TIME Innovation

Five Best Ideas of the Day: October 14

The Aspen Institute is an educational and policy studies organization based in Washington, D.C.

1. Fix the system, don’t fight individual diseases: Why Ebola may change how aid dollars are spent on healthcare in Africa.

By Lesley Wroughton at Reuters

2. Plan for a global body to regulate the great promise of genetics — balancing unfettered innovation with sensible rules to prevent abuse.

By Jamie F. Metzl in Foreign Affairs

3. Because it increases disease and exacerbates resource scarcity, the Pentagon sees climate change as a threat multiplier.

By Laura Barron-Lopez in the Hill

4. The U.S. should call out Egypt’s rising authoritarian leadership and the plight of repressed people there.

By the Editorial Board of the Washington Post

5. Successful community collaborations build civic confidence for increasingly audacious projects that can improve lives.

By Monique Miles in the Collective Impact Forum blog

The Aspen Institute is an educational and policy studies organization based in Washington, D.C.

TIME Ideas hosts the world's leading voices, providing commentary and expertise on the most compelling events in news, society, and culture. We welcome outside contributions. To submit a piece, email ideas@time.com.

TIME Genetics

Gene-Therapy Trial Shows Promise Fighting ‘Bubble Boy’ Syndrome

The immune system-related disease affects about 1 in 100,000 babies each year

A new gene-therapy treatment is showing promise in treating a rare and severe congenital condition that involves extreme immune-system deficiencies.

“Bubble boy” syndrome, an X-linked condition, takes its name from a famous case in which an affected boy, vulnerable to infection, lived inside a plastic bubble that protected him from the world’s germs. Outside of such sterile environments, babies with the syndrome seldom live longer than a year, the Wall Street Journal reports.

The condition has for decades bested medical researchers, despite occasional bouts of optimism — hope for one previous gene-therapy treatment was felled when some recipients developed leukemia.

Gene-therapy treatment works, essentially, by replacing unperforming genes with functional ones. Dysfunctional cells are removed from the child’s immune system and exposed to a genetically engineered virus that can reprogram the cells to function properly, explains Reuters. Those cells are then reinserted back into the patient.

In the earlier treatment, the virus to which the cells were exposed apparently activated a part of their genetic code that leads to leukemia, Reuters says.

But initial results reported in the New England Journal of Medicine show that none of the nine babies from the U.S. and Europe who received the latest treatment are exhibiting any signs of cancer.

Of the nine infant participants in the research — who were between 4 and 10½ months old when they began receiving the therapy — eight were still alive 16 to 43 months later, without living in a protective “bubble.” (The ninth child died four months after treatment began from an earlier infection he had been fighting.)

Out of the eight boys still living, the treatment upped blood T-cell levels, rebuilding the immune system, of seven. In the case of the eighth child, the treatment did not rebuild his immune system, but a successful stem-cell transplant has kept him in improved health, Reuters reports.

TIME Addiction

Addicted to Coffee? It’s Probably in Your Genes

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A new genetic explanation for your caffeine cravings

If you feel like you literally could not survive a day without coffee, you might have your genes to thank (or blame).

A new genome-wide study published in Molecular Psychiatry has identified genetic variants that may have a lot to do with your coffee obsession. Researchers from Harvard School of Public Health and Brigham and Women’s Hospital looked at more than 120,000 coffee drinkers and found six markers linked to responsiveness to caffeine—some of which had been previously identified as being related to smoking initiation and other types of potentially addictive behaviors, but had never before been linked to coffee consumption, says Marilyn Cornelis, research associate in the Department of Nutrition at Harvard School of Public Health and lead author of the study.

MORE: You Asked: Is Coffee Bad For You?

Caffeine is a drug—a fact many of us forget until we madly crave a double shot. “There is controversy as to whether it can be addictive, and some of the genes that come up in the study suggest that’s quite possible,” Cornelis says. “The stimulating effects caffeine has would suggest that caffeine is a major driving in habitual coffee consumption at the genetic level.”

