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Root vegetables like carrots were found to contain chemicals of emerging concern.

Pharmaceuticals Found in Low Levels in Wastewater-Irrigated Produce

With 99% of California’s agricultural lands ravaged by drought, some farmers in the state are considering an alternative to freshwater: treated sewage.


 “In water-short regions of the world like Israel, like the Western U.S., like Australia, we will increasingly use recycled water,” says Richard Luthy, professor of environmental engineering at Stanford University. However, two new studies from Israel and California raise questions about whether using treated wastewater to irrigate crops could expose consumers to the low levels of pharmaceuticals that persist in wastewater, even after treatment.

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 One study investigated the fate of chemicals of emerging concern (CECs)—compounds and molecules with no standardized regulations that could have negative health and environmental effects—in the agricultural environment. The results,
 <a href="http://pubs.acs.org/doi/abs/10.1021/es5017894">
 published in July
 </a>
 in the Journal of Environmental Science and Technology by a team at the Hebrew University of Jerusalem, revealed that root vegetables absorbed CECs when irrigated with treated wastewater artificially spiked with excess CECs as well as from unaltered treated wastewater.
 <a href="http://pubs.acs.org/doi/abs/10.1021/es502868k">
 The other
 </a>
 , conducted by a team at the University of California, Riverside, has been accepted for publication by the same journal. The researchers used similar techniques, discovering that over half of the vegetables irrigated by un-spiked treated wastewater had taken up CECs.


 However, neither study nor experts in the field could conclusively say how the presence of CECs in produce might affect public health. “It’s something that’s on the radar screen that we’re looking at, but it’s something that as yet has not appeared as problem,” says Luthy, who wasn’t affiliated with either study. “That’s not the same thing as saying that we shouldn’t look for it.”


 California has a long history of such reuse, going back as far as 1910 when San Francisco’s Golden Gate Park was irrigated with wastewater. Now, around 13% of California’s wastewater is reused, and around 35% of that is devoted to agriculture. The practice of re-using treated wastewater is far more common in Israel, which repurposes 75% of its total effluent for agriculture.


 A 2010 review paper published in the Journal of Environmental Monitoring, however found that CECs persist even in treated wastewater. Treatment removes some CECs, such as the non-steroidal anti-inflammatory drug (NSAID) ibuprofen and the endocrine disruptor BPA, but not others, including carbamazepine, a seizure medication, or diclofenac, an NSAID. Researchers
 <a href="http://www.pbs.org/wgbh/nova/next/body/pharmaceuticals-in-the-water/">
 are uncertain
 </a>
 whether the concentrations found in water supplies pose any threat to public health.


 Furthermore, how CECs behave in farm fields remains poorly understood. “Nobody who designed a drug imagined that a drug would eventually be in the soil, so no one knows what the fate of these drugs are in the soil,” says Benny Chefetz, professor of agricultural and soil chemistry at The Hebrew University of Jerusalem and a senior author on the first study. Chefetz’s team tested an artificial worst-case scenario by using treated wastewater spiked with excessive amounts of CECs to irrigate carrots and sweet potatoes.

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 They found that, depending on the compound’s properties and the soil’s characteristics, some drugs, including the seizure medications carbamazepine and lamotrigine, were absorbed by the edible roots and transported to the leafy portions of the plants. Others, including the NSAIDs ibuprofen and diclofenac, were not.


 Chefetz hopes that these results can help direct wastewater treatment plants to remove only the drugs that most likely to be absorbed by crops. “For instance, ibuprofen, which is well used in the U.S., is very easily removed in the soil system, so you don’t need to put a lot of energy to remove it from the treated wastewater,” he says.


 The second study, led by Jay Gan, a professor of environmental chemistry at University of California Riverside, also found that produce could absorb CECs from irrigation. The investigators spiked treated wastewater with fixed concentrations of 15 compounds and used it to irrigate half of a field of vegetables; the other half was irrigated with un-spiked treated wastewater. In the un-spiked half, around 64% of the edible portions of the vegetables absorbed at least one CEC, and 90% did in the spiked half.


 While detectable, the concentrations weren’t high. “In the edible tissues, the levels were very, very low,” Gan says. “Especially if you compare to what people normally take in a medication scenario, it’s probably four or five orders of magnitudes smaller.”


