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Archive for the ‘Longevity’ Category

The 10 new cars owners keep the longest are mostly sports cars, SUVs – INSIDER

Friday, October 11th, 2019

The new cars that owners keep the longest before reselling are mostly sports cars and SUVs, according to a study by car search engine iSeeCars.com.

Most owners keep their new cars for an average of 8.4 years, but the ten vehicles on the list averaged 9.7 to 11.4 years.

Almost all the sports cars on the list with the exception of the Porsche 911 in the coupe body style are the convertible versions. iSeeCars CEO Phong Ly claims this is because convertibles are the least-driven type of car and typically amass 60% fewer miles than the average car.

Read more: The 10 cars owners ditch after less than a year more than any other, according to data

"Sports cars typically aren't daily drivers and don't accrue high mileage as a result, so it takes them longer to show signs of wear and tear," Ly said in a prepared statement. "Because sports cars aren't typically used as primary vehicles, owners likely aren't as concerned with having the latest and greatest technology and safety features."

iSeeCars.com analyzed over 5 million cars to identify which models were kept the longest before being sold by their original owners between January 1, 2014 and December 31, 2018. Cars owned for less than five years were excluded from the data set.

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Push-ups? Here’s what can really help you live to a ripe old age – The Australian Financial Review

Friday, October 11th, 2019

The problem with any of these approaches is that you would just be training for a particular test, which misses the point. It's not the push-up itself that makes you live longer; it's that you are still strong and nimble enough to execute one.

What these tests have in common is they're good shorthand of things that matter for longevity: overall health, fitness and muscle strength. A fit person walks faster than someone out of shape, and getting up off the floor is tricky for people with weak bones and muscles.

"Frailty is a really bad thing starting in middle age, and even worse as you get older," says Michael Joyner, a physician and human physiology researcher at the Mayo Clinic.

One way to think of longevity is "not as some magic property of a body, but as the lucky state of not having a fatal disease", says Steve Cole, professor of medicine and psychiatry and bio-behaviouralsciences at the UCLA School of Medicine. "By and large, people don't die of being old; they die of disease." Therefore, the study of longevity is a way of looking at disease risk or the rate of disease development, he says.

Over the years, various drugs and nutritional supplements have been studied for their potential to help us live longer, but nothing has been shown to work in humans to the extent that would be required for the Food and Drug Administration's approval, says Gordon Lithgow, chief academic officer at the California-based Buck Institute for Research on Aging.

While researchers continue searching for a pill to extend life, you'll have to try these verified methods.

The most powerful way to promote longevity and improve your long-term health is also simple and, depending on how you do it, free.

"There's no question that exercise is the biggest anti-ageing medicine there's ever going to be - it's really huge," Lithgow says.

"Hands down, nothing compares to exercise," says Laura Carstensen, founding director of the Stanford Center on Longevity. "The great thing is that most people can do it, and you don't need 10,000 steps per day to get the benefits." It takes remarkably little exercise to get longevity benefits.

Even 10 to 15 minutes a day provides measurable rewards, says Michael Joyner, a physician and human physiology researcher at the Mayo Clinic. Going from sedentary to even just a bit of exercise is where you get the biggest payoffs. The health benefits - such as reducing your risk of heart disease and diabetes - increase with greater amounts of exercise, until you get to about an hour of exercise per day. After that, the rewards start to level off.

"Almost anyone doing more than that is doing it for things other than health," Joyner says.

Go ahead and train for that Ironman if that's what you want, but if you're exercising for health and longevity, you don't need to run a marathon. Work by Iowa State University epidemiologist Duck-Chul Lee suggests that even running a little less than 10 minutes a day could decrease your mortality risk by about 30 per cent.

But you don't have to run. Walking or other moderate activities are just as good if you're looking for a longevity boost.

Some of the early evidence for the heart benefits of moderate exercise came from studies in the 1950s by British epidemiologist Jeremy Morris showing that conductors on double-decker buses, who spent their shifts walking up and down, had lower rates of coronary heart disease and thus lived longer than bus drivers who spent their workday sitting. Since then, studies showing the cardiovascular benefits of exercise have been "incredibly consistent", Joyner says.

But there's more. Physical activity also reduces the risk of diabetes, which one study found shaved six years off life expectancy.

And it keeps your brain healthy, too. "Exercise has better effects on cognitive performance than sitting around playing brain games," Carstensen says. A 2006 study in Neuroscience found that exercise spurs the brain to release growth factors that promote new connections between neurons, keeping the brain healthy. There's even research suggesting that strength training can reverse some age-related changes in your muscles.

There seems to be something about keeping an active lifestyle, too.

When you look at centenarians as a group, they might not be Arnold Schwarzeneggers, but they typically maintain a high level of physical function, says author Bill Gifford, who interviewed quite a few of them while writing his book, Spring Chicken: Stay Young Forever (Or Die Trying). "They can go up and down stairs, probably because they never stopped going up and down stairs," Gifford says.

His research for the book spurred him to make sure he was exercising at least a little bit every day.

Extend your life span while you sleep. It sounds like a bad infomercial, but it turns out that sleeping well is a good way to keep your body healthy for the long haul. Sleep is a time when your brain gets caught up on maintenance. In 2013, a team led by Maiken Nedergaard at the University of Rochester Medical Center published a study in Science concluding that sleep helps the brain clear out metabolic waste that accumulated during waking hours, providing a kind of restorative maintenance.

Skimp on sleep, and you hinder this important work.

If you've ever missed a night of slumber, you know that sleep deprivation hampers your mood and makes it hard to think clearly, but it can have severe consequences for your metabolic health, as well. Take someone who needs seven hours of sleep a night and restrict them to only five hours of shut-eye for five nights and they experience metabolic changes that look a lot like diabetes, says Satchidananda Panda, who studies circadian biology at the Salk Institute for Biological Studies.

Indeed, numerous studies have shown that sleep deprivation can decrease insulin sensitivity - a measure of how well your body regulates blood sugar - and increase your risk of diabetes. A 2015 meta-analysis found that Type 2 diabetes risk was higher in people who sleep less than seven hours or more than nine hours, compared with people who got seven to eight hours a night.

So why is sleeping more than nine hours associated with greater mortality? "People who sleep 14 hours per day are probably not healthy," Carstensen says, but it's hard to say right now whether it's possible to get too much sleep. Most people are on the other end of the spectrum.

Regularly sleeping too long may indicate a health problem

The consensus among sleep researchers is that seven to eight hours of sleep is ideal, but that's just a best guess based on the current data, Carstensen says.

"The biggest problem is that most of the data is self-reported and people are really bad at that," Carstensen says.

The advent of sleep trackers can help with the measurements, but they aren't always accurate, so avoid fixating too much on the exact numbers or you may end up in a cycle of anxiety that prevents you from sleeping. The problem is common enough that researchers have coined a term for it - orthosomnia.

Don't make a habit of skimping on sleep during the week with the idea that you'll catch up on the weekends. It doesn't take many nights of short sleep to reduce insulin sensitivity, and a small study published this year in Current Biology found that recouping on sleep over the weekend didn't entirely make up for the metabolic problems that developed during sleep deprivation. Furthermore, when volunteers in the study were given the opportunity to catch up on sleep over the weekend, they ended up shifting their body clocks so that it became harder to get up on Monday morning.

(Getting enough sleep every night might also improve your work life. In the throes of writing his book, Gifford made a decision to start prioritising sleep over work. His deadline was fast approaching, and he'd been getting up early and staying up late. Allowing his body to sleep as long as it needed to led to a "radical transformation in my ability to write", Gifford says. "I'd been trying to work 14 hours per day, and then suddenly I was getting twice as much done in six or seven hours.")

Forget all those headlines you've seen about "anti-ageing diets" and anti-aging "superfoods".

"These notions are generally not supported by science," Lithgow says. That's not to say diet isn't important, only that "nutrition is just a very difficult science", he says.

Severely restricting calories in lab animals makes them live longer, but "it's not clear that it works in humans", Lithgow says. Although there's plenty of evidence that it's not good to overeat, he says, whether drastically limiting food intake can extend life in people remains an open question. The joke, of course, is that calorie restriction will surely make your life seem longer.

It might be possible to get some of the benefits of calorie restriction without giving up so much food. Intriguing work by Panda suggests that restricting the timing of when you eat, rather than the amount, might provoke some of the healthy metabolic changes that reduce the risk of diabetes. Most of these studies have been done in mice, however, and Panda acknowledges that the human studies are small.