MORE: How Coffee Might Lower the Risk of Heart Failure

The results might help add nuance to coffee research, she says, which generally treats everyone as the same. It could also help pinpoint people who’d most benefit from coffee consumption, and who should stick to decaf. “We assume that any health effects from one cup of coffee will be the same for everyone, but this data suggests that’s not true,” Cornelis says.

Scientists have known for a long time that genetics play a role in coffee consumption and caffeine response, Cornelis says. “But it’s only until just recently that we’ve actually been able to pinpoint these exact genetics. That’s an important step forward in the research.”

TIME medicine

New Genes Found that Determine Your Height

The latest analysis doubles the number of genes connected to height

How tall you are is strongly related to the genes you inherit, and previous studies suggested that as much as 80% of the variance in height among people is due to their DNA.

And in the largest genetic study of height-related genes to date, scientists involved in the appropriately titled GIANT consortium (Genetic Investigation of Anthropometric Traits) identified 423 genetic regions connected to height — which could explain as much as 60% of that genetic component.

Dr. Joel Hirschhorn, leader of the GIANT consortium at Boston Children’s Hospital, Harvard Medical School and the Broad Institute of MIT says that for a trait like height, which isn’t determined by a single gene but likely the combined effects of multiple genes involved in multiple different processes from bone growth to cell growth, the new findings are like finding biggest nuggets of gold in a riverbed. The latest analysis, published in the journal Nature Genetics, describes the gene variants most commonly shared among people (not the rare mutations) that likely contribute to height.

They emerged from a sweep of the genomes of more than 250,000 people of various heights, and from correlating their stature with their genetics. Many of the known and familiar factors related to height, including those dealing with skeletal growth and collagen that are mutated in people with medically short stature, for example, appeared in the study, confirming their role in determining how tall people get.

But there were also some surprises — genetic regions that previous had never been thought to be related to height, including a gene known to be involved in cell growth but not in skeletal functions. “It’s a mix ranging from completely known things, to those that make sense to things that are completely surprising and things we don’t even know what to think about them,” says Hirschhorn.

What the group has identified are gene regions of interest, and a new round of studies will have to delve deeper into those areas to isolate specific genes — and the proteins they make, such as growth factors, enzymes, or other agents — that are actually responsible for determining height. But it’s a critical first step, and could lead to potential new ways of treating medical conditions of short stature or gigantism that can have health negative health effects on the heart and joints.

TIME Genetics

New Study Makes Great Strides in Understanding Human Height

Nearly 700 gene variants linked to height have been identified

What makes tall people tall and short people short is becoming less of a mystery to scientists. An international team of researchers has identified nearly 700 gene variants in more than 400 gene regions that are connected to height — an estimated 20 percent of all the gene variants that play a role in determining one’s size.

The findings of the study were published in the journal Nature Genetics, Reuters reports. It is believed to be the biggest study of its kind to date.

Scientists believe that about 80 percent of a person’s height is hereditarily determined, with environmental factors such as nutrition determining the rest. The average height of humans around the world has risen throughout the last few generations as world nutrition generally improves.

Researchers studied the genomes of 253,288 people from Europe, North America and Australia, all with European ancestry and found 424 gene regions with 697 gene variants that are linked to height. Many of the genes identified were not previously known to have an effect on skeletal growth.

“For over 100 years, [height has] been a great model for studying the genetics of diseases like obesity, diabetes, asthma that are also caused by the combined influence of many genes acting together,” Dr. Joel Hirschhorn, a pediatric endocrinologist and geneticist at Boston Children’s Hospital and the Broad Institute. “So by understanding how the genetics of height works, we can understand how the genetics of human disease works.”

[Reuters]

TIME Sex/Relationships

How Previous Sexual Partners Affect Offspring

At least, if you’re a fly. But the research suggests that it may be time to take into account more than just DNA when it comes to our offspring

It’s a long-held belief among animal breeders that pure-bred progeny are best produced by females who have never mated before. Call it puritanical or ridiculous, but in breeding, it’s been a long-standing practice—even though there has never been much science to back it up. Now, however, researchers at University of New South Wales in Australia believe they may finally have some evidence to give that notion some scientific support.