 Chafetz and his team found that carrots and sweet potatoes irrigated with un-spiked treated wastewater also absorbed the seizure drugs carbamazepine and lamotrigine. Based on the amounts measured, the investigators estimated that a half a carrot a day could chronically expose a child to enough low doses of lamotrigine that it might eventually pose a health risk.


 However, the specific implications for public health remain unclear. “The conclusion isn’t as straight forward as we’d like it to be, because there are still a lot of questions,” says Tomer Malchi, a graduate student who worked with Chefetz on this study. For instance, it is unknown how these anti-convulsants might affect a fetus if a pregnant woman were to consume them with her produce.


 Gan, who has collaborated with Chefetz in the past but not on these two recent studies, urges caution. “There are not really any relevant EPA threshold standards, and to try to guess if [CECs] can really cause problems is really hard,” he says. He and his co-authors note in their own study that a person’s annual CEC exposure via produce was only 3.69 micrograms in a year, or “three orders of magnitude smaller than that in a single medical dose for one compound.”


 Chefetz agrees that his team’s results shouldn’t be cause for panic. “The bottom line is not that the treated wastewater is unsafe—I’m not saying that,” he says.


 “A lot of people would be like, ‘Is there a red light? Stop?’ And I’d say no, no,” Malchi says. “It’s a little orange light, and we need to see what this means.”


 Photo credit:
 <a href="https://www.flickr.com/photos/29487672@N07/14760573314">
 swong95765/Flickr (CC BY)
 </a>

Bioengineers Hack PCs and Phones to be Cheap Disease Detectors

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 Scientists have reinvented the technology that makes analyzing crime scene DNA and diagnosing infectious diseases possible—for 1/500
 
 th
 
 the cost.
 

 Today, we can distinguish human genetic material at crime scenes and detect the DNA of infectious agents in blood using a reliable, heat-dependent process called PCR. The catch is that PCR equipment usually runs into the multiple thousands of dollars—a significant barrier in resource-limited settings.
 

 So scientists at the University of California, Santa Barbara designed a system that combines the wasted heat from an over-clocked computer with the imaging capacity of a mobile phone. It works just like regular PCR, but “for a fraction of the cost,” writes Faye Walker, an author of the study. Scientists eager to convert their PCs and phones to PCR machines can find
 <a href="http://pubs.acs.org/doi/full/10.1021/ac5022419">
 the how-to guide
 </a>
 published by members of Tom Soh’s lab in September’s issue of Analytical Chemistry.
 
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<img alt="" class="richtext-image full-width" src="https://staging.pbs.org/wgbh/nova/media/images/heatsink_JNKYJaj.width-990_NiPcKnt.jpg"/>
<figcaption>Computer processors can throw off a lot of heat, which is often wasted but which can be put to good use.
 
 </figcaption>
</figure>

 “I think the cost effectiveness, particularly, is going to be a very attractive feature,” said Susan Montgomery, the epidemiology team lead of the Parasitic Diseases Branch at the CDC. “The equipment that’s needed for the way PCR is done in laboratories now is expensive.”
 

 PCR works by mixing a miniscule amount of DNA with chemicals and running it through cycles of heating and cooling on a machine called a thermal cycler to copy the DNA billions of times. This amplification increases the amount of DNA to levels that, when mixed with fluorescent dyes, can be seen under UV light.
 

 Kareem Ahmad, another author on the study, first considered harnessing a PC’s heat for biomedical research four and a half years into his PCR-intensive PhD. Ahmad had built a PC at home to watch movies and noticed the computer’s fan whirring loudly while he watched Netflix. When he checked the computer’s internal temperature, he saw it approaching 70˚ C. He remembers thinking, “I wonder if it could be hot enough to do PCR?”
 

 Ahmad found inexpensive software online that could cycle the internal temperature of a computer, just like a PCR machine. The next day, he decided to run a PCR experiment using the computer instead of a thermal cycler as the heat source. “The second time I did that experiment, it worked, which was unlike every other project I had worked on up until that point,” Ahmad said.
 
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<img alt="" class="richtext-image full-width" src="https://staging.pbs.org/wgbh/nova/media/images/heat-sink-pcr1.width-990_7tg5BC9.jpg"/>
<figcaption>A closeup of Kareem Ahmad's heat-sink PCR thermocycler
 
 </figcaption>
</figure>

 Over the next two years, the PC-Phone-PCR (P3) system evolved until it eventually included a camera phone outfitted with a special filter and tubes pre-loaded with the necessary chemicals and fluorescent dye. Ahmad—who graduated with his PhD six months after the initial experiments—handed off the work to Faye Walker, “who did an excellent job of putting it across the finish line,” he said.
 