Although Panda is confident enough in the results to have written a book, The Circadian Code, which includes instructions on how to try it, some scepticism is warranted, Joyner says.

"Time-restricted eating has shown some interesting results in small studies," Joyner says, but "will it be sustainable over time in the real world? This is important because most dietary strategies work only if they are adhered to."

He says he wonders whether the metabolic benefits that Panda has found with time-restricted eating is really about the timing or simply related to people eating less when their dining hours are restricted. One thing shown repeatedly in anti-ageing studies is that things that initially look like magic bullets never live up to their initial hype, Joyner says.

What does seem clear, however, is that metabolic health is important for long-term health, because it keeps diabetes in check and that insulin sensitivity in particular appears crucial.

Given what we know right now, a Mediterranean diet - with its heart-healthy emphasis on fish, vegetables, fruits, nuts, healthy fats like olive oil, whole grains and limited consumption of red meat - "is probably the best approach for improving longevity", Carstensen says.

But the benefits are pretty modest. If you hate eating that way, then the payoff probably won't feel worth it to you, she says. At least try to eat a diet rich in fruits and vegetables.

The idea of red wine as a health elixir became popular in the 1980s with the observation that rates of coronary heart disease were low in France, despite the predominance of a diet relatively high in fat and cholesterol. The French penchant for a glass of red wine with dinner was proposed as an explanation for this "French Paradox", popularisingthe notion of red wine as heart helper.

Subsequent studies have indeed found that moderate alcohol consumption may reduce the risk of coronary heart disease, and a two-year randomisedclinical trial in Israel showed that people with Type 2 diabetes who were assigned to drink a glass of red wine with dinner every night experienced some improvements in blood markers associated with cardiovascular disease risk.

But other studies suggest that alcohol may raise the risk of many cancers, and a report published last year in the journal Lancet concluded that there's no amount of alcohol that improves health. What gives?

"Alcohol studies are very much like nutrition studies - based almost exclusively on self-reports, and we know that people are really bad at self-reporting," Carstensen says. "Most people, when they say they're drinking two drinks per day, are probably consuming more. We don't know the amounts that people are consuming nor do we know what else they do."

There's some evidence that people who abstain from alcohol are sicker or less healthy than those who imbibe a little.

"That probably reflects not a lack of alcohol in their system, but something about their world - that they're sick or isolated or don't have friends to meet at the pub," Carstensen says. "I've never seen a study that's really controlled for all of those factors." Which means that the studies calculating the health consequences of alcohol consumption depend on consumption figures that are inherently unreliable and may fail to account for other factors that could be at play.

Drinking to excess - more than one or two drinks a day - is unhealthy, and will take a toll on your longevity - no doubt about it. But taking the published studies together, "I don't think we have a lot of evidence that moderate alcohol is bad for you," Carstensen says. At the same time, she'd "be very hesitant to recommend that people who don't drink should start".

In today's world, it's easy to live in a state of chronic stress, and the problem isn't just that stress feels lousy. It also makes you more susceptible to diseases that could shorten your life.

Researchers are now learning that many conditions associated with older age - such as cancer, heart attacks and Alzheimer's disease - share a common ingredient: inflammation.

Under normal conditions, inflammation is simply the body's response to injury - it's how the body heals cuts and wounds and other insults, Cole says. "Inflammation by itself is not inherently evil." But when we're feeling chronically threatened or under siege, our bodies amp up their inflammatory machinery to ready our biological response to injury, and that inadvertently fuels the development of an array of age-related diseases, where inflammation is a common fertiliser, Cole says.

Research has identified chronic stresses that can provoke harmful biological changes, including living in poverty, caregiving for a dying spouse, losing a loved one, suffering post-traumatic stress disorder, and experiencing prejudice.

"Any way of feeling threatened or insecure seems to be enough to activate the body to produce more inflammation," Cole says. "This is one of the best defined connections between the world as we experience it and how we end up generating a body that's a fertile ground for the development of these diseases."

Your chance of developing chronic inflammation also rises with the passing years. "Inflammation seems to be a general sign of aging, where our inflammatory processes are being turned on or accumulated," Lithgow says. "Age-related inflammation is very much like inflammation from an injury, but now it's coming on without a source of infection."

What's the antidote? "Obviously we should all just be happy," Cole says with a laugh, as if it were that easy. He knows that it's not and says you probably can't eliminate stress from your life, but you can find ways to manage it. Identify the recurring stressors in your life, and work on a plan to diffuse them.

Wellness strategies such as yoga, tai chi and meditation can reliably help diffuse stress, Cole says, although he acknowledges that they often don't make a huge difference.

Forging connections with other people has been found to be a powerful way to manage stress and improve your overall wellbeing.

"People who report having stronger relationships live longer than people who are socially isolated," Carstensen says. A meta-analysis published in 2015 calculated that loneliness and social isolation were associated with 29 per cent and 26 per cent increases in mortality risk, respectively, and living alone was linked to a 32 per cent increase risk of dying.

What's clear is that people who have a strong sense of purpose and meaning in their lives have a markedly lower risk of death than those who don't.

"How we can bottle that and make it useful is more of a challenge," says Cole, who has studied loneliness and longevity.

Telling a lonely person to stop being lonely doesn't work, Cole says, "but if you can go to the lonely person and say, 'Hey, we really need your help. Is there anything you can do to help others?' - that is incredibly powerful. The mechanism here seems to be turning attention away from yourself and your own suffering and toward a community or cause greater than yourself."

Centenarians tend to have a sense of purpose in their lives.

"It's really important that people who are entering the later phases of life have a clear purpose, something to get up for every day," Lithgow says. That thing can be anything from looking after a grandchild or working or tending a garden.

Many centenarians continued working into their 80s, 90s and beyond, Lithgow says, and usually these jobs are in environments where they interact with younger people.

Interacting with other generations can keep older people engaged, and some retirement communities and nursing facilities are now taking steps to give their residents opportunities to connect with kids - for instance, placing kindergarten classrooms in nursing homes.

Most of the proven tips for living a long, healthy life are not products that you buy, but good lifestyle habits that you adopt (or bad ones, such as smoking, that you either quit or never take up and are clearly associated with diminished longevity).

Even something as simple as always wearing a seat belt can reduce your chances of dying early. Most of the things that make up a longevity lifestyle are simple - exercise, eat (and drink) healthily, sleep adequately, stay engaged - if only people would do them.

"To me, the bottom line is: Live a reasonably moderate life and you'll be OK," Carstensen says.

Washington Post

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Insilico Medicine Becomes the Face of AI Drug Discovery – Nanalyze

Friday, October 11th, 2019

In many industries, theres usually one or two companies that become nearly synonymous with their particular market. One of the most obvious examples is Coca Cola (KO). Think about it: We still refer to a soda as a coke, even though the soft drink manufacturer allegedly abandoned using cocaine in its formulation long ago. In emerging technologies like artificial intelligence, its more difficult to pinpoint a clear leader in many cases. Nvidia (NVDA) is still the obvious choice for AI chips. After that, there are very few household names that represent anything close to a pure play in AI technology. However, one name has emerged in the last few years that has become the face of AI drug discovery: Insilico Medicine.

Regular readers will certainly recognize the startup as a key player in the longevity industry. Weve profiled the company on several lists here and here related to drug discovery, as part of our ongoing coverage of life extension science. September was a particularly good month for the Rockville, Maryland startup. At the beginning of the month, it published a paper in Nature Biotechnology that detailed its efforts to design and validate a drug candidate for treating fibrosis and other diseases in just 46 days, shaving off months if not years from the discovery process, not to mention saving millions of dollars. A week later, the five-year-old startup completed a $37 million Series B, bringing its total disclosed funding to $51.3 million.

Insilico Medicine co-founder and CEO Alex Zhavoronkov

We recently caught up with Insilico Medicine co-founder and CEO Alex Zhavoronkov, who is on a crusade to prove that automation will be a big part of the future of healthcare. We talked about the companys recent achievement in accelerating the drug discovery process; its open challenge to big pharma; Insilicos numerous partnerships and joint ventures; the difficulties in getting funding for longevity therapy research and development; and the AI hype surrounding healthcare in general.