Working with flies, Angela Crean, a research fellow at the evolution and ecology research center, picked up on her mentor’s work of looking at how male factors can influence offspring outside of the DNA in his semen.

“The genetic tests showed that even though the second male fertilized the eggs, the offsprings’ size was determine by the condition of the first male,” she says of her findings, published in the journal Ecology Letters. “The cool thing is that the non-genetic effects we are seeing are not necessarily tied to the fertilization itself.”

Cool, or really disturbing. The implications of the study are that any mates a female has had may leave some legacy—in the form of physical or other traits that are carried in the semen (but not the DNA-containing sperm)—that could show up in her future offspring with another mate.

While there’s a growing body of work showing that a mother’s diet, her smoking status, and other lifestyle habits can have an influence on her offspring, the data on similar factors on the father’s side is just emerging. With flies it’s known, for example, that males who eat a maggot-rich diet while they’re mere larvae, develop into larger than average adults, and on top of that, sire larger than average offspring as well. Males fed a meager maggot diet tend to be smaller have have smaller progeny.

Eager to learn how this was happening, Crean conducted a series of mating experiments with female flies when their eggs were immature. At that stage, the eggs are more receptive to absorbing factors in semen, but because they aren’t fully developed, they can’t be fertilized and won’t result in baby flies. When she and her colleagues “mated” these females with males who were larger, then allowed the females to actually mate with smaller males once they were mature, the offspring turned out to be large, just like the first males the females had sexual contact with. Genetically, they were the offspring of the second, smaller male, but physically, they resembled the larger males.

The same was true when they reversed the experiment and first exposed the females to smaller flies and then mated them with the larger ones.

To be sure that the was indeed due to something in the semen, Crean repeated the studies with an unfortunate group of male flies who had their genitalia glued down so they could not pass on any semen during their encounters. (“It’s horrifying but seemed nicer than cutting them off,” she says.) When these males, both large and small, were the first “mates” for females, their size did not have an effect on the offspring when the female mated with her second mate and had offspring. In other words, those offspring were large if the second male was large, and small if the second male was small.

Crean says the idea of a female’s previous mates having an effect on their offspring isn’t unheard of. In fact, this very idea, called telegony, was proposed by ancient scholars such as Aristotle but dismissed with the advent of genetics. But new findings about epigenetics — how our behaviors, such as diet, smoking and drinking — can affect our genes and how those changes can be passed on, make the idea of such non-genetic inheritance possible. “This could be seen as a maternal effect [such as diet or smoking] where the mother’s environment are her previous mating partners,” she says. “We have to realize that it’s not just DNA that gets passed on. It opens up the opportunity for all these other pathways that we had excluded.”

And while flies aren’t people, what are the chances that the same phenomenon is occurring in human reproduction? “It’s something we definitely don’t want to speculate about yet with humans,” she says. “There is no direct scientific evidence for that at all.” At least, for now.

TIME Parenting

The Pain of Passing My Disability on to My Child

Parenting
Cecilia Cartner—Getty Images

When my daughter was six weeks old, we received official word that she had inherited my bone disorder, a condition that would likely cause her many fractures and possibly painful corrective surgeries

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This article originally appeared on Patheos.

When my oldest daughter Leah was born, many people made the same observation: “Look at those fingers! So long and skinny…just like yours, Ellen.” Right after she was born, my husband went with her for a bath as I was stitched up after my c-section. When he returned, he mentioned that her eyes were a “funny color.” All of those observations, straightforward and innocent on the surface, let me know that some of my darkest fears were probably being realized.

My daughter’s long, skinny fingers and toes, the bluish color in the whites of her eyes—these were signs that Leah had inherited a scrambled gene that would wreak havoc on her skeleton. When she was six weeks old, we received official word that Leah had indeed inherited my bone disorder, osteogenesis imperfecta (OI)—a condition that would likely cause her many fractures (I had about three dozen before the age of 11) and possibly painful corrective surgeries. I clutched her fiercely against my chest and told God that he had damn well better take care of this child. That day 14 years ago was the hardest day of my life.