 Using the final P3 product, the scientists in the lab could detect parasites in human blood by adding blood to the pre-loaded tubes, boiling them briefly, placing them in the computer’s heat sink, cycling the computer’s temperature, and—under UV or blue light—using the camera to detect the presence of the now-fluorescing parasite DNA. They then used the same computer that provided the heat source to analyze the photos and determine which tubes contained blood positive for parasite infection.
 

 “I’m almost kicking myself for not coming up with it sooner, because it seems like—once you realize it—it seems like such a simple, obvious thing,” Ahmad said.
 

 “I love the idea of making things with what you have, that solve problems that you have in the field,” said Dr. Darvin Scott Smith, chief of infectious disease and geographic medicine at Kaiser Permanente. Smith would like to see this technology tested in environments where the scientists anticipate it being used and eventually see it tested on multiple diseases.
 

 Montgomery, the CDC epidemiologist, added that field-testing the P3 system, “will go a long way, I think, to pushing the argument forward that this is something that could be used in a disease control setting.”
 

 Ahmad hopes the P3 system’s practicality will make it widely adoptable. “To me, what’s cool about this technology is that it’s not actually that sophisticated, and it’s not something that is beyond the reach of most people,” he said. “It’s something that’s almost democratic.”
 
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 Photo credits:
 <a href="https://www.flickr.com/photos/jstownsley/388362245/">
 J.S. Townsley/Flickr (CC BY-NC-ND)
 </a>
 , Kareem Ahmad

You May Be Born to Feel Carsick

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 If you spent your last road trip staring queasily at the horizon, chances are you might be one of around 33% of people who suffer from motion sickness.
 

 Motion sickness, it turns out, might not just be a matter of willpower and intestinal fortitude. Personal genetics company 23andMe has mined the genomes sequenced from the spit of over 80,000 customers to conduct the first ever
 <a href="http://www.genome.gov/20019523">
 genome-wide association study
 </a>
 of motion sickness. They discovered that variation in certain genes may predispose a person to the dizziness and nausea thought to result from conflicting sensory signals about whether the body is in motion, or standing still.
 
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<img alt="" class="richtext-image full-width" src="https://staging.pbs.org/wgbh/nova/media/images/dizzy_crop.width-990_wLUqazc.jpg"/>
<figcaption>23andMe found common genetic variations in people who get carsick.
 
 </figcaption>
</figure>

 Using an online questionnaire, participants self-reported how carsick they get from never (a score of zero) to frequently (a score of three). Variations in single bits of genetic code—also known as single nucleotide polymorphisms, or SNPs—in 35 regions of the genome associated with balance, glucose regulation, and eye, ear, and brain development occurred more frequently in people who scored higher on the carsickness scale.
 

 The many different kinds of motion sickness make it difficult to draw broad conclusions from a questionnaire that specifically examined carsickness, explained motion sickness expert and University of Minnesota professor of kinesiology Thomas Stoffregen.
 

 “People get sick in cars, but they get sick in ships, and they get sick at the movies, and they get sick while they’re playing video games, and they get sick in all kinds of different situations,” he said, adding “the fact that there are some genes that line up with the answers that people gave on these online questionnaires does not, does not, does not in any way imply that the genes are causally related to motion sickness.”
 

 From the genetics perspective, Steven McCarroll, assistant professor of genetics at Harvard Medical School, said that there are very few genome wide association studies that have been conducted on this scale–and is optimistic about future studies that take advantage of the databases collected by companies like 23andMe.
 

 “When I realized that they had studied this common phenotype in 80,000 people it’s clear that they had a lot of statistical power,” he said. “I think that it’s just tremendously exciting that communities can organize over the internet and bring amazing statistical power to a problem that required really large cohorts to answer a question like this.”
 

 The
 <a href="http://www.eurekalert.org/pub_releases/2015-02/e-2su020215.php">
 announcement
 </a>
 of 23andMe’s results—published in the journal Human Molecular Genetics—comes just days after President Obama announced his $215 million Precision Medicine Initiative, which many hope will use the genetic data collected in databases like 23andMe’s to usher in a new age of genetically guided treatment and therapeutic development.
 