We wont spend too much time dissecting Insilicos latest achievement, as thats already gotten plenty of press. You can find a good deep dive into the paper and its significance by Margaretta Colangelo, a managing partner at Deep Knowledge Ventures, which made some of the first investments in the company about five years ago. It wasnt just the fact that Insilico Medicines new AI platform, called Generative Tensorial Reinforcement Learning (GENTRL), accomplished the feat of designing and validating a drug in such a short timeframe. It was also the first time anyone had combined two AI techniques known as generative adversarial networks (GANs) and generative reinforcement learning for drug discovery. Both Colangelo and Zhavoronkov refer to the achievement as pharmas AlphaGo moment, referring to Google DeepMinds defeat of a professional Go player.

Insilico Medicines AI platform, called Generative Tensorial Reinforcement Learning (GENTRL), combines two AI techniques known as generative adversarial networks and generative reinforcement learning for drug discovery. Credit: Insilico Medicine

Zhavoronkov first presented the paper at a conference in Basal, Switzerland, hometown to two of big pharmas biggest players Roche and Novartis. The choice of venue was obviously intentional, as Insilico has actively sought the spotlight since it was founded in 2014 in order to prove the value of AI to improve human health and quality of life. In 2015, for example, a group of Zhavoronkovsstudents and colleagues founded, Youth Laboratories, listing him as an adviser. It was a machine vision company that focused on aging and skin health which made headlines in 2016 for hosting an online beauty contest, Beauty.AI, that was judged solely by machines and attracted a bit of controversy for picking mostlyfair-skinned people. That led to yet another project, Diversity.AI, an effort to use machine learning to make sure we all have an equal opportunity to be spied on marketed to. Last year, the company was named to CB Insights prestigious AI 100 list.

But back to Insilicos primary focus: defeating age-related disease. Zhavoronkov believes his companys AI platform has advanced to the point where it could automate drug pipeline development from end to end and produce a marketable drug within 24 months or less with the right kind of backing. So while its efforts have focused on pre-clinical activities like identifying drug targets and developing therapeutic molecules around those specific disease targets, Insilicos AI also boasts predictive powers.

Insilico Medicine applies artificial intelligence throughout the drug development pipeline. Credit: Insilico Medicine

We also work with some of our pharma partners on predicting clinical trial outcomes; we also analyze clinical trials data, said Zhavoronkov, who is looking to partner with a major pharmaceutical company on an XPRIZE-type challenge where Insilico races against the clock to develop the first drug fully developed using artificial intelligence and one that targets a rare disease. If no contenders emerge, Zhavoronkov said he still believes it will be possible to develop a viable drug using AI within four or five years.

He noted that investment banks are also interested in Insilicos AI predictive analytics around clinical outcomes. The reason for the attention is obvious: If investors can leverage a tool that can better predict the chance of success or failure of a particular drug, that would surely influence how much money if any they are willing to put into a particular project or company. Weve noted previously that venture capitalists are increasingly turning toward AI to guide their investments into the hottest startups.

While Insilico awaits to see what big pharma company will emerge to take up its challenge, it has plenty of other partnerships and ventures to juggle. In fact, the company just announced today a new collaboration worth up to $200 million with one of Chinas biggest pharmaceutical companies, Jiangsu Chia Tai Fenghai Pharmaceutical Co. The goal of the collaboration is to accelerate drug discovery for triple-negative breast cancer using artificial intelligence.

We actually started making those kind of advanced partnerships where we would plan to take products into [clinical trials] only recently, Zhavoronkov said, for about the last year or so.

He noted that his company has about 16 ongoing collaborations, including several with one of the key players in the longevity industry Juvenescence. One of the more advanced joint ventures with Juvenescence is with a company called Generait Pharmaceuticals that is targeting senescent cells, which are cells that have stopped dividing but continue to secrete inflammatory molecules that damage nearby cells and tissues, leading to disease and an earlier death. Generait has already identified several disease targets but Zhavoronkov could not go into details at this time.

A sampling of some of the deals and partnerships brokered by Insilico Medicine. Credit: Insilico Medicine

Another joint venture between Juvenescence and Insilico, which also includes the nonprofit Buck Institute for Research on Aging, is Napa Therapeutics. Insilico has already done its part and Napa is now working on several potential drug molecules that could help boost the levels of an oxidized compound called nicotinamide adenine dinucleotide (NAD+), which is involved in getting the power plant of the cell called the mitochondria revved up again. So far, the molecules look very good, Zhavoronkov said.

Many [partnerships] are with smaller companies, you know, where we do get less money up front, but we do get the data, he noted. We need their pre-clinical data so we can train [our algorithms].

While Zhavoronkov is obviously pleased to have just pocketed $37 million from investors like Chinese AI tech giant Baidu and a pharmaceutical firm like Eli Lilly and Company, he feels that respect for the longevity industry is still lacking. For example, few of Insilicos major investors backed the company because they are specifically interested in life extension science, according to Zhavoronkov.

They invested not because of longevity. I actually need to divest of some of my longevity-focused programs, he explained. They invested because of the generative chemistry. It works; they know it works. Thats a major disruption. So thats why they invested. They didnt consider longevity; longevity is not being perceived as credible in financial circles yet.

Legitimacy is also difficult to build when there is so much hype around artificial intelligence.

There are lots and lots of scientific charlatans very often re-positioning very old technology as AI, he said. Suddenly, every statistician within big pharma became an AI scientist.

In terms of direct competitors, Zhavoronkov noted that he deeply respects the work being done by San Francisco-based Atomwise, but the technology from others is mostly smoke and mirrors. Thats why Insilico is focused on publishing its work in peer-reviewed journals in order to back up its claims. The company has published about 60 papers in the last five years.

Thats because Zhavoronkov believes that there is nothing more important than longevity, whether youre talking about the big-picture economics of healthcare or living more productive, healthier years in the twilight of life.

The goal is to create the longevity economy, he said. So, in the next couple years, as we ingest a little bit more data and develop more advanced algorithms, we will be able to go after more complex problems.

If the longevity industry does live up to its lofty goals of becoming the biggest industry in human history, Insilico Medicine will likely play a major role in that success. Even if we dont all end up living as old as Moses, the potential to cure some of humanitys most debilitating diseases is too good to ignore. And, right now, no one is ignoring Insilico Medicine.

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‘NCIS’: How the Cast Feels About Not Receiving an Emmy – Showbiz Cheat Sheet

Friday, October 11th, 2019

Most would agree NCIS is a great show. It has a huge fan base and is one of the most-watched television dramas. However, the shows following hasnt translated into an Emmy award (at least not yet). Heres how the NCIS cast feels about the series being passed over for an Emmy after all these years.

Mark Harmon told Entertainment Tonight host Kevin Frazier he knows how fortunate he is to be part of NCIS. Harmon said he tells actors who decide to leave the show that theyre leaving a special place with a lot of support. He also reminds them theyre leaving one of the top shows in the world:

And if we can talk about awards or talk about whatever, the longevity of this show, I tell young actors all the time. I say, Hey, are you gonna leave? Thats great. Good luck. And I said, But you come here, and you have a chance to work every day with friends who are going to support you. You work with a tremendous safety net underneath you here that nobodys going to let you fail. And I said, And theyre paying you. And, oh yeah, by the way, its the number one show in the world.

Harmon told Frazier the people who are part of NCIS genuinely enjoy being there. He says its a family environment where everyone comes together to just chat and talk about whats going on in their personal lives. I think its great that people love it, and people enjoy it. And we all sit here and laugh and talk about our day and how we approach it. But theres a bunch of professionals here who know what theyre doing. And I dont know that this kind of thing in network television is going to happen again, Harmon said.

Frazier asked the cast how they feel about doing such great work but never receiving an Emmy. This show has done Emmy-caliber work, but youve never won an Emmy. When you think about that, does it bother you? he asked. Rocky Carroll, who plays NCIS Director Leon Vance, says he isnt bothered about the lack of an Emmy when he thinks about the fate of shows that have one multiple Emmy awards. I think of all the shows that have won multiple Emmys that are not on the air, that have run their course. And, you know, I say that jokingly, but there are a lot of shows that have stood on the podium and accepted Emmys, but theyre in the Where are They Now? file now. And were still here, Carroll said.

Brian Dietzen (Jimmy Palmer) says not receiving an Emmy doesnttake away from the fact that theyre a talented cast:

I do think that 16 years, longevity doesnt preclude it from having some pretty awesome performances. I mean, whether its guest stars or some of the people in these chairs. There have been some amazing performances this year. The fact that we dont get recognized for awards season, its a bummer. I think wed all love to see that happen and whatnot, but that doesnt mean that the good work isnt happening right here. The fact that the people who do watch this show, see that and appreciate it, I think thats kind of what we hang our hat on.