I have spent much of the past 10 years or so writing about genetics and disability and the choices made possible by increasingly sophisticated technologies that allow parents to choose, to some extent, what sort of child they might have. I have talked to dozens of potential parents who, like me, have some serious genetic baggage and fear putting its weight on their children’s shoulders. And I have talked to some people who wonder whether, if their child does inherit some genetic menace that wreaks havoc on that child’s health and well-being, will they regret that they took such chances with a genetic lottery stacked against them?

I tell such people that I think it’s impossible, barring extreme psychological dysfunction, to regret your own child’s existence. And I tell them about my daughter Leah, who is bearing the weight of my own genetic baggage on her fragile skeleton, who has, yes, broken a dozen bones and deeply mourned the losses that come when yet another broken bone messes with our plans. I have watched Leah sink into a place that is really dark and really sad. But I have other stories to tell about Leah, not just the dark and sad ones.

There’s this story: One Sunday morning several months ago, I slipped on some black ice when going to get our newspaper. Landing hard on my back, I broke two ribs and a shoulder bone, and partially collapsed a lung—the kind of injuries that stronger-boned people incur when they fall from trees and roofs. I managed to crawl from the frozen front walk into our entrance hall, but couldn’t go any farther. While I lay there waiting for the ambulance to arrive, as my husband reassured my two younger children and called my mom to come stay with the kids, as I struggled to breathe, Leah sat next to me on the floor. She just sat there, silent. At one point, I said to her, “You know, Leah, don’t you? You know how I’m feeling.” I wasn’t talking just about the pain, but also the crushing disappointment of a regular day ruined, the weightier knowledge of the ruined days to come. I was talking about feeling powerless in the face of something as stupidly mundane as ice, and being betrayed by the fragile body gaining the upper hand on the strong spirit. Leah nodded. Yes, she knew.

A few months later, I was heading to pick Leah up from church choir practice. I was dreading it, because I knew that Leah would be getting some bad news at the rehearsal. For Leah, singing is a passion, and when she joined our church choir about three years ago, she found another family, a community. The choirmaster was a young man called Dr. Roberts. Dr. Roberts is a talented musician but also a gifted teacher. Leah will, I’m sure, remember him for the rest of her life as the kind of teacher and mentor who changed her life. I knew that during this particular rehearsal, Dr. Roberts was planning to let the kids know that he had taken a job in New York City and would be leaving. I knew Leah would be devastated.

She came out from the church to the parking lot and with tears streaming down her face, she said, “You know Mom? This is his dream, this job he’s taking in New York. It’s good. It’s just all good.”

So it seems that, at not quite 15 years old, Leah knows what love looks like. She knows how to help carry another’s burden. She knows that sometimes an empathic presence is more helpful than words. She knows about wanting the best for someone you care about, even when their best is your worst. That she is capable of such wisdom at such a young age is proof to me that I can never regret anything about the person Leah is and is becoming, brittle bones and all.

I want to be perfectly clear, though, about what I don’t mean. I hate those clichés about how we should be grateful for the shitty stuff in our life because it teaches us so much, about how “Everything happens for a reason.” I don’t believe that one bit.

But I’m beginning to understand that Leah’s inheritance from me is not merely a faulty gene and a fragile skeleton, but also the truest kind of compassion—the kind that arises when you know what pain looks like and feels like, and you recognize another’s need, and know just what to do.

Do I regret that Leah inherited my fragile bones? I don’t love it. I even sometimes hate it.

But while I sometimes wish I could have spared her that particular genetic fate, I’m also profoundly grateful that it was not in my power to decide what kind of kid I would get.

Because I never could have predicted, much less devised, the wounded and gracious person my daughter is becoming.

Ellen Painter Dollar is the author of No Easy Choice: A Story of Disability, Parenthood, and Faith in an Age of Advanced Reproduction (Westminster John Knox, 2012). She blogs about faith, family, disability, and ethics at Patheos. Dollar also serves on a working group sponsored by the Yale University Interdisciplinary Center on Bioethics, exploring bioethical issues related to health care and people with disabilities.