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 Photo credit:
 <a href="https://www.flickr.com/photos/areyoumyrik/308908967/in/photolist-5LU1TV-tieSF-9GZkPo-dcAYb-druhJP-7kiuj2-6vx4EG-77rvh-7knoA3-6m4Mwp-5Jr5A-7knotb-7knowy-7knoqw-tiePX-76GzE6-29oiRM-29sFcu-4f1Sq1-fAUHr-6EzpQf-tieNG-5Tfe7t-Jar3A-kxb2s5-9UdxCW-pPeQGL-r7w3U-69vNtQ-MAW5-4v2eM7-7bfYZ4-fvxFc-MpSDi-98yoDw-2tdoEF-dcAzw-6Am9XB-kB7o9-3KL88-6dnmg6-6aXw9e-gs31c-7vMLKw-7jsdJs-9XoqDA-4GiN5a-56jgPv-nchET-mJuPd">
 are you my rik? / Flickr (CC BY-ND 2.0)
 </a>

In Once-Mysterious Epigenome, Scientists Find What Turns Genes On

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 Over a decade ago, the Human Genome Project deciphered the “human instruction book” of our DNA, but how cells develop vastly different functions using the same genetic instructional text has remained largely a mystery.
 

 As of yesterday, it became a bit less mysterious. A massive NIH consortium called the Roadmap Epigenomics Program published eight papers in the journal Nature which report on their efforts to map epigenetic modifications, or the changes to DNA that don’t alter its code. These subtle modifications make genes more or less likely to be expressed, and the collection of epigenetic modifications is called the epigenome.
 
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<img alt="" class="richtext-image full-width" src="https://staging.pbs.org/wgbh/nova/media/images/dna-molecule.width-990_pj3aq3G.jpg"/>
<figcaption>A handful of new studies provide epigenetic roadmaps to understanding the human genome in action.
 
 </figcaption>
</figure>

 One of the eight studies
 <a href="http://www.nature.com/nature/journal/v518/n7539/full/nature14248.html#f2">
 mapped over 100 epigenomes
 </a>
 characterizing every epigenetic modification occurring in human tissue cells. “These 111 reference epigenome maps are essentially a vocabulary book that helps us decipher each DNA segment in distinct cell and tissue types,” Roadmap researcher Bing Ren, a professor of cellular and molecular medicine at the University of California, San Diego, said in
 <a href="http://www.nih.gov/news/health/feb2015/niehs-18.htm">
 a news release
 </a>
 . “These maps are like snapshots of the human genome in action.”
 

 This kind of mapping has challenged the field because of the huge amount of data needed to make sense of the chaotic arrangements of genes and their regulators. “The genome hasn’t nicely arranged the regulatory elements to be cheek by jowl with the elements they regulate,” Broad Institute director
 <a href="http://www.nytimes.com/2015/02/19/health/scientists-shed-light-on-circuits-that-control-genes.html">
 Eric Lander told Gina Kolata
 </a>
 at The New York Times. “It can be very hard to figure out which regulator lines up with which genes.”
 

 Here’s how Lander described the detective process used to Kolata:
 
<blockquote>

 If you knew when service on the Red Line was disrupted and when various employees were late for work, you might be able to infer which employees lived on the Red Line, he said. Likewise, when a genetic circuit was shut down, certain genes would be turned off. That would indicate that those genes were connected, like the employees who were late to work when the Red Line shut down.
 
</blockquote>

 Diseases can be linked to epigenetic variations as well. For example, another of the eight papers published yesterday
 <a href="http://www.nature.com/nature/journal/v518/n7539/full/nature14252.html">
 proposed
 </a>
 that the roots of Alzheimer’s disease lie in immune cell genetic dysfunction and epigenetic alterations in brain cells.
 

 Creating an epigenetic road map is a huge step, but it’s just a first step. As Collins wrote in 2001 when the human genome had been mostly mapped, “This is not even the beginning of the end. But it may be the end of the beginning.”
 
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 Photo Credit:
 <a href="http://commons.wikimedia.org/wiki/File:DNA-molecule2.jpg">
 ynse / Wikimedia Commons
 </a>

The new test could lengthen the useful life of antibiotics  such as clindamycin, one of the most essential drugs, according to the World Health Organization.