Read more: InsideCote de Pablo and Mark Harmons Sweet Relationship

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How long do timing belts last? | HowStuffWorks

Sunday, September 29th, 2019

Your car's timing belt is responsible for maintaining the precision that's crucial to your engine's functions. Essentially, it coordinates the rotations of the camshaft and crankshaft so the engine's valves and pistons move in sync. The expected lifespan of your timing belt is specific to your car and engine configuration, usually between 60,000 and 100,000 miles. (You can check your owner's manual or look online for your car's service schedule.)

The manufacturer's recommended intervals are a safe guideline; you probably won't need to replace your belt any earlier [source: Allen]. However, if you're approaching your service interval and have doubts about the belt's condition, you might as well get it replaced a little early. It'll be less expensive than waiting until after the belt breaks.

Why is it important to replace the timing belt on such a strict schedule? The belt is a synthetic rubber strap that contains fiber strands for strength. It has teeth to prevent slipping, which fit into the grooves on the end of the camshaft and crankshaft. It's a simple part for such an important function, and when it snaps, things get a lot more complicated. Unlike many car parts that gradually lose function as they wear out, a timing belt simply fails. Whether the belt breaks or a couple of teeth strip, the end result is the same. One minute, your car will be running perfectly; the next minute, it won't. You're in trouble if your car has an "interference engine," in which the valves are in the path of the pistons. If the camshaft or crankshaft moves independently in an interference engine, there will be at least one valve/piston collision. The fragile valves will bend, and you'll be faced with a costly repair.

It's easy to check the belt for signs of premature wear -- just locate it in the engine bay (usually under a plastic or metal shield that should be easy to remove) and check it for drying, fraying and discoloration.

The belt itself is inexpensive, probably costing less than $20 at an auto parts store. Your mechanic will probably charge several hundred dollars (or more) for a belt replacement service, though. Those hours spent dismantling and reassembling the engine bay add up quickly.

You can replace the timing belt yourself if you have access to the necessary equipment. In some cars, it's a straightforward procedure -- remove the engine covers and shrouds, line up the camshaft and crankshaft, slip off the old belt, and slip on the new one. Sometimes, though, it's a lot more complicated. For example, the timing belt might loop through a motor mount, in which case the mount would need to be removed to access the belt. You'd need an engine hoist or stand to safely remove and replace the mount [source: Juran].

Keep in mind that an error in this job, such as improperly turning the engine by hand or failing to coordinate the shafts, will cause the same damage as a snapped belt. Make sure you understand the procedure before getting started.

Need more help with the do-it-yourself approach? The next section will point you in the right direction.

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How long do windshield wiper blades last? | HowStuffWorks

Sunday, September 29th, 2019

Windshield wiper blades don't get the respect they deserve. They remove rain, snow and sometimes even ice and dirt from the windshield of your car and they do it quickly and smoothly, at the push of a button. They endure extremes of temperature, from sub-zero winter weather to scorching desert sunshine. They may have to operate for hours at a time. And yet they're made out of thin, flexible rubber -- not exactly the sort of material that can take this kind of abuse indefinitely.

This makes windshield wiper blades one of the hardest working -- yet least durable -- parts of your car. Over time, they'll crack, become misshapen or lose their flexibility. And don't think that just because you live in a sunny dry climate without much rain -- Southern California, for instance -- that your wiper blades will last longer. In fact, the heat and lack of moisture can damage the blades even if you never turn them on. Similarly, extremely cold weather can make the blades stiff and easily fractured.

Most experts say that wiper blades need to be changed every six to 12 months, though this depends both on weather conditions and on what the blades are made out of. Ordinary rubber blades have the shortest lifespan, halogen-hardened rubber blades last a bit longer, and silicone blades have the longest lifetimes of all, perhaps exceeding a year even under intense use. Of course they also cost more than ordinary rubber blades.

You'll know when your wiper blades need to be replaced because you'll see streaking as they wipe the moisture from the windshield or even large gaps where no water is being removed. They may start making squeaking or chattering sounds (though this can also happen if you run the wipers when the windshield is mostly dry). If left unchanged for too long, the material of the blade can shred and break loose from the arm. This can actually cause damage to your windshield, as the metal or hard plastic of the arm scrapes across the glass. You don't want this to happen.

Fortunately, you won't necessarily have to replace the entire blade assembly. Most blade arms will accept rubber refills, giving you the option of replacing only the part that's damaged. However, blade arms can become bent over time, so make sure that the refill is all that you need to replace in order to fix the problem.

For more information about windshield wiper blades and other related topics, follow the links below.

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Longevity | UNH Human Resources

Tuesday, April 23rd, 2019

Definition

Longevity is an extra pay increment awarded to Hourly-Paid staff (Operating Staff) with a current hire dateprior to July 1, 2011,to recognize length of service to the University System. Longevity payments are not treated as benefits eligible, but are taken into account when computing the regular rate for overtime purposes to conform with FLSA regulations.

Longevity increments for Operating Staff are as follows:

For purposes of longevity only, a year of service will be equal to a calendar year of employment, i.e., 12 consecutive months from date of hire equals one calendar year. If an employee held a flex-year appointment of 50% for 10 years, the total years of service for longevity purposes would be 10 years.

The longevity increment, awarded each pay period, is calculated by multiplying the base pay for that pay period by the longevity percentage. Longevity is not included in vacation or earned time payout on termination.

Length of employment will start from the first day of status employment of at least 50% time for employees with a current hire date prior to July 1, 2011.

Longevity increments shall be effective on the staff member's anniversary date of employment.

Staff members will not have their longevity affected by absences due to illness, accident or leaves of absence. Exceptions to this is when an accident is incurred at a staff member's secondary employment outside the University System.

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About the Center – Stanford Center on Longevity

Wednesday, March 27th, 2019

Life expectancy is ballooning just as science and technology are on the cusp of solving many of the practical problems of aging. What if we could not only have added years but spend them being physically fit, mentally sharp, functionally independent, and financially secure? At that point, we no longer have a story about old age. We have a story about long life.- Laura L. Carstensen, A Long Bright Future

In less than one century, life expectancy has increased by an average of 30 years in developed regions of the world. Quite suddenly, there are more people living longer in the world than ever before in human history and they are accounting for an increasingly greater percentage of the world population. Improved longevity is, at once, among the most remarkable achievements in all of human history and one of our greatest challenges. These added years can be a gift or a burden to humanity depending upon how they are used.

The mission of the Stanford Center on Longevity is to redesign long life. The Center studies the nature and development of the human life span, looking for innovative ways to use science and technology to solve the problems of people over 50 by improving the well-being of people of all ages.

Meeting these challenges includes changing our public policies as well as personal behavior. Redesigning long life means appreciating the unique challenges of aging, as well as the great value older people contribute to a society.

The Center aims to use increased life expectancy to bring about profound advances in the quality of life from early childhood to old age. To inspire change of this scale, the Center works with academic experts, business leaders and policy makers to target important challenges and opportunities for aging societies. By fostering dialogue and collaboration among these typically disconnected worlds, the Center aims to develop workable solutions to urgent issues confronting the world as the population ages.

Over 140 Stanford faculty members are Center affiliates. Their research foci include a broad range of topics, including behavioral economics and decision making, age-related changes in cognition, assistive robotics, the potential of stem cells, and technology developments that reduce cost and improve healthcare delivery.

The Center was founded by two of the worlds leading authorities on longevity and aging. Laura Carstensen PhD, is the founding director. A professor of psychology at Stanford, she has won numerous awards, including a Guggenheim Fellowship, and her research has been supported for more than 20 years by the National Institute on Aging. Thomas Rando MD, PhD, professor of neurology and neurological sciences, is deputy director. His research on aging has demonstrated that is possible to identify biochemical stimuli that can induce stem cells in old tissues to repair injuries as effectively as in young tissues. This work has broad implications for the fields of regenerative medicine and stem cell transplantation.