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TIME Ideas hosts the world's leading voices, providing commentary and expertise on the most compelling events in news, society, and culture. We welcome outside contributions. To submit a piece, email ideas@time.com.

TIME Mental Illness

Schizophrenia Linked to 108 Genes

In a groundbreaking study, researchers reveal a host of new genes involved in schizophrenia, making it possible to develop desperately needed treatments

It took 80,000 genetic samples, seven years and the work of 300 scientists from around the world, but scientists now have the most complete dossier on schizophrenia ever.

In an historic paper published in the journal Nature, the Schizophrenia Working Group of the Psychiatric Genomics Consortium identified 108 new regions on the genome linked to the psychiatric disorder, which is associated with hallucinations and psychotic episodes and affects about 1% of people worldwide.

The genetic clues are the most dramatic hints that experts have gotten so far about what causes that mental illness. Schizophrenia has had a rocky history in the psychiatric community, with some doctors early on not even recognizing it as a disorder, and others debating whether its origins were biological or caused by traumatic events or other experiences. Now, by comparing the genomes of people with and without the disorder, it’s clear that at least some of the psychotic symptoms can be traced to changes in the genes.

“For the first time, we are starting to see the underlying biological basis of the disease, and that can lay the foundation for understanding the disorder, and eventually developing treatments,” said Eric Lander, founding director of the Broad Institute of MIT and Harvard, where about one third of the DNA samples were sequenced.

MORE: Older Fathers Linked to Kids’ Autism and Schizophrenia Risk

The study used genome wide association, a technique that sequences the genomes of affected and unaffected individuals, and then compares where they differ. Those DNA differences may be hints about why people develop schizophrenia in the first place, and therefore lead to new drugs or treatments.

The 108 genetic regions aren’t all located in specific genes, nor is it known yet if this is what actually causes schizophrenia. But, like evidence at a crime scene, they may point to certain molecular pathways that are responsible for the mental illness. It’s already known that some of the identified regions, for example, are involved in how adaptable or plastic the brain is, and in regulating the immune system, a connection that experts have previously not investigated before. Other genes may also reveal new ways to potentially treat the disease, a significant improvement over the existing therapies, which only address one brain system, involving dopamine. “Thorazine was approved in 1954 as the first anti-psychotic medication, and every antipsychotic since then has relied on the same fundamental mechanism of action,” Steve Hyman, director of the Broad Institute’s Stanley Center for Psychiatric Research and professor of stem cell and regenerative biology at Harvard University said. “And their efficacy has plateaued since the 1960s.”

MORE: Most Common Psychiatric Disorders Share Genetic Roots

Having a greater suite of potential areas of inquiry, the researchers hope, will attract pharmaceutical companies back to the field of mental illness. “We now have more than 100 genes pointing to distinct pathways – calcium channels, glutamate, the immune system – this is concrete stuff, and it means that the pharmaceutical companies who left [this area of drug development] because they didn’t have anything concrete to work on, are beginning to get their toes in the water, and are thinking of jumping back in the water,” says Lander.

The genetic windfall can also help scientists piece together how genetic changes may work in tandem to cause symptoms of psychoses. They warn that these advances, and new treatments, may not come in the next year, but they may be able to provide better answers to questions about which drugs may work better in which patients, and in finding ways to detect and hold off symptoms of schizophrenia earlier, before they become debilitating. All of the genetic information released in the paper will be deposited in a public database for researchers to access and advance the understanding of the disorder.

TIME Genetics

How Our Social Networks Impact Our Health

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A new study says we may be genetically similar to our friends Digital Vision.—Getty Images

We share more than similar interests with our friends, we share genetics too

We might think we pick our pals based on who will best complement us—the old “opposite attracts” adage—but there may be something else at play. A new study published in the journal in the journal Proceedings of the National Academy of Sciences of the United States (PNAS) shows we are more genetically similar to our friends than to strangers. In fact, we’re about as genetically equivalent to our friends as we are our fourth cousins.