Quick Test That Measures a Patient’s Own Proteins Could Slash Antibiotic Overuse

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 If you’ve ever been prescribed antibiotics to fight the flu, you’ve experienced first-hand how difficult it is for doctors to distinguish between bacterial infections and viral infections (the flu is the latter). Oftentimes, doctors will prescribe antibiotics just in case it’s a bacterial infection so the patient will recover sooner. Early administration of antibiotics can halt bacterial infections before they spiral out of control, but the practice has led to the overuse of our most precious drugs.


 Fortunately, a team of researchers
 <a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0120012">
 announced
 </a>
 yesterday that they may have solved this problem in the form of a blood test. It works by detecting the proteins produced by a patient’s own body in response to infection to quickly determine whether they have been sickened by a bacterial strain or a virus. It returns a result within minutes rather than the hours or days required with typical clinical tests.


 Today’s tests aren’t just slow, they also require that the infectious agent has multiplied enough inside the patient’s body that the levels are high enough to be detected, and can misidentify the root cause when a person has concurrent infections. To overcome these hurdles, scientists from Israeli biotech company MeMed looked to the patient’s own body to see which molecules the immune system produces when fighting off different kinds of infections.

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 The test performed well, properly identifying the type of infection most of the time. The researchers even report that it is more accurate than typical clinical diagnostics. Here’s Smitha Mundasad, reporting for BBC News on the new test:


 It relies on the fact that bacteria and viruses can trigger different protein pathways once they infect the body.


 A novel one, called TRAIL, was particularly high in viral infections and depleted during bacterial ones. They combined this with two other proteins – one is already used in routine practice.


 The rapid test could slow the rampant spread of antibiotic resistance in bacteria. Inappropriately prescribing antibiotics to to combat a virus like the flu or using too low of a dose of antibiotics encourages bacteria to evolve traits that protect them from commonly used drugs.


 Antibiotic misuse is not a small problem. The CDC estimates that nearly half of all antibiotics should never have been prescribed in the first place, and antibiotic resistant bacteria infect around 2 million people each year in the United States, killing over 23,000 of those infected.


 Virus expert Jonathan Ball from the University of Nottingham is cautiously optimistic, telling the BBC’s Mundasad that while MeMed’s new test might reduce inappropriate antibiotic use, “It will be important to see how it performs in the long term.”

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<a href="https://www.flickr.com/photos/lamentables/308945428">
 lamentables/Flickr (CC BY-NC-SA)
 </a>

By testing a patient&#x27;s blood, doctors may be able to determine whether an infection is viral or bacterial in a matter of minutes.

Scientists Genetically Modify Human Embryos

It was, perhaps, inevitable. Once we gained the ability to modify the DNA of an organism, it was only a matter of time before we turned that technology on ourselves and our offspring.


 Now, Chinese scientists have edited the genome of a human embryo. Their work was
 <a href="http://link.springer.com/article/10.1007/s13238-015-0153-5/fulltext.html">
 quietly published
 </a>
 late last week, on a Saturday, in the little-known, open-access journal
 
 Protein &amp; Cell
 
 , an unusual way to introduce a first-of-its-kind study.

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 Typically, such results usually appear in the pages of a handful of respected journals like
 
 Science
 
 or
 
 Nature
 
 and are surrounded by a flurry of publicity. The lead researcher, Junjui Huang of Sun Yat-sen University in Guangzhou, attempted to publish in several journals but was turned down out of ethical concerns. David Cyranoski and Sara Reardon unearthed the paper and brought it to wider attention in
 <a href="http://www.nature.com/news/chinese-scientists-genetically-modify-human-embryos-1.17378">
 an article
 </a>
 they published late yesterday in
 
 Nature
 
 ’s news section.


 The journals may also have balked at the mediocrity of the science itself. “It came up with relatively non-break through results,” says George Church, a professor at Harvard University. It was “a fairly technical paper that didn’t provide any brand new insights.”


 “Ethically, it is of huge significance,” says Arthur Caplan, a professor of bioethics at New York University. “The paper is much more interesting as an ethics paper than it is as a science paper. The science isn’t going to be impacted in any way by the appearance of this paper.”