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About the Center - Stanford Center on Longevity

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List of British monarchs by longevity – Wikipedia

Saturday, March 23rd, 2019

Wikimedia list article

This is a list of British monarchs by longevity since the Union of the Crowns of England, Scotland and Ireland in 1603. To maintain consistency within the table, the dates of birth and death for each monarch are given in New Style. Two measures of the longevity are giventhis is to allow for the differing number of leap days occurring within the life of each monarch. The first column is the number of days between date of birth and date of death, allowing for leap days; the second column breaks this number down into years, and days, with the years being the number of whole years the monarch lived, and then days after his or her last birthday. Elizabeth II (queen since 6 February 1952), is the longest lived British sovereign.

*Updated daily according to UTC. While Queen Victoria lived for only 4 days more than George III in terms of years and days format, she actually lived for five days more because there were 20 leap days during Victoria's life and only 19 leap days during the life of George III.

If Charles, Prince of Wales, were to accede to the throne, he would immediately be ranked 8th with an age of 70years, 119days. If instead his son, William, Duke of Cambridge, were to accede any time before September 2030, he would be ranked 18th.

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Longevity – SNPedia

Monday, February 18th, 2019

Research on longevity, which can also be thought of as maximal lifespan, is more popularly associated with extending human life than with the more strict connotation of life expectancy (more at Wikipedia). Heredity and other factors (such as birth order and age of the mother at the time of the person's birth) influence longevity. [1]

There are at least 3 potentially overlapping classes of SNPs (or other genetic polymorphisms) that can be considered to affect longevity. First, many SNPs may influence susceptibility to diseases that shorten longevity; these can be found in SNPedia associated with those diseases, and related information is summarized on the heritability page. Second, some SNPs are being discovered based on their prevalence in people who live beyond average human lifespan; these SNPs may enhance longevity. Third, certain SNPs may be to able to affect longevity only in certain environmental contexts, for example SNPs that shorten or lengthen longevity only if an individual with a given genotype is also exposed to certain diets or toxins (such as cigarette smoke).

SNPs from the latter two categories include:

A 2017 GWAS analysis of parental longevity in 300,000 UK Biobank participants of European descent found 10+ SNPs to be associated with combined mothers' and fathers' attained age (and a few others just with paternal or maternal age); these 10+ SNPs and the longevity-associated allele were [PMID 29227965]:

Overall, it's useful to realize that SNPs are likely to influence your risk of dying from 9 of the top 10 causes of death (in developed countries), as noted below (based on 2000 US data):

10.1126/science.1190532 identified 150 snps however numerous questions about the plausibility of the results, led to it's eventual retraction.

http://genomics.senescence.info/download.html

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LONGEVITY | meaning in the Cambridge English Dictionary

Saturday, February 2nd, 2019

Early growth determines longevity in male rats and may be related to telomere shortening in the kidney.

Different letters above the columns indicate significant differences in longevity, the number within the columns indicates the number of replicates.

He commented that infection longevity might be conducive to multiple infections or that species may occupy different sites within the snail, making coexistence possible.

The aging lung the contribution of elastin and collagen, which are insoluble extracellular proteins characterized by their longevity, strength and resistance to destruction.

While very similar features have been found to increase ' happiness', we find them to be somewhat significant in explaining longevity.

If so, then increased longevity is much less of a problem than improved technology linked to increased expectations.

Of course, other factors might also be influential, including revisions in expectations of longevity.

In addition, it is not known whether patients' expectations of their longevity affect their psychological wellbeing.

Under this hypothesis, gigantism is viewed as a host adaptation that improves host survival beyond the longevity of the parasite.

I also present the alternative hypothesis, discussing why higher levels of initial political competition may increase the longevity of a democracy.

Prolonged longevity in both societies also means that family carers have been ageing, and periods of care have often become prolonged.

Otherwise, how can we account for his longevity and for his remarkable comebacks ?

Whilst the impact of increasing longevity has been significant, the effect has been much less than that of interest rates.

Therefore, control strategies that can limit transmission as well as drug pressure and thereby extend longevity of antimalarials in malaria endemic areas should be considered.

The natural longevity of the mongoose is not known, but some individuals have been reported to survive up to 13 years in captivity.

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LONGEVITY | meaning in the Cambridge English Dictionary

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Animal Longevity and Scale

Friday, January 25th, 2019

A useful line of analysis is to consider the effect of scale changes for creatures which aresimilar in shape and only differ in scale. As the scale of an animal increases the body weight and volume increase with the cubeof scale. The volume of blood flow required to feed that bulk also increases with the cube of scale. The cross sectional area of the arteries and the veins required to carry that blood flow only increases with the square of scale. There are other area-volume relationships which impose limitations on creatures. Some of those area-volume constraints, including the above one, are:

Thus to compensate for the body needs which increase with the cube of scale but the areas increase with only the square of scale the average blood flow velocity must increase linearly with scale. Blood flow velocity is driven by pressure differences. The pressuredifference must be great enough to carrying the blood flow to the top of the creature and great enough to overcome the resistance in the arteries and veins to the flow. The pressure required to pump blood from the heart to the top of the creature is proportional to scale.The pressure difference required to overcome the resistance to flow through the arteries intothe capillaries and back again through the veins is more difficult to characterize in terms of scale.The greater cross sectional area reduces the resistance but the long length increases resistance. The net result of these two scale influences seems to be that the pressure difference required to drive the blood through the bulk of the creature is inversely proportional to scale. The pressure difference imposed would be the maximum of the two required pressure differences.

Shown below are the typical blood pressures for creatures of different scales.

The linear regression of the logarithm of pressure on the logarithm of height yields the following result:

The linear regression of the logarithm of pressure on thelogarithm of weight yields:

If blood pressure were proportional to scale then the coefficient for *log(Height) would be 1.0 and for *log(Weight) would be 0.333 since weight to proportional to the cube of scale.The regression coefficients are not close to the theoretical values but they are of the proper order of magnitude for accepting blood pressure as beingproportional to scale.

The volume of the heart of a creature is proportional to the cube of scale. The volumeof the blood to be moved is also proportional to the cube of scale. From the previous analysis the flow velocity is proportional to scale. Therefore the time required to evacuatethe heart's volume is proportional to scale. This means that the heartbeat rate is inverselyproportional to scale. The following table gives the heart rates for a number of creatures.

A regression of the logarithm of heart rate on the logarithm of weight yields the followingequation:

If heart rate were exactly inversely proportion to scale the coefficient for *log(weight)would be -0.333. This is because scale is proportional to the cube root of weight.The coefficient of -0.2 indicates that the heart rate is given an equation of the form

One salient hypothesis is that the animal heart is good for a fixed number of beats. This hypothesis can be tested by comparing the product of average heart rate and longevity for different animals. Because the heart rate is in beats per minute and longevity is in years thenumber of heart beats per lifetime is about 526 thousand times the value of the product. Thedata for a selection of animals are:

Although the lack of dependence is clear visually the confirmation in terms of regression analysis is:

The t-ratio for the slope coefficient is an insignificant 0.15, confirming that there is no dependence of lifetime heartbeats on the scale of animal size.

If a heart is good for just a fixed number of beats, say one billion, then heart longevity is this fixed quota of beats divided by the heart rate. From the above equation for heart rate,lifespan (limited by heart function) would be proportional to scale raised to the 0.6 power.

The data for testing this deduction are:

For the data in the above table, admittedly very rough and sparse, the regression of the logarithm of the lifespan on thelogarithm of weight gives

Thus the net effect of scale on animal longevity is positive. Taking into account that weight is proportional to the cube of the linear scale of an animal the above equation in terms of scale would be

This says that if an animal is built on a 10 percent larger scale it will have a 6 percentlonger lifespan.

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Longevity | Smallville Wiki | FANDOM powered by Wikia

Tuesday, January 1st, 2019

Longevity is the ability to live or persist for extended periods of time.

Unlike some of their other abilities like superhuman strength, speed, stamina, and invulnerability, this ability appears to manifest for Kryptonians a while later after they get introduced to an environment under a yellow sun, and as such, this ability seems to require a certain amount of storage of rays given off by a yellow sun for it to take effect [citationneeded]

The Kryptonian machine computer program called Brainiac appeared to operate indefinitely. [citationneeded]Davis Bloome can live for very long periods of time. [citationneeded]

Among Kryptonians, blue kryptonite can hinder this ability. Dax-Ur aged while wearing a blue kryptonite rock on his wrist.

Darkseid was present on Earth during its darkest points in history but was banished away by Orion's bow.

Curtis Knox is an immortal, the source of his immortality was never discovered, he was around centuries before the first meteor showers occurred.