Though the latest findings were primarily reserved to a group of white people of European origin, the researchers say their findings suggest there is a genetic factor at play beyond physical appearance. Though the researchers say we only share about 1% of our genes with our friends, these underlying markers may make noteworthy patterns when it comes to who we decide to spend our time with, and could even influence our health.

The study is the second to recently show that the people we are closest to are also genetically similar to us. In May, another study published in PNAS found that people also tend to be genetically similar to their spouses. But why?

These questions are central to the work of researchers, James Fowler, a professor of medical genetics and political science at the University of California, San Diego, and Dr. Nicholas Christakis, a social scientist at Yale University. The pair have been building a growing body of research about why we choose our friends, and what evolutionary benefits these choices might have.

“Sharing genes with friends appears to enhance your utility to them,” says Dr. Christakis. “Consider the hypothetical example of speech. If you evolve the capacity to speak, its use to you is greatly enhanced if you form ties with others who have evolved the same capacity.” On the other hand, the researchers found that we tend to hang out with people whose immune system make up is different from ours, which also makes genetic sense, since evolutionarily we don’t want to be susceptible to the same illnesses as our best friend or partner. We could pass it to each other, and then who takes care of who?

In the past, the researchers have looked at how social contagion can spread generosity and have reported thar people are more likely to light up a cigarette if their friends do. And in a 2007 study, the pair showed that friends can influence our weight more than genetics or family members, showing that when a study participant’s friend become obese, there was a 57% greater chance that the participant would also become obese too. They believe it’s not just that we share lifestyle behaviors with our friends, but that friends change our opinions on what we believe to be appropriate social behavior. Conversely, friends could also help us stay on a weight loss plan for the same reasons. The researchers also show that social networks could also have the potential to predict epidemics given that most are set up in a similar way, where certain people are more connected and popular than others, and subsequently more likely to come in contact with disease.

In earlier studies on friendship and genetics, Christakis and Fowler suggested that genetics can influence social behavior in networks of friends, even impacting whatever predispositions those friends already have. For example, if someone is genetically predisposed to alcoholism, and they end up associating with people of similar genotypes who are more likely to have alcohol available, that could be a problem for them. But on the other hand, if that same person chooses a group of friends with a different make-up, alcohol may not be frequently present, and their predisposition remains un-triggered.

That means friendships might modify the way our own genes are expressed, the authors propose. Meaning human evolution is not just limited to the influence of physical and biological environments, but social ones as well.

TIME Friendship

Study: BFFs May Have Similar DNA

RyanJLane—Getty Images

Really close friends might be as genetically similar as fourth cousins

Next time someone says “You would really like my friend, she’s just like you,” try to refrain from giving her the side eye. It turns out she might have some science to back her up. According to a new study from Yale University and the University of California at San Diego, good friends are often genetically similar, and can share as much as 1% of the same gene variants. In genetic terms, that’s a lot. As close as, say, fourth cousins.

“This gives us a deeper accounting of the origins of friendship,” says Nicholas Christakis, professor of sociology, evolutionary biology, and medicine at Yale, who co-authored the study with James Fowler, professor of medical genetics and political science at UC San Diego. “Not only do we form ties with people superficially like ourselves, we form ties with people who are like us on a deep genetic level. They’re like our kin, though they’re not.”

To do their study, which was published in July in the Proceedings of the National Academy of Sciences, Christakis and Fowler looked at 1.5 million gene variants from the Framingham Heart Study, a dataset which has details on the friendships and genetics of its participants. Most of the participants were of European descent. Researchers genetically compared pairs of friends with pairs of strangers from among the same 1,932 subjects they studied. None of the pairs were related to each other.

The study found that, oddly, close friends are often genetically similar in their sense of smell. But it also concluded that friendship may play a role in evolution. The genes that were shared by friends saw the most “evolutionary activity”, or have evolved the fastest over the past 30,000 years. Whether the friendship or the genetic similarity came first is up for debate. Do we seek out genetically similar friends or do our friendships and mating affect what genes get passed on

“Human beings are one of the few species who form long-term, non-reproductive relationships with other members of our species,” says Fowler. “This role of affiliation is important. It ties into the success of our species.”

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