<h2>
 Familiar Methods, Unfamiliar Sources
</h2>

 Much of the paper’s experimental method retraces well-trodden ground. The team used the CRISPR-Cas9 genome editing technique, a relatively new but powerful and widely-used method that allows scientists to modify genes more rapidly than before. Though the molecular machinery was first demonstrated as an editing technique in 2012, scientists have quickly become adept at wielding it, to the point where researchers at various levels—from undergraduates to tenured professors—are using it in labs around the world.


 The Chinese team’s target was the gene responsible for β-thalassaemia, an inherited blood disorder that can lead to severe anemia. In that sense, they were on the right path. “I think there’s tremendous promise in genome editing for blood disorders, and other disorders, but particularly blood disorders,” says Dr. Daniel Bauer, a professor and blood disorder researcher at the Harvard Stem Cell Institute. But, he adds, this and other disorders could be corrected by altering a person’s blood stem cells. In that case, “one wouldn’t necessarily need to modify the germ line to have a benefit in this kind of blood disorder,” he says. Dr. Suneet Agarwal, an assistant professor at the Harvard Medical School who studies gene therapy and bone marrow disorders, agrees. “I don’t think it’s safe to try and achieve a clinical cure with this type of technology. We already know that it has a long way to go in terms of its development.”

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 Huang and his team said they collected embryos with the mutation from a nearby fertility clinic, according to Cyranoski and Reardon’s reporting, though little else is known about how they were created or obtained, Caplan points out. The researchers chose to modify
 <a href="http://humrep.oxfordjournals.org/content/27/suppl_1/i22.full.pdf">
 tripronuclear zygotes
 </a>
 , which are single-celled embryos that have an additional set of chromosomes. Humans, having two copies of each chromosome, are diploid. So while a triploid embryo may develop for several days or weeks, it ultimately has an extremely low chance of survival.


 Using tripronuclear zygotes allowed the researchers to study whether their edits took hold and how they affected early development. Since the embryos were unable to develop into viable fetuses, it provided the team with a modicum of ethical cover. But it also prevented them from saying anything about the viability of the modified embryos.


 Even then, the results weren’t promising. The researchers started out with 86 embryos, but just 71 made it to the end of the study. Of those, 54 were tested, and the team discovered that only 28 had successfully been modified. Worse, the CRISPR scissors missed their target often enough to be worrying. Two of the six embryos Huang’s team sequenced for off-target mutations were found to contain mistaken edits.

<h2>
 Ethical Concerns
</h2>

 Despite the fact that the embryos weren’t viable, many scientists are concerned that Huang and his group plowed ahead before the rest of the community had arrived at a consensus on how to proceed. Back in the 1970s, when researchers first discovered how to splice new bits of DNA into a genome, a technology known as recombinant DNA, they held a conference at Asilomar in California in 1975 to hash out a number of guidelines. In January of this year, scientists met in Napa, California, to do the same for genome editing. They identified a number of guidelines, including calling for a moratorium on any modifications to the earliest phases of development, known as the germline.


 “When you cross the germline bright line, you’re also opening the door to eugenic reasons—improvement, enhancement—not just disease,” Caplan says. The scientific community, he adds, hasn’t “even talked about that very much.”

<div class="pullquote">

 “The paper is much more interesting as an ethics paper than it is as a science paper.”

</div>

 Modifying the germline is ethically debatable, possibly perilous, but also potentially powerful. With current gene therapies, clinicians must modify every targeted cell in the body, which could number in the trillions. But in a zygote, the stage at which the Chinese group worked, they only have to modify one. As the embryo divides, every subsequent cell should retain the modifications. But if the editing technique fails to cut in the right place, as it did in several of the Chinese group’s modified embryos, every cell will also carry unintended edits, potentially introducing new, deleterious mutations. Furthermore, in the Chinese study, not every cell in the tested embryos contained the modifications. That kind of defeats the purpose of editing the germline.

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 Still, Church thinks this sort of experimentation should be happening, just at a more careful pace. “I’m one of the advocates of going forward cautiously,” he says. “This is one of the experiments I’m sure everybody would like to see.” Though there weren’t any breakthrough results—if the Chinese group had succeeded, Church points out, their work would certainly have been considered “more important”—he does see some value from their work. “It’s important for other safety and efficacy steps, and they even mention ways that you could improve the efficiency and specificity in the future.”


 Kevin Esvelt, a technology development fellow at Harvard’s Wyss Institute, thinks this study could help put the brakes on any fast-movers in the field. “It’s a basic first step that provides a nice cautionary tale warning against clinical attempts any time soon.”