Clark Kent was initially afraid of this ability while he was an adolescent, fearing the that he would eventually outlive everyone including the ones he loves. After his friend Ryan dies, he learns that time is valuable, and that he shouldn't take someone's life for granted, as it will end sometime. When the Crystal of Air gets stained with human blood, a second meteor shower is triggered, and the Black Ship ventures to Earth, bringing Aethyr and Nam-Ek to Earth. Here, they attempt to get Kal-El to join them in making Earth a utopia and a new Krypton in which they would rule forever but Clark denies them and traps them in the Phantom Zone. After Clark becomes mortal when Jor-El removes his abilities, he gets shot and dies at 7:18 AM. Jor-El inhabits Lionel's body and revives Clark, restoring his powers, so he can complete his Kryptonian destiny because "his mortal journey has ended".

Later on, his cousin Kara reminds him that trying to love Lana and live with her till she grows old is a foolish idea because he will out live her. Clark later accepts this ability, as shown while he was talking with John Jones, admitting that eventually "they'll all be gone".

Please add quotes about longevity and immortality here.

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Longevity – Wellness – Sharecare

Tuesday, January 1st, 2019

Maintaining your muscle mass through the ages has an aesthetic appeal. You will automatically look better because you will be toned and shapely with less sagging-and-floppy arms, and less fat.

Ideally, a well-rounded and comprehensive exercise program includes cardio work, strength training, and stretching. Each of these activities affords you unique benefits that your body needs to achieve and maintain peak performance. Cardio work, which gets your heart rate up for an extended period of time, will burn calories, lower body fat, and strengthen both your heart and lungs; strength training (use of weights or elastic bands, or even your own body weight as resistance in some cases) will keep your bones strong and prevent the loss of lean muscle mass that naturally occurs with age; and stretching will keep you flexible and less susceptible to joint pain. All three of these forms of exercise will keep your body moving and also help you to maintain good posture, which will instantly make you look younger. The type of activity you do is not nearly as important as how often you do it, and how long you do it. Because exercise lowers stress for up to twenty-four hours, its important to avoid being a weekend warrior and make it a goal of keeping a semi-daily routine.

Dont forget that the benefits of exercise are cumulative. Another fact science has proven is that you dont have to sweat it out on a treadmill for a full sixty minutes. You can do ten minutes here, twenty minutes there. (Like calories, it all adds up!) Sprinkle pockets of workout times into your day -- at lunch, after dinner, or in the fifteen minutes right after you get up and the house is still quiet.

No matter which form or type of exercise you choose to do, its positive impact on your skin and overall looks cannot be underestimated. I don't know anybody who is fit and who looks older than she should, do you?

From The Mind-Beauty Connection: 9 Days to Less Stress, Gorgeous Skin, and a Whole New You by Amy Wechsler.

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What does longevity mean? – Definitions.net

Saturday, December 1st, 2018

Longevity

The word "longevity" is sometimes used as a synonym for "life expectancy" in demography - however, the term "longevity" is sometimes meant to refer only to especially long lived members of a population, whereas "life expectancy" is always defined statistically as the average number of years remaining at a given age. For example, a population's life expectancy at birth is the same as the average age at death for all people born in the same year. Longevity is best thought of as a term for general audiences meaning 'typical length of life' and specific statistical definitions should be clarified when necessary.Reflections on longevity have usually gone beyond acknowledging the brevity of human life and have included thinking about methods to extend life. Longevity has been a topic not only for the scientific community but also for writers of travel, science fiction, and utopian novels.There are many difficulties in authenticating the longest human life span ever by modern verification standards, owing to inaccurate or incomplete birth statistics. Fiction, legend, and folklore have proposed or claimed life spans in the past or future vastly longer than those verified by modern standards, and longevity narratives and unverified longevity claims frequently speak of their existence in the present.

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How You Can Increase Your Longevity

Saturday, November 10th, 2018

If you live longer than the average person, then you could be said to havelongevity. Striving for your maximum potential age is thegoal oflongevity. This potentially can be reached by practicing healthy behaviors and attitudes.

Longevity is defined as "long life" or "a great duration of life." The term comes from the Latin word longaevits. In this word, you can see how the words longus (long) and aevum (age) combine into a concept that means an individual who lives a long time.

The most important part of this definition is the comparative nature of it. Long life implies longer than somethingand that something is the average lifespan.

Biologists sometimes define longevity as the average lifespan expected under ideal conditions. It's hard to say what's ideal. Plenty of medical research is ongoing about the "right" amount and type of exercise to get, the best diet to eat to maximize longevity, and whether certain pharmaceuticals or supplements can help improve your longevity.

Lifespans have increased pretty dramatically over the last century or so, in large part due to advances in medicine that have nearly eliminated certain deadly infectious diseases.

The average baby born in 1900 lived about a half-century. Nowadays, the life expectancy of people in the United States is nearly 79 years on average81 years for women and 76 years for men, and in some countries, life expectancy is even longer.

It's very possible that humanity's true longevity might be much higher. Humans might live longer if they can create the ideal conditions of a healthy diet and exercise.

You may think that your genes determine your longevity, but the truth is genetics account for a maximum of 30 percent of your life expectancy. The rest comes from your behaviors, attitudes, environment, and a little bit of luck.

You may have heard about various life extension techniques. Keep in mind that none of them have been proven in humans and most are just theories. The only proven way to live longer is to live a healthy life.

If you want to beat the average and maximize your longevity, what should you do? Here's a list of things to consider:

Make a commitment today to make one healthy change a week. Before you know youll be feeling better and on the road to longevity.

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Live forever or die trying. r/longevity – reddit

Saturday, November 10th, 2018

Let us continue our funding efforts for our future health. Our regular donations will help to speed up Scientific Research to prevent and reverse age-related diseases. You can consider following research groups suggested by members or any other research group working on longevity.

SENS Research Foundation: They fund research that uses regenerative medicine to repair the damage underlying the diseases of aging (about SENS)

LEAF/lifespan.io Various Campaigns such as Become a Lifespan Hero, NAD+ Mouse Project, MouseAge Project

Other options: LEAF on Amazon Smile, eBay, Humble Bundle

Crowdfunding project for the translation of the book Ending Aging (by Aubrey de Grey) into Portuguese.See Donation link and leafscience.org Article

Dog Aging Project: "The University of Washingtons Dog Aging Project is dedicated to promoting healthy aging in people and their companion animals."

National Institute on Aging (NIA) : "NIA, one of the 27 Institutes and Centers of NIH, leads the federal government in conducting and supporting research on aging and the health and well-being of older people". (mission)

The Longevity Research Institute. "They are designing and launching mouse studies for interventions.." read more on this Reddit Comment

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Thanks to following members of this subreddit who have shared their donation efforts. These are based on their public comments on this subreddit. Please share your donation efforts here. It will motivate others to participate.

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The Longevity Summit 2018 | The Economist Events

Saturday, November 10th, 2018

In 2017, for the first time, The Economist brought together Asian business leaders, political decision-makers and health-care entrepreneurs to discuss how to make longevity a source of healthy innovation. At the Longevity Summit 2018, The Economist will build on this momentum to foster thinking on the topic of living to 100.

The event will answer the following key questions:

About the 2018 summit:

The worlds over-60 population is already nearing a billionand its still growing. Low fertility rates and increasing life expectancy have the United Nations predicting that by 2050 there will be 2.1 billion of these older people, and around half of them will live in Asia.

Longevity is a polarising issue. Optimists enthuse about advances in biotechnology and the market power of a silver economy; doomsayers fear skyrocketing health-care costs and inadequate workforces. A more plausible, middle position is to see the challenges associated with an ageing population as inextricably linked with their solutions. Governments and businesses need healthy populations to sustain demand, productivity and growth. And as people age, they want to stay healthy, engaged and purposeful. Happily, these are complementary demands.

But across Asia, progress in meeting the challenges of ageing has been patchy. Japan and Singapore have made great strides in helping their populations cope with longevity. Hong Kong, Taiwan and Korea are catching up by embracing new ideas and policy solutions. Philippines, Vietnam and Malaysia enjoy demographic buoyancy, with younger populations for the moment, but in the coming decades they will face the same pressures as their greying neighbours. What lessons can Asias longevity leaders share when it comes to engaging the over-60 population in the economy and society? Can the longevity dividend offset the costs of increased demand for health care and social services?

