine. Varicella coverage was 93.6% among the 39 states and DC that have a 2-dose varicella vaccine requirement.

Some states are strengthening their requirements for exemptions. In 2015, California removed religious and philosophic exemptions for kids in public and private schools and Vermont removed philosophic exemptions. Schuchat recommended parents find out what their states’ vaccination exemption rates are.

Getting routine vaccines in childhood is estimated to prevent 322 million cases of disease and 732,000 early deaths among kids, the CDC points out in its report. The benefits of vaccination are not just for health. Routine vaccination could save $1.38 trillion.

TIME diabetes

Antibiotics Are Linked To Type-2 Diabetes

Antibiotic use is associated with type-2 diabetes diagnoses, the latest research reveals

A new study published in the Journal of Clinical Endocrinology & Metabolism finds that people who develop type-2 diabetes used significantly more antibiotics—even 15 years before they were diagnosed—than people without the disease.

The researchers used data from citizens of Denmark, since the country has a single-payer national health insurance system with detailed health and pharmacy records. Using national health registries, the researchers looked at 170,504 people who had type-2 diabetes and tracked their prescriptions for antibiotics. They matched those people with 1.3 million other Danish citizens of the same age and sex who did not have diabetes and compared data from the two groups.

People with type-2 diabetes were more likely to receive more courses of antibiotics (0.8 prescriptions per year) than those who didn’t have the disease (0.5 prescriptions per year). An increased use of antibiotics was detected up to 15 years before people with type-2 diabetes were even diagnosed; an increased usage was also found after diagnosis.

MORE: How This Common Drug Can Have Lasting Effects On Kids

The study wasn’t designed to be able to determine a cause, but the authors point out two interpretations of the results. One is that people who go on to develop type-2 diabetes are more vulnerable to infections years before they’re diagnosed, so it would make sense for them to take more antibiotics. The other theory is that antibiotics raise the risk of type-2 diabetes.

This second theory is derived largely from research in rodents, and it’s the one that compels Dr. Martin Blaser, professor of medicine and microbiology at New York University Langone Medical Center and a longtime researcher of the effects of antibiotics. (Blaser was not involved with this study but is familiar with the research.)

“When you take antibiotics,” he says, “you change the composition of the microbiota”—your personal collection of bacteria in the body that communicates with human cells. Blaser has a hypothesis for how this might work in children who develop type-1 diabetes: the change in composition from taking antibiotics also alters metabolism, possibly making people more likely to become diabetic. “This work coming out that antibiotics might be affecting adults in a similar fashion is a little surprising to me, but in no way shocking,” he says. “I thought by the time you’re adult things are pretty much fixed, but maybe they’re not.”

The results of the study are not conclusive. But Blaser says they add to the body of research about the potential risks of antibiotics. “It’s evidence consistent with the idea that antibiotics have cost—not just monetary cost, but a biological cost in terms of potentially causing long-term effects,” he says. “As we’re studying it more and more, it suggests that things may bounce back, but it may not be the same normal, and it may predispose to other diseases—including important diseases, common diseases, like type-2 diabetes.”

TIME Diet/Nutrition

Should I Eat Salmon?

5/5 experts say yes.

This food from the sea is a no-brainer for all five of our experts.

A small 3-oz serving of wild salmon has about 156 calories and 23 grams of protein, plus 6 grams of fat. Omega 3 fatty acids are salmon’s claim to fame, “providing anywhere between 2-3 grams per 3-oz. serving,” says Julia Renee Zumpano, a registered dietitian at the Center for Preventive Cardiology Cleveland Clinic. (To put that into perspective, that’s the nutrient equivalent of taking three days’ worth of soft gels of fish oil in supplement form.) “Omega 3 fatty acids can help reduce blood triglycerides, blood pressure, and reduce swelling.”

“Wild is better than farmed,” says Dr. David Katz, director of the Yale University Prevention Research Center, an assertion with which most of our experts agree. Zumpano points out that farmed salmon may contain more saturated fat, calories, pollutants and antibiotics than wild salmon. (Salmon does have low mercury levels, however, according to the FDA.)

Farmed salmon may not deliver as many omega-3s, says Peter D. Nichols, senior principal research scientist at CSIRO Food, Nutrition & Bioproducts in Australia who’s researched long-chain omega-3 (LC Omega-3) oils. “The content of the LC Omega-3 has generally decreased in farmed salmon both in Australia and globally,” he says. “The LC omega-3 content is about half of what it used to be, although we should also note that this is still generally 10-100 fold higher than most other food groups.”

Not all farmed salmon is bad, though, says Tim Fitzgerald, director of impact in the oceans program at the Environmental Defense Fund. “Although most generic farmed salmon—often labeled ‘Atlantic’ in stores—still comes with a variety of environmental concerns, a number of new companies are upping their game and showing that salmon farming doesn’t have to be on everyone’s ‘avoid’ list,” he says. A few of his favorite sustainably farmed salmon standouts are Atlantic Sapphire, Kuterra and Verlasso. Fitzgerald also likes arctic char as an alternative to farmed salmon. “It’s closely related to salmon—so looks and tastes very similar, it’s farmed responsibly, and has a price point somewhere between Atlantic and wild Alaskan salmon.”

For the overall most sustainable salmon, choose wild Alaskan salmon, says Kimberly Warner, a senior scientist at Oceana, a nonprofit focused on ocean conservation. “Wild Alaskan salmon are managed well in the U.S.,” she says. It’s expensive, but you’ll be getting an especially good deal during the summer salmon season (and buying fish in season means the fish is most likely to be honestly labeled, she says).

But don’t forget: not every fish worth eating comes on ice. “Virtually all canned salmon is wild-caught in Alaska,” Fitzgerald says, “so you can get all of the environmental and health benefits for just a few dollars.”

salmon
Illustration by Lon Tweeten for TIME

Read Next: Should I Eat Tilapia?

TIME Sex/Relationships

Couples Who Do This Together Are Happier

A study shows that giggling in tandem is a good indicator the relationship's going to last.

Study after study has shown that laughing is good for the soul. But now we know something else: sharing giggles with a romantic partner keeps the lovey-dovey feelings going, according to a study published in the journal Personal Relationships.

Laura Kurtz, a social psychologist from the University of North Carolina, has long been fascinated by the idea of shared laughter in romantic relationships. “We can all think of a time when we were laughing and the person next to us just sat there totally silent,” she says. “All of a sudden that one moment takes a nosedive. We wonder why the other person isn’t laughing, what’s wrong with them, or maybe what’s wrong with us, and what might that mean for our relationship.”

Kurtz set out to figure out the laugh-love connection by collecting 77 heterosexual pairs (154 people total) who had been in a relationship for an average of 4 years. She and her team did video recordings of them recalling how they first met. Meanwhile, her team counted instances of spontaneous laughing, measured when the couple laughed together as well as how long that instant lasted. Each couple also completed a survey about their relational closeness.

“In general, couples who laugh more together tend to have higher-quality relationships,” she says. “We can refer to shared laughter as an indicator of greater relationship quality.”

It seems common sense that people who laugh together are likely happier couples, and that happier couples would have a longer, healthier, more vital relationship—but the role that laughter plays isn’t often center stage. “Despite how intuitive this distinction may seem, there’s very little research out there on laughter’s relational influence within a social context,” Kurtz says. “Most of the existing work documents laughter’s relevance to individual outcomes or neglects to take the surrounding social context into account.”

Kurtz noted that some gender patterns emerged that have been reported by previous studies. “Women laughed more than males,” she notes. “And men’s laughs are more contagious: When men laugh, they are 1.73 times more likely to make their partner laugh.”

There’s also evidence that laughing together is a supportive activity. “Participants who laughed more with their partners during a recorded conversation in the lab tended to also report feeling closer to and more supported by their partners,” she says. On the flip side, awkward chuckles, stunted grins and fake guffaws all are flags that there may be something amiss.

This harkens back to a classic psychological experiment conducted in 1992, where 52 couples were recorded telling their personal, shared histories. The team noted whether the couples were positive and effusive or were more withdrawn and tired in telling these stories, then checked in with the couples three years later. They saw a correlation in how couples told stories about their past and the success of their partnership: the more giddy the couple was about a story, the more likely they remained together; the less enthusiastic the couple was, the more likely the couple’s partnership had crumbled.

While there are cultural differences in laughter display—Kurtz says that Eastern cultures tend to display appreciation with close-mouthed smiles, not the heartier, toothy laughs that are more Western—there’s no question that laughter is important. “Moments of shared laughter are potent for a relationship,” she says. “They bring a couple closer together.”

TIME Cancer

Genetic Test Impacts Chemo Choices In Surprising Ways

568857577
Maciej Frolow—Getty Images

A study investigates for the first time how a gene-based test is affecting women’s decisions to get chemotherapy

In the new era of personalized medicine, having more information on hand is considered the ideal situation for making more customized, and ideally, effective decisions about medical care.

And in a new study of breast cancer patients, researchers show that a relatively new genetic test for evaluating tumors is doing just that. It’s just that the test isn’t necessarily leading to the decisions that experts expected.

The Oncotype DX Breast Cancer Assay is a test approved by the U.S. Food and Drug Administration to help women decide how likely their breast cancer is to recur. The score, from zero to 100, is for women with breast tumors that have not spread to the lymph nodes. It places women on a scale of probability, based on an analysis of 21 genes in her tumor. Most doctors and patients use the score to decide, in part, whether the woman should receive chemotherapy following surgery.

MORE: A Major Shift in Breast Cancer Understanding

In previous studies, about 20% to 30% of doctors say they changed their recommendation about chemotherapy based on the Oncotype DX score. But none of the studies looked at how Oncotype DX affected the likelihood a woman would undergo chemotherapy rates in a real-world setting— outside of a trial. In clinics, says Michaela Dinan, assistant professor in medical oncology at the Duke Cancer Institute, many other factors contribute to treatment decisions, including fear, family history and physician advice. So she and her colleagues conducted a review of data on more than 44,044 breast cancer patients to see how the Oncotype test affected chemotherapy decisions.

MORE: Here’s the Amount of Exercise That Lowers Breast Cancer Risk

The results, published in JAMA Oncology, showed that overall, the test had no effect on their decision. Women who were tested were no more or no less likely to opt for chemotherapy than those not getting Oncotype DX. Younger age and a higher risk disease were more likely to predict chemotherapy use than the assay.

While many assumed that the test would lead to fewer treatments, Dinan’s data shows that how the testing affects chemotherapy decisions is less predictable. When Dinan delved further into the numbers, she found an interesting pattern. Those rated as having high-risk breast cancer according to the National Comprehensive Cancer Network guidelines were less likely to get chemo than women who were not tested. And among people with low-risk disease, those getting the genetic test were more likely to get chemotherapy than low-risk patients who did not.

Because the study did not take into consideration what the Oncotype DX scores were, it’s possible, for example, that women considered high risk who received intermediate or low Oncotype DX scores decided not to undergo chemotherapy since the testing showed their response might not be as positive as they might have expected. On the other hand, women who have low risk disease and receive an intermediate test score might decide to undergo chemotherapy since the intermediate risk might represent a slightly higher risk of recurrence than they were anticipating.

“It’s a more nuanced finding,” says Dinan. “The Oncotype DX test is impacting the receipt of chemotherapy, but the impact isn’t in one direction or another in terms of whether people are more or less likely to get chemotherapy.”

As more options for personalized treatments make their way into the clinic, Dinan says it’s worth remembering that they shouldn’t dictate decisions but inform them. “The nuanced finding of the difference between high risk and low risk patients says to me that whether or not a woman with early stage breast cancer undergoes chemotherapy is going to be affected by a number of different factors, not just this assay. It’s a personalized discussion about the individual patient’s case.”

TIME Research

Marijuana Does Not Affect Brain Volume, Study Finds

TIME.com stock health brain
Illustration by Sydney Rae Hass for TIME

The latest research adds to the debate over marijuana's effects on the brain

Using marijuana does not cause changes in brain volume, a new study suggests.

Public health experts have cited concerns that using marijuana could be associated with structural changes in the brain. However, a new trial comparing the brains of marijuana users and non-users to their siblings reveals that marijuana use likely does not cause changes in brain volume.

In the study, published in the journal JAMA Psychiatry, researchers looked at a large group of siblings ages 22 to 35. Of the 483 people, 262 reported ever using marijuana, even just once. The researchers then split the men and women into groups: sibling pairs who had never used marijuana, sibling pairs where both had reported using marijuana, and sibling pairs where one had used marijuana and one had not. Overall, they noticed that people who reported using marijuana had smaller volumes in certain parts of the brain—like the left amygdala, which is involved in emotional processing. However, these differences still fell within a range of volume that is considered normal.

The researchers hypothesized that in the sibling pairs where one had used marijuana and one had not, they would see differences in brain volume. But instead, they found that the exposed and unexposed siblings had the same amygdala volume. “We found no evidence for the causal influence of cannabis exposure on amygdala volume,” the authors concluded.

The researchers suggest that differences in volume could be due to other factors, like genetics or living environment. “Our study suggests that cannabis use, or at least the simple index of it that we used, does not directly impact changes in brain volumes,” says study author Arpana Agrawal, an associate professor at Washington University School of Medicine. “Instead, any relationship that we did see between cannabis use and brain volumes was due to predisposing factors that influence both cannabis use and brain volumes.”

The study did not find that brain volume has any effect on whether or not a person uses marijuana.

Another study, also published by different authors in the same journal, found that using marijuana could alter the brains of males at high risk for schizophrenia in potentially meaningful ways.

More research needs to be done to understand whether marijuana does or does not have potentially harmful effects on the brain, or whether the risks are different from one person to the next.

Your browser is out of date. Please update your browser at http://update.microsoft.com