 Despite many scientists’ reservations, this research isn’t likely to stop. Huang is hoping to refine his technique, Nature reports, either by tweaking his CRISPR-Cas9 system or using another gene editing technique like TALENs, which is more accurate and should lead to fewer off-target mutations. Furthermore, Huang’s group is not alone, Cyranoski and Reardon report. Four other groups in China are rumored to be working on editing human embryos.


 To give the scientific community and the general public more time to consider the issue, Caplan thinks we should ask researchers to stop voluntarily. “I think we should have a moratorium,” he says. “Journals should not accept papers right now.”


 “This experiment stirs attention to the fact that we need to have both national and international discussions about how to proceed, if at all,” Caplan adds. “But if we’re going to do it, we don’t do it by publishing a meaningless experiment in a third-tier journal. That’s not the way to begin.”


 Image credit: Yorgos Nikas/Wellcome Images (CC BY-NC-ND)

Chinese scientists used the CRISPR-Cas9 editing technique to alter the genome of a “nonviable” human embryo.

Early studies suggest that cheese may be protective against heart disease.

For a Healthy Heart, You May Have to Eat More Cheese

Go ahead, finish off that wheel of Brie, that brick of cheddar, or that blob of mozzarella. Your heart may thank you.


 Last month, a group of Danish scientists investigated why the French don’t seem to suffer from cardiovascular disease as much as their high saturated fat, high cholesterol diets would suggest. The researchers looked to diet to explain this so-called French Paradox, and what do the French eat a lot of? Cheese. In 2013, the French led the pack in
 <a href="http://i100.independent.co.uk/article/the-10-countries-in-the-world-that-eat-the-most-cheese-revealed--gkKzi-d6vg">
 cheese consumption worldwide
 </a>
 —closely followed by Iceland and Finland.


 So the team had 15 young-to-middle aged men follow three different diets for two weeks at a time. Each diet had the same amount of calories: one was high in 1.5% milk fat, another was high in cheese, and a third allowed butter but no other dairy.

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 The scientists then took a close look at the men’s urine and feces to see what came out after the dairy went in. Men on the milk and cheese diets excreted higher levels of molecules called short-chain fatty acids which are thought to be anti-inflammatory and lower levels of a molecule called TMAO, made by gut microbes when they break down animal-based foods and linked to cardiovascular disease. The authors speculated that the cheese and milk might be altering gut bacteria to somehow make more of the beneficial short chain fatty acids and less of the potentially damaging TMAO.


 “The most interesting thing to me is the short chain fatty acid and immunology angle,” says Kevin Bonham, a post-doctoral scholar who studies the microbial communities in cheese and writes for the Scientific American blog,
 <a href="http://blogs.scientificamerican.com/food-matters/">
 Food Matters
 </a>
 .
 
 “
 
 The study size is pretty small, but at the same time it it’s certainly suggestive of an interesting link.”


 This study, despite being funded by a dairy company, aligns with other work in the field that draws correlations between cheese and dairy consumption and protective effects in cardiovascular and metabolic disease, says Gökhan Hotamisligil, chair of genetics and complex diseases at the Harvard School of Public Health.

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 Not everyone is sold on cheese’s benefits, though. Kim Williams, a cardiologist at Rush University Medical Center, president of the American College of Cardiology, and a vegan, is less certain that diet explains the French Paradox. “I spent a lot of time in Paris and other parts of France, and what you don’t see is inactive people who are overweight,” he says, adding that further studies need to be done to first tease out the lifestyle factors that are contributing to it and second to compare the risk for cardiovascular disease of animal-based diets versus plant-based diets. “It shouldn’t just be more cheese versus less cheese or cheese versus butter, it actually should be a plant-based diet versus the animal products,” he says.


 “Whether or not cheese will solve French paradox, I think, remains to be seen,” Hotamisligil says. Nevertheless, “As a big cheese lover, I am loving to read these sort of findings,” he jokes. “Wine is good, cheese is good, so I’m all set.”

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<a href="https://www.flickr.com/photos/matupplevelser/4644484638">
 Photo credit: Gunnar Magnusson (CC BY-ND 2.0)
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A new study suggests that eating cheese may be good for you, and it has some sound science to back it up.

R.A. Becker

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