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The Longevity Summit 2018 | The Economist Events

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Buckyballs, health and longevity state of knowledge …

Thursday, October 25th, 2018

By Vince Giuliano

Image source

The popular life extension blogs have been lit up recently with exchanges related to a recent publication that reports that a homogenized solution of olive oil and C60 carbon buckyballs fed to middle age rats extends their lifespans by an average of 90%. If this result stands up it is truly amazing. Compared with other longevity interventions such as rapamycin feeding or calorie restriction which at best extend lifespans by 15-20%, the 90% figure is off the scale. So I decided to delve into the research literature to clarify what is known and what is not known about C60 carbon fullerenes as related to biological impacts and health. I report on this expedition here. I also chime in with my own hypotheses about the mechanisms through which the C60-olive oil cocktail extends rats lifespans, assuming it really does. The main points I will be documenting are:

Image source

C60 buckyball Image sourceBuckminister Fuller

What is a C60 fullerene?

From wickipedia: A fullerene is any molecule composed entirely of carbon, in the form of a hollow sphere, ellipsoid or tube. Spherical fullerenes are also called buckyballs, and they resemble the balls used in football (association football). Cylindrical ones are called carbon nanotubes or buckytubes. Fullerenes are similar in structure to graphite, which is composed of stacked graphene sheets of linked hexagonal rings; but they may also contain pentagonal (or sometimes heptagonal) rings.[1] The first fullerene molecule to be discovered, and the familys namesake, buckminsterfullerene (C60), was prepared in 1985 by Richard Smalley, Robert Curl, James Heath, Sean OBrien, and Harold Kroto at Rice University. The name was an homage to Buckminster Fuller, whose geodesic domes it resembles. The structure was also identified some five years earlier by Sumio Iijima, from an electron microscope image, where it formed the core of a bucky onion.[2] Fullerenes have since been found to occur in nature.[3] More recently, fullerenes have been detected in outer space.[4] According to astronomer Letizia Stanghellini, Its possible that buckyballs from outer space provided seeds for life on Earth.[5]

C60 buckyballs and longevity of rats, mice and other lower species

I start out with the publication that has initiated the current buz, The prolongation of the lifespan of rats by repeated oral administration of [60] fullerene published in August 2011. The study reported was designed to assess the toxicity of C60 in an olive oil suspension, not to assess impact on lifespans of rats. The result that not only was the suspension not toxic but radically increased the livespans of the rats was a surprise to the researchers. Countless studies showed that [60]fullerene (C60) and derivatives could have many potential biomedical applications. However, while several independent research groups showed that C60 has no acute or subacute toxicity in various experimental models, more than 25 years after its discovery the in vivo fate and the chronic effects of this fullerene remain unknown. If the potential of C60 and derivatives in the biomedical eld have to be fullled these issues must be addressed. Here we show that oral administration of C60 dissolved in olive oil (0.8 mg/ml) at reiterated doses (1.7 mg/kg of body weight) to rats not only does not entail chronic toxicity but it almost doubles their lifespan. The effects of C60-olive oil solutions in an experimental model of CCl4 intoxication in rat strongly suggest that the effect on lifespan is mainly due to the attenuation of age-associated increases in oxidative stress. Pharmacokinetic studies show that dissolved C60 is absorbed by the gastro-intestinal tract and eliminated in a few tens of hours. These results of importance in the elds of medicine and toxicology should open the way for the many possible -and waited for- biomedical applications of C60 including cancer therapy, neurodegenerative disorders, and ageing.

A nice thing about this publication is that it describes the experimental conditions in meticulous detail. For example, getting a good solvent vector for administration of C60 to animals has been a serious problem. Unlike many other studies which employed water-based solutions of C60 with poor or uncertain bioavailability and toxic effects, this study used an olive oil brew. Fifty mg of C60 were dissolved in 10 ml of olive oil by stirring for 2 weeks at was increased to 60% for 10 min and then hold constant for the remaining 7 min of ambient temperature in the dark. The resulting mixturewas centrifugedat 5.000gfor each sample run. At least 10 column volumes of the initial composition were ushed 1 h and the supernatant was ltered through a Millipore lter with 0.25 mmporosity.

There were several sub-studies reported in this paper. In the chronic toxicity and longevity sub-study, only 18 rats middle-aged were involved divided into three cohorts of six rats each: a) a control cohort fed normal rat chow, b) a cohort fed food plus olive oil by gavage, and c) a cohort feed the C60-olive oil brew by gavage (forced feeding). The rats were housed three per cage and acclimated for 14 days, before dosing. Three groups of 6 rats (10 months old, weighing 465.31(10 months old,were administered daily for one week, then weekly until the end of the second month and then every two weeks until the end of the 7th month, by gavages with 1 ml of water or olive oil or C60 dissolved in olive oil (0.8 mg/ml), respectively. All rats in cohort (a) were alive until week 18 of the experiment and all were dead by week 38. All rats in cohort (b). were alive until week 36 and all were dead by week 58. In cohort (c). all rats were alive until week 60 and all dead by week 66 (the last one being sacrificed at week 66). Between weeks 38 and 60 all the control rats were dead and all the C60-fed rats were alive and well. Olive oil alone produced a weighted average of 18% life extension while the weighted average for the C60-olive oil brew was 90%. Remarkably, no rats in cohort (c) contracted cancers.

In the sub-study of oxidative stress, the C60-olive oil mix almost completely protected against carbon tetrachloride oxidative liver damage. Sixty rats randomly divided into 10 groups of 6 rats were pre-treated daily for 7 days by oral gavages (og groups) or by i.p. injection (ip groups). Groups A (GAog and Groups B and C (GBog, GCog and GBip, GCip) were pre-treated with 1 ml of olive oil while groups D and E (GDog, GEog and GDip, GEip) were pre-treated with 1 ml of C60-olive oil Twenty-four hours before sacrice, groups GA, GC and GE were i.p. injected with a single dose of CCl4 (1 ml/kg bw) while GB and GD, used as controls, were administered with a 0.9% NaCl aqueous solution under the same conditions. The animals were subsequently sacrificed and their livers examined. the liver sections of GA and GC animals co-treated with water and CCl4 or with olive respectively, showed important damage including many inammatory areas as well as large necrotic areas with ballooning necrotic cells associated with an important steatosis (Fig. 4). In contrast, microscopic examination of the liver sections of GE animals co-treated with C60-olive oil and CCl4, revealed few necrotic areas with some ballooning cells without apoptosis limited to some cords of hepatocytes (Fig. 4).

The study also investigated the pharmacodynamics and pharmacokinetics of C60 administration. The results of this pharmacokinetic study show for the rst time that C60 is absorbed by the gastro-intestinal tract (Fig. 1). In the case of highly hydrophobic drugs (Log P > 5) it is well known that the absorption of the molecules by the gastro-intestinal tract occurs via the mesenteric lymphatic system after association with developing lipoproteins in the enterocytes rather than via the portal blood [40]. Therefore, as the octanol/water partition coefcient of C60 is estimated to be 6.67 [41], the absorption of C60 occursvia the mesenteric lymphatic system rather than via the portal blood. The elimination half-lives indicate that C60 is completely eliminated from blood 97 h after administration irrespective of the route of administration. The elimination process follows a non-urinary route because unmodied C60 was not detected in urine samples taken up 48 h after administration. Previous investigations showed that C60 is mainly eliminated through the bile ducts [21] .

Conclusion: The effect of pristine C60 on lifespan emphasizes the absence of chronic toxicity. These results obtained with a small sample of animals with an exploratory protocol ask for a more extensive studies to optimize the intestinal absorption of C60 as well as the different parameters of the administration protocol: dose, posology, and treatment duration. In the present case, the treatment was stopped when a control rat died at M17, which proves that the effects of the C60 treatment are long-lasting as the estimated median lifespan for C60-treated rats is 42 months. It can be thought that a longer treatment could have generated even longer lifespans. Anyway, this work should open the road towards the development of the considerable potential of C60 in the biomedical eld, including cancer therapy, neurodegenerative disorders and ageing. Furthermore, in the eld of ageing, as C60 can be administered orally and as it is now produced in tons, it is no longer necessary to resort to its water-soluble derivatives, which are difficult to purify and in contrast to pristine C60 may be toxic

A 2008 publication also indicated that a fullerene is capable of extending the lifespans of mice: A carboxyfullerene SOD mimetic improves cognition and extends the lifespan of mice. In lower organisms, such as Caenorhabditis elegans and Drosophila, many genes identified as key regulators of aging are involved in either detoxification of reactive oxygen species or the cellular response to oxidatively-damaged macromolecules. Transgenic mice have been generated to study these genes in mammalian aging, but have not in general exhibited the expected lifespan extension or beneficial behavioral effects, possibly reflecting compensatory changes during development. We administered a small-molecule synthetic enzyme superoxide dismutase (SOD) mimetic to wild-type (i.e. non-transgenic, non-senescence accelerated) mice starting at middle age. Chronic treatment not only reduced age-associated oxidative stress and mitochondrial radical production, but significantly extended lifespan. Treated mice also exhibited improved performance on the Morris water maze learning and memory task. This is to our knowledge the first demonstration that an administered antioxidant with mitochondrial activity and nervous system penetration not only increases lifespan, but rescues age-related cognitive impairment in mammals. SOD mimetics with such characteristics may provide unique complements to genetic strategies to study the contribution of oxidative processes to nervous system aging.

Another 2011 publication Polyhydroxy Fullerenes (Fullerols or Fullerenols): Beneficial Effects on Growth and Lifespan in Diverse Biological Models indicates that fullerenes can extend the lifespans of certain more primitive organisms. The publication reports Recent toxicological studies on carbon nanomaterials, including fullerenes, have led to concerns about their safety. Functionalized fullerenes, such as polyhydroxy fullerenes (PHF, fullerols, or fullerenols), have attracted particular attention due to their water solubility and toxicity. Here, we report surprisingly beneficial and/or specific effects of PHF on model organisms representing four kingdoms, including the green algae Pseudokirchneriella subcapitata, the plant Arabidopsis thaliana, the fungus Aspergillus niger, and the invertebrate Ceriodaphnia dubia. The results showed that PHF had no acute or chronic negative effects on the freshwater organisms. Conversely, PHF could surprisingly increase the algal culture density over controls at higher concentrations (i.e., 72% increase by 1 and 5 mg/L of PHF) and extend the lifespan and stimulate the reproduction of Daphnia (e.g. about 38% by 20 mg/L of PHF). We also show that at certain PHF concentrations fungal growth can be enhanced and Arabidopsis thaliana seedlings exhibit longer hypocotyls, while other complex physiological processes remain unaffected. These findings may open new research fields in the potential applications of PHF, e.g., in biofuel production and aquaculture. These results will form the basis of further research into the mechanisms of growth stimulation and life extension by PHF.

C60 is a powerful antioxidant

This point is long known and confirmed in a number of studies. From (2007) Medicinal applications of fullerenes: Results published in 1999 have shown that fullerenes have a potential as biological antioxidants. The antioxidant property is based on the fact that fullerenes possess large amount of conjugated double bonds and low lying lowest unoccupied molecular orbital (LUMO) which can easily take up an electron, making an attack of radical species highly possible. It has been reported that up to 34 methyl radicals have been added onto a single C60 molecule. This quenching process appears to be catalytic. In other words the fullerene can react with many superoxides without being consumed. Due to this feature fullerenes are considered to be the worlds most efficient radical scavenger and are described as radical sponges (Krusic et al 1991). The major advantage of using fullerenes as medical antioxidant is their ability to localize within the cell to mitochondria and other cell compartment sites, where in diseased states, the production of free radicals takes place. Experiments on rats done by Najla Gharbi and coworkers proved this remarkable trait. They showed that aqueous C60 suspensions prepared without using any polar organic solvent, not only have no acute or sub acute toxicity in rodents, but also protect their livers against free-radical damage (Gharbi et al 2005).

The 2005 publication [60]fullerene is a powerful antioxidant in vivo with no acute or subacute toxicity confirms both this and another point made in the recent rat study: C60 does not engender toxicity in rodents. In the present work, we report the effects of C(60)-pretreatments on acute carbon tetrachloride intoxication in rats, a classical model for studying free-radical-mediated liver injury. Our results show that aqueous C(60) suspensions prepared without using any polar organic solvent not only have no acute or subacute toxicity in rodents but they also protect their livers in a dose-dependent manner against free-radical damage. To be sure, according to histopathological examinations and biological tests, pristine C(60) can be considered as a powerful liver-protective agent.

The 2011 report Antioxidant activity of fullerene C60 against OH free radicals: A Quantum Chemistry and Computational Kinetics Studyreports Fullerenes are considered to be the worlds most efficient radical scavenger, and represents an attractive tool for biological applications. Indeed, it have been demonstrated in vivo and in vitro, that fullerenes and related structures reduce the toxicity of free radical assault on neuronal tissue, reacting readily and at a high rate with free radicals, which are often the cause of cell damage or death. Although there is strong evidence that antioxidant activity is an intrinsec property of fullerenes, the mechanism of radical scavenging and neuroprotection are still unclear. In this work, we have studied the reaction between fullerene C60 and hydroxyl radicals, using high level quantum chemistry and computational kinetics methods. Energy profiles are calculated using different basis sets, and reaction rate constant are reported for the first time. The presence of nonpolar environments seems to enhance the reactivity of fullerene molecule toward OH radicals, compared to the gas phase. Energetic considerations show that, once a first radical is attached to the fullerene cage, further additions are increasingly feasible, suggesting that fullerene can act as OH radical sponges. They also protect their livers in a dose-dependent manner against free-radical damage. To be sure, according to histopathological examinations and biological tests, pristine C(60) can be considered as a powerful liver-protective agent.

C60 has low toxicity and can cross the blood-brain barrier and may lead to many medical applications.

The 2012 publication C60 fullerene derivatized nanoparticles and their application to therapeutics reports Fullerenes can be formed into many new materials and devices. They have a wide range of applications in medicine, electronics, biomaterials, and energy production. An overview of the nanostructure and the physical and chemical characteristics of fullerene-drug derivatives is given. The biological behavior of fullerene derivatives shows their potential to medical application fields because C(60) is rapidly absorbed by tissues and is excreted through urinary tract and enterons, which reveals low toxicity in vitro and in vivo studies. Nanomedicine has become one of the most promising areas of nanotechnology, while many have claimed its therapeutic use against cancer, human immunodeficiency virus (HIV), and neurodegenerative disorders. Water-soluble C(60) fullerene derivatives that come from chemical modification largely enhance the biological efficacy. The blood-brain barrier (BBB) is a physical barrier composed of endothelial tight junctions that restrict the paracellular permeability. A major challenge facing neuropharmacology is to find compounds that can be delivered into the brain through the bloodstream. Fullerene C(60) was demonstratively able to cross the BBB by hybridizing a biologically active moiety dyad, which provides a promising clue as a pharmacological therapy of neural disorders.

Fullerene C60 is neuroprotective

The 2001 publication Fullerene-based antioxidants and neurodegenerative disorders reports: Water-soluble derivatives of buckminsterfullerene (C60) derivatives are a unique class of compounds with potent antioxidant properties. Studies on one class of these compounds, the malonic acid C60 derivatives (carboxyfullerenes), indicated that they are capable of eliminating both superoxide anion and H2O2, and were effective inhibitors of lipid peroxidation, as well. Carboxyfullerenes demonstrated robust neuroprotection against excitotoxic, apoptotic and metabolic insults in cortical cell cultures. They were also capable of rescuing mesence-phalic dopaminergic neurons from both MPP1 and 6-hydroxydopamine-induced degeneration. Although there is limited in vivo data on these compounds to date, we have previously reported that systemic administration of the C3 carboxyfullerene isomer delayed motor deterioration and death in a mouse model of familial amyotrophic lateral sclerosis (FALS). Ongoing studies in other animal models of CNS disease states suggest that these novel antioxidants are potential neuroprotective agents for other neurodegenerative disorders, including Parkinsons disease.

C60 derivative and hybrid structure compounds are also being studied for their neurprotective as well as other medical properties. See for example [Study of the neuroprotective action of hybrid structures based on fullerene C60]. The neuroprotective action of hybrid structures based on fullerene C60 with attached proline amino acid has been studied. Hybrid structures contained natural antioxidant carnosine or addends with one or two nitrate groups. It has been shown that all studied compounds had antioxidant activity and decreased the concentration of malondialdehyde in homogenates of the rat brain.

Fullerene C60 might be useful for the treatment of Alzheimers disease.

The 2012 publication Fullerene C60 prevents neurotoxicity induced by intrahippocampal microinjection of amyloid-beta peptide reports: The dynamics of the state of hippocampal pyramidal neurons after intