When International Space Station commander Barry Wilmore needed a wrench, Nasa knew just what to do. They “emailed” him one. This is the first time an object has been designed on Earth and then transmitted to space for manufacture.

Made In Space, the California company that designed the 3D printer aboard the ISS, overheard Wilmore mentioning the need for a ratcheting socket wrench and decided to create one. Previously, if an astronaut needed a specific tool it would have to be flown up on the next mission to the ISS, which could take months.

This isn’t the first 3D printed object made in space, but it is the first created to meet the needs of an astronaut. In November astronauts aboard the ISS printed a replacement part for the recently installed 3D printer. A total of 21 objects have now been printed in space, all of which will be brought back to Earth for testing.

“We will use them to characterise the effects of long-term microgravity on our 3D-printing process, so that we can model and predict the performance of objects that we manufacture in space in the future,” explained Mike Chen from Made in Space.

Chen also explained the process of sending hardware to space. First, the part is designed by Made In Space in CAD software and converted into a file-format for the 3D printer. This file is then sent to Nasa before being transmitted to the ISS. In space the 3D printer receives the code and starts manufacturing.

“On the ISS this type of technology translates to lower costs for experiments, faster design iteration, and a safer, better experience for the crew members, who can use it to replace broken parts or create new tools on demand,” Chen said.


Few concepts in popular psychology have gotten more attention over the last few decades than self-esteem and its importance in life success and long-term mental health. Of course, much of this discussion has focused on young people, and how families, parents, teachers, coaches, and mentors can provide the proper psychological environment to help them grow into functional, mature, mentally stable adults.

Research shows that low self-esteem correlates with poorer mental health outcomes across the board, increased likelihood of suicide attempts, and difficulty developing supportive social relationships. Research also shows that trying to raise low self-esteem artificially comes with its own set of problems, including tendencies toward narcissism, antisocial behavior, and avoiding challenging activities that may threaten one’s self-concept.

This division in the research has led to a division amongst psychologists about how important self-esteem is, whether or not it’s useful to help people improve their self-esteem, and what the best practices are for accomplishing that.

In one camp, you have people who believe improving self-esteem is of paramount importance. On the other side of the fence are those who feel the whole concept of self-esteem is overrated and that it’s more critical to develop realistic perceptions about oneself.

But what if we’ve been asking the wrong questions all along? What if the self-esteem discussion is like the proverbial finger pointing at the moon?

New research is suggesting this may indeed be the case, and that a new concept — self-compassion — could be vastly more important than self-esteem when it comes to long-term mental health and success.

Why the Self-Esteem Model Is Flawed

The root problem with the self-esteem model comes down to some fundamental realities about language and cognition that Acceptance and Commitment Therapy (ACT, pronounced all as one word) was designed to address.

The way psychologists classically treat issues with self-esteem is by having clients track their internal dialog — especially their negative self talk — and then employ a number of tactics to counter those negative statements with more positive (or at least more realistic) ones. Others attempt to stop the thoughts, distract themselves from them, or to self sooth.

Put bluntly, these techniques don’t work very well. The ACT research community has shown this over and over again. There are many reasons that techniques like distraction and thought stopping tend not to work — too many to go into all of them here. For a full discussion, see the books Acceptance and Commitment Therapy or Get Out of Your Mind and Into Your Life. For the purposes of our discussion here, we will look at one aspect of this: How fighting a thought increases its believability.

Imagine a young person has the thought, “There is something wrong with me.” The classic rhetoric of self-esteem forces this person to take the thought seriously. After all he or she has likely been taught that having good self-esteem is important and essential for success in life. If they fight against the thought by countering it, however, that means the thought is confirmed. The thought is itself something that is wrong with the individual and has to change. Every time they struggle against it, the noose just gets tighter as the thought is reconfirmed. The more they fight the thought, the more power they give it.

This is a classic example of why in ACT we say, “If you are not willing to have it, you do.”

The simple fact is, we can’t always prevent young people from experiencing insecurity and low self-esteem. Heck, we can’t eliminate those feelings in ourselves. All people feel inadequate or imperfect at times. And in an ever-evolving, ever-more complex world, there is simply no way we can protect our young people from events that threaten their self-esteem — events like social rejection, family problems, personal failures, and others.

What we can do is help young people to respond to those difficult situations and to self-doubt with self-compassion. And a couple of interesting studies that were recently published show that this may indeed offer a more useful way forward not only for young people, but for all of us.

What Is Self-Compassion?

Before we look at the studies, let’s take a moment to define self-compassion.

Dr. Kirstin Neff, one of the premier researchers in this area, defines self-compassion as consisting of three key components during times of personal suffering and failure:
1. Treating oneself kindly.
2. Recognizing one’s struggles as part of the shared human experience.
3. Holding one’s painful thoughts and feelings in mindful awareness.

Given this context, the negativity or positivity of your thoughts isn’t what’s important. It’s how you respond to those thoughts that matters. Going back to the example above — “There is something wrong with me” — instead of fighting against that thought or trying to distract yourself from it, you could notice this thought without getting attached to it (become mindful), understand that it is common to all humans and part of our shared experience as people, and then treat yourself kindly instead of beating yourself up.

Does this approach really work better than simply improving self-esteem?

It seems it does.

A just-published longitudinal study that followed 2,448 ninth graders for a year found that low self-esteem had little effect on mental health in those who had the highest levels of self-compassion. That means that even if they had negative thoughts, those thoughts had minimal impact on their sense of well-being over time as compared to peers who didn’t have self-compassion skills.6

This suggests that teaching kids who suffer from self-esteem issues to be more self-compassionate may have more benefit than simply trying to improve their self-esteem.

The question is: How do we do that?

As it turns out, this is exactly where ACT excels.

Using ACT to Enhance Self-Compassion

Knowing that enhancing self-compassion has been shown not only to mitigate problems with self-esteem, but also impacts other conditions including traumatic stress. Jamie Yadavaia decided to see in his doctoral project if we could enhance self-compassion using ACT.

The results were promising.

A group of 78 students 18 years or older was randomized into one of two groups. The first group was put in a “waitlist condition” which basically means they received no treatment. The other group was provided with six hours of ACT training.

As anticipated, ACT intervention led to substantial increases in self-compassion over the waitlist control post-treatment and two months after the intervention. In this group self-compassion increased 106 percent — an effect size comparable to far longer treatments previously published. Not only that, but the ACT treatment reduced general psychological distress, depression, anxiety, and stress.

At the heart of all these changes was psychological flexibility, this skill seemed to be the key mediating factor across the board, which makes sense. After all, learning how to become less attached to your thoughts, hold them in mindful awareness, and respond to them with a broader repertoire of skills — like self-kindness, for example — has not only been posited in the self-compassion literature as a core feature of mental health but proven time and again in the ACT research as essential for it.

Taken together these studies have an important lesson to teach all of us.

It’s time for us to put down the idea that we have to think well of ourselves at all times to be mature, successful, functional, mentally healthy individuals. Indeed, this toxic idea can foster a kind of narcissistic ego-based self-story that is bound to blow up on us. Instead of increasing self-esteem content what we need to do is increase self-compassion as the context of all we do. That deflates ego-based self-stories, as we humbly accept our place as one amongst our fellow human beings, mindfully acknowledging that we all have self-doubt, we all suffer, we all fail from time to time, but none of that means we can’t live a life of meaning, purpose, and compassion for ourselves and others.


A 70 year old man who dumped almost a quarter of a tonne of pornography in a Japanese park is unlikely to be charged, police said Tuesday, because the stash belonged to an ill friend. Hideaki Adachi was spotted unloading 17 sacks of films and magazines, which included around 500 VHS video tapes, from the back of a truck at a small park in the western Japanese city of Osaka.

Adachi was arrested on suspicion of illegally dumping the 200 kilograms (440 pounds) of porn, but was released the next day after telling police he had found the trove in a storehouse belonging to a bedridden friend, police told AFP.

“He wanted to get rid of them out of goodwill for his friend,” a spokesman said.

Asked if he had left the library in the park with the intention of giving the material away, the spokesman said officers thought not, because “the videos were not laid out to be seen”. Adachi, who worked as a volunteer in the park helping homeless people, had hoped that the huge collection of adult materials would be picked up and taken to a proper disposal site.


Earlier this month, in Kansas City, Missouri, the Jackson County Sheriff’s Department was out looking for people. And when they spotted a subject, they went after them, in a sting operation the likes of which this country has never seen.

What made this operation especially unusual was the man behind it: a fellow in a red hat — known to these men only as “Secret Santa.”

Every year this anonymous, wealthy businessman gives out about a hundred thousand dollars worth of hundred dollar bills to random strangers. But this year, instead of doing it all himself, he deputized these deputies to give away much of it.

“Let’s start with a thousand,” Secret Santa said as he gave the deputies the money.

And so, armed to the teeth with Benjamins, the officers went out to do Santa’s bidding. They specifically went after people they thought would appreciate it most. Cars driving while dented — or out on Bondo — were likely targets.

“Merry Christmas,” a deputy said while handing money to a driver.

“You’re kidding. Oh my God, no,” answered the driver in disbelief.

Most people weren’t just blown away — most people were moved to tears. Their reactions were a combination of really needing the money and being caught off guard.

We saw Jessica Rodriguez, a mother of three, get pulled over. While the deputy walked to her car, Rodriguez talked to someone on her cell phone to tell them she’d been pulled over for “no cause.”

“How you doing, m’am?” the deputy asked her.

“I’m good until you pulled me over,” she answered.

“Okay, well, on behalf of Secret Santa, he wants you to have this, OK?” the deputy said as he handed her money.

Rodriguez told the deputy he saved her Christmas.
“I wasn’t going to be able to get my kids anything,” she told him.

“Well, I hope you may be able to get your kids something with it,” he said.

As always, creating moments like that is the main mission here. But this year “Secret Santa” also had a secret agenda.

“What do you want the officers to get out of this?” I asked him.

“Joy,” he answered. “You know, as tough as they are they have hearts that are bigger than the world.”

Let’s face it, it hasn’t been a good year for law enforcement — but for the vast majority of decent officers who will never make headlines — Secret Santa offered this gift.

A chance to be bearer of good news for a change, a chance to really help the homeless, to thank the law-abiders, to see hands up in celebration and then be assaulted in the best possible way.

There were a lot of hugs. Our body cameras took a real beating, but it was worth it — just to see people trust again and to see cops surrender.


The Abraham Lincoln Presidential Library and Museum wants all armchair historians to volunteer for a special project they can do from home.

The library needs help transcribing 30,000 pages of historical documents.

Volunteers would get a look at the document, then type out what they see. Officials say the papers give unique insight into the day-to-day experience of living in Illinois during the Civil War.

Documents like these would ordinarily not be transcribed, leaving researchers to dig through them as they try to find something related to their topic. But in crowdsourcing the project, the library hopes to create a searchable database available to researchers around the world.

If you’re up for the challenge, visit ChroniclingIllinois.org and click on “Transcriptions.” That takes visitors to a page with links at the top and bottom to create an account. After you sign up, a confirmation will be sent to your email. Click on it and then go back to the Transcriptions page to select a document and begin.


Thanks to Beth Pieper for bringing this to the attention of the It’s Interesting community.

By Peter Shadbolt for CNN

A bio-drone that dissolves after use leaving no trace it ever existed may sound like the stuff of a James Bond film, but NASA and a team of researchers are actually building one.

Made from a substance that combines mushroom fibers and cloned paper wasp spit, the drone might resemble a propeller-powered egg carton, but its designers say it has the ability to fly into environmentally sensitive areas and leave almost no trace.

Lynn Rothschild, the NASA developer guiding students from Stanford-Brown-Spelman working on the project, says the drone could be made to disappear simply by ditching it into a stream or puddle.

She said her interest in unmanned aerial vehicles was sparked by work on environmentally sensitive areas in her Earth Science group at NASA.

“Periodically, UAVs get lost — for example on coral reefs or in other sensitive habitats,” she said in an interview with the project team.

“As I started to hear about this, I thought, ‘Well, wouldn’t it be useful if the UAV was biodegradable, so if it crashed somewhere that was sensitive, it wouldn’t matter if it dissolved.”

The mushroom-like substance known as mycelium, which makes up the chassis of the drone, is being hailed as the new plastic — a plastic that has the advantage of degrading quickly.

The team grew cellulose “leather” to coat the fungal body of the flying craft and then covered the sheets with proteins sourced from the saliva of paper wasps — a water resistant material that the insects use to cover their nests.

The circuits are printed from silver nanoparticle ink in an effort to make the machine as biodegradable as possible.

Despite a heavy preponderance of biological parts, the team said the project had its limits.

“There are definitely parts that can’t be replaced by biology, ” said Stanford University’s Raman Nelakanti.

At its first short flight at the International Genetically Engineered Machine competition in Boston, the team used a standard battery, motor and propellers to fly the drone.

Nevertheless, the team is working on making other parts biodegradable and is studying how to build its sensors from modified E. coli bacteria, the bacteria most commonly found in the intestines of humans and animals.

The team said that ultimately the drone could be sent into areas where it might not be expected to return such as wildfires or nuclear accidents, sending data and never coming back.

While the parts degrade naturally, the team also experimented with enzymes that would help the drone self-destruct, breaking it down further on impact.

Creating a drone that does not infect the environment has been another challenge for the team.

“If you have living organisms acting as biosensors and the plane crashes, there certainly could be problems as the plane interacts with the environment,” Rothschild said.

“Hopefully people could think of this in advance, and design such that this never becomes a problem.

“For example, on crashing, the cells might die. Or the cells could be attenuated. There are all sorts of other processes to keep them from contaminating the environment. But that, to me, is the largest concern with a biological UAV – having living things on the UAV.”


Erika Check Hayden
Nature Medicine 20,1362–1364(2014)doi:10.1038/nm1214-1362Published online 04 December 2014

In 1889, the pioneering endocrinologist Charles Edouard Brown-Séquard told Parisian doctors that he had reinvigorated himself by injecting an extract made from dog and guinea pig testicles. Thousands of physicians began administering the extract—sold as “Elixir of Life”—to their patients. Though other researchers looked derisively on his salesmanship, his was among the early investigations that led to the eventual discovery of hormones.

The quest to end aging, rife with bizarre and doomed therapies, is perhaps as old as humanity itself. And even though researchers today have more sophisticated tools for studying aging, the hunt for drugs to prevent human decay has still seen many false leads.

Now, the field hopes to improve its track record with the entrance of two new players, Calico, which launched in September 2013, and Human Longevity, which entered the stage six months later. South San Francisco–based Calico, founded by Google with an initial commitment of at least $250 million, boasts an all-star slate of biotechnology industry leaders such as Genentech alums Art Levinson and Hal Barron and aging researchers David Botstein and Cynthia Kenyon. Human Longevity was founded by genome pioneer Craig Venter and hopes to use a big data approach to combat age-related disease.

The involvement of high-profile names from outside the aging field—and the deep pockets of a funder like Google—have inspired optimism among longevity researchers. “For Google to say, ‘This is something I’m putting a lot of money into,’ is a boost for the field,” says Stephanie Lederman, executive director of the New York–based American Federation for Aging Research, which funds aging research. “There’s a tremendous amount of excitement.”

The lift was badly needed; in August 2013, a major funder of antiaging research, the Maryland-based Ellison Medical Foundation, founded by billionaire Larry Ellison, had said it would no longer sponsor aging research. But so far, neither Calico nor Human Longevity has progressed enough to know whether they will be able to turn around the field’s losing track record, and the obstacles they face are formidable, say veterans of antiaging research.

“We’ve made inroads over the past 20 years or so,” says molecular biologist Leonard Guarente of the Massachusetts Institute of Technology in Cambridge, who has founded and advised high-profile companies in the space. “But I think there’s a long way to go.”

Pathway to success?

Calico appears to be taking the approach that worked for Barron and Levinson at Genentech, the pioneering biotechnology company that has become among the more successful drug companies in the world by making targeted medicines—largely engineered proteins—that disrupt disease pathways in diseases such as cancer. The hallmark of Genentech’s approach has been to dissect the pathways involved in disease and then target them with biotechnology drugs. This past September, Calico announced an alliance with AbbVie, the drug development firm spun out of Abbott Laboratories in 2013. In that deal, Calico and AbbVie said they would jointly spend up to $1.5 billion to develop drugs for age-related diseases including neurodegenerative disorders and cancer.

Such an approach is representative of one way to cure aging: targeting the diseases that become more prevalent as people grow older. This follows the argument that treating such diseases is itself treating aging. The opposing view is to see aging as an inherently pathological program that, if switched off or reprogrammed, could be halted. But because regulators don’t consider the progression of life itself a disease, the semantic debate is moot to drug companies: they can only get drugs approved by targeting diseases that become more common with age, such as cancer, diabetes and neurodegenerative disorders.

Calico has a close view on disease targets. In another September announcement, the company revealed one of its first development areas: drugs related to a class of compounds called P7C3s, which appear to protect nerve cells in the brain from dying by activating an enzyme called nicotinamide phosphoribosyltransferase that inhibits cell death. The P7C3 compounds, discovered in 2010 by researchers at University of Texas Southwestern in Dallas, have been tested in numerous models of neurodegenerative diseases associated with aging, including Alzheimer’s disease and Parkinson’s disease.

The AbbVie and P7C3 deals signal that Calico may focus on a traditional drug development strategy aimed at developing drugs that affect molecular players in the aging process in animal models. That approach makes sense to many who have been in the field for a long time, who say there is still much to learn about the molecular biology of aging: “The way Calico has said they are approaching this is the right way, which is to understand some fundamental aspects of the aging process and see how intervening in them affects that process,” says George Vlasuk, the chief executive of Cambridge, Massachusetts–based Navitor Pharmaceuticals and former head of the now defunct antiaging company Sirtris Pharmaceuticals.

But so far that approach has been difficult to translate successfully into interventions that delay aging or prevent age-related disease. For the most part, the biology of aging has been worked out in animal models; Kenyon’s foundational discoveries, for instance, were made in Caenorhabditis elegans roundworms. But the legion of companies that have failed to commercialize these discoveries is large, and some in the field now think that further progress can be made only by studying human aging. Screening for drugs that affect lifespan in model organisms such as yeast and nematodes is a gamble, says physician Nir Barzilai of the Albert Einstein College of Medicine in New York, who leads a large study of human centenarians. “I’m not sure those are going to be so important.”

Human focus

Craig Venter is squarely in the camp of those who believe the focus must shift towards humans. His Human Longevity is taking a big data dive into human aging, planning to sequence the genes of up to 100,000 people per year and analyze a slew of phenotypic data about them, including their protein profiles, the microbial content of their bodies and digitized imagery of their bodies. “We’re trying to get as much information as we can about humans so that we can find the components in the human genome that are predictive of those features,” Venter told Nature Medicine. “The model organism approach has largely failed. There’s only one model for humans, and that’s humans.”

Venter has a point, according to Judith Campisi, a cell and molecular biologist at the Buck Institute for Age Research in Novato, California. “We now have lots of targets, so I think there’s room for optimism,” she says. “But we’re still swimming in a sea of ignorance about how all these pathways and targets are integrated and how we can intervene in them safely.”

Michael West, CEO of the California-based regenerative medicine company BioTime, knows this well. In 1990, West founded a company, Geron, with $40 million from Silicon Valley venture capitalists such as Menlo Park, California–based Kleiner Perkins, dedicated to activating an enzyme called telomerase to forestall human aging. Telomerase activity, discovered in 1984, extends telomeres—the ends of chromosomes, thought to function as timekeepers of the age of a cell. But researchers soon found that human cancer cells have overactive telomerase, and it’s now thought that telomerase serves a highly useful function as a defense against unchecked cell growth that could lead to cancer1. Geron has shifted its telomerase strategy to blocking telomerase to fight cancer; it no longer works on longevity. “The focus on aging was abandoned,” West says.

Other companies, however, carried forward with the search for drugs against aging, inspired by a 1982 finding that mutating some genes in roundworms could enable them to live longer2. For example, one mutant lived for an average of 40% to 60% longer than normal, and at warm temperatures more than doubled its maximum life expectancy from 22 to 46.2 days. It was the first demonstration that aging was not an inevitable process. The work triggered a flurry of activity to find genes linked to aging and use them in interventions to stave off age-related disease.

Companies rooted in this strategy include Elixir Pharmaceuticals, cofounded in 1999 by Guarente and Kenyon, and Sirtris, established in 2004 by one of Guarente’s former students, David Sinclair. Kenyon had discovered genes in nematodes that extended life; with Guarente, she hoped to make drugs that could do this in humans. Guarente and Sinclair founded different companies, but both were interested in a pathway discovered at MIT that, they believed, acted similarly to a drastic treatment, called calorie restriction, long known to extend the lives of rats. If the rats were fed 40% fewer calories than normal, they could live up to 20–40% longer than the average rat. Guarente’s lab discovered that boosting the dose of genes called sirtuins could prolong the lives of roundworms3, and Sinclair published similar evidence in yeast. They thought that sirtuins worked through the same pathway as calorie restriction and that this same pathway was targeted by a naturally occurring compound called resveratrol found in red grapes and red wine. Both companies began looking for chemicals similar to resveratrol that, they predicted, might ultimately cure aging.

Sirtuin stepbacks

UK-based GlaxoSmithKline bought Sirtris for $720 million in 2008, a move seen as an important endorsement of that “calorie restriction mimetic” strategy. But other researchers were not able to reproduce some of Sinclair’s key studies4—for instance, those showing that resveratrol exerted its antiaging effects through sirtuins. It was also later found that the kind of diet fed to lab mice could affect whether or not sirtuins extended their lifespans; those eating a very high-fat diet seemed to benefit5, but it wasn’t clear that this was the most relevant model for human beings. Similar arguments about diet composition have yielded conflicting results for calorie restriction studies in monkeys and have raised the question of whether animal models of caloric restriction that appear to find a benefit are really just proving that bringing fat animals down to normal weight helps keep them disease free, thus extending lifespan.

Last year, GSK closed Sirtris, absorbed its drug development work and laid off some of Sirtris’s 60 employees. Elixir shut down some time after 2010, having burned through $82 million in venture capital.

The Sirtris experience underscored the unpredictability of aging research. Since the field does not agree on biological readouts of aging, such as altered signaling of certain pathways or expression of particular molecules that serve as proximate measurements of the aging process, the only way to do these studies was to follow animals until they died in order to record their lifespan.

The US National Institute on Aging stepped in, organizing a 1999 meeting that led to the Interventions Testing Program, aimed at bringing some order to the field. The program would systematically run experiments of candidate life extension treatments in mice at three separate sites. The hope was that the studies, which began in 2004, would help identify candidate life extension interventions that most deserved to be taken forward.

Already, most researchers agree, the program has succeeded in building more consensus around some drugs. One of the winners from the program so far, for instance, has been rapamycin, a relatively old drug given to kidney transplant recipients and some patients with cancer. In 2009, the drug was shown to extend the lives of genetically diverse mice7. (Resveratrol failed to prolong mouse lifespan in these same studies.) It was also shown to work in much older mice—the equivalent of about 60-year-old people—than had been studied in previous experiments, a situation that researchers say is much more relevant to the way antiaging drugs would be used in human patients. “You’re not going to give these drugs to teenagers,” says Matthew Kaeberlein of the University of Washington in Seattle. “You’ll probably want to give them to people who are certainly post-reproductive, and perhaps in their 60s and 70s.”

Strong signals

Rapamycin suffers from some of the same issues as previous failed antiaging treatments. It’s an old, unpatentable drug, like resveratrol, and has side effects such as a diabetes-like syndrome when given to transplant patients, who continue to take the drug for life after their surgeries. The side effects are worrying for a potential medicine that might be given over years to delay aging. But the signal from the rapamycin studies in mice is so strong that it’s now seen as one of the most promising leads in aging research, even despite these problems. Navitor, for instance, is looking for compounds that influence the mTOR, short for the ‘mammalian target of rapamycin’, pathway, through which rapamycin seems to extend lifespan. The pathway has the potential to influence a wide range of diseases, including neurodegenerative, autoimmune, metabolic and rare diseases and cancer. That’s been enough to entice investors to fund a $23.5 million financing in the company in June. By targeting a specific branch of the mTOR pathway, Navitor hopes they can elicit the benefits of rapamycin without its side effects.

Vlasuk says that companies like his now focus on treating age-related diseases rather than trumpeting the potential to cure aging itself and all associated maladies. “I’m acutely aware that I don’t want to be caught up in the same hype cycle that Sirtris was at one time,” Vlasuk says.

The field is also maturing in other ways. For instance, there’s a growing realization that the people who wish to take life extension drugs will be more old than young, but that it might be difficult to reverse age-related pathology once it has already set in.

Meanwhile, young researchers are taking the field in new directions. In May, three groups published results of experiments in which they transferred blood or blood products from young to old mice. They showed that the technique can rejuvenate muscle, neurons and age-related cognitive decline. A batch of companies is now forming to translate the finding into people; one, privately funded Alkahest, has begun enrolling patients into a study that will test whether blood donated from young adults and infused into patients with mild to moderate Alzheimer’s disease can improve their symptoms. Importantly, says regenerative biologist Amy Wagers of the Harvard Stem Cell Institute in Cambridge, Massachusetts, one of the pioneers of this approach, it seems to reverse some signs of age-related disease: “This notion that you can do some good even after pathology begins means its much more likely that we can come to a place where we can support people with more healthy aging,” she says.

The challenge of clinical trials for aging-related illnesses is familiar to the brains behind the newest antiaging companies. One solution could be to prove that an intervention prevents the sick from becoming sicker. It’s long been suspected, for instance, that the diabetes drug metformin has antiaging properties, but it can have potential side effects because it inhibits glucose production by the liver, so it can’t be given to healthy people. This year, however, UK-based researchers reported in a large retrospective trial that patients with diabetes taking metformin lived a small but significantly longer time than both diabetics taking another class of drugs and healthy people who were not taking metformin.

Barzilai has been impressed enough by these and other findings to try to round up funding for an international clinical trial to test whether metformin or some other drug improves health of the elderly by delaying the onset of a second disease in those who begin taking it when they are newly diagnosed with diabetes. He argues that second diseases, which can include cancer, become much more likely once a patient has been diagnosed with a first. Preventing the onset of a second disease is a way of extending longevity, he argues, by reducing the disease burden in any one patient. “Let’s show that we can delay aging and delay the onset of a second disease,” he says. “If we can do that, we can make FDA [the US Food and Drug Administration] change its review process and look at better potential drugs that delay aging.”

The challenges of testing treatments in patients with age-related diseases, such as Alzheimer’s, are formidable. Hal Barron knows this well; he presided over a failed Genentech trial of an antibody called crenezumab, which was designed to alleviate symptoms of mild to moderate Alzheimer’s disease. Still, that hasn’t deterred him or Levinson from going all in on neurodegenerative diseases with Calico.

“Art Levinson is one of the smartest guys around in terms of his perception of what drug discovery can do,” Vlasuk says. “His involvement in Calico and the group that he’s assembling there and the backing that Google has provided for this has really opened a lot of people’s eyes.” The question now is what Levinson, Venter and others are seeing—and whether it will be enough to lead aging research to finally fulfill its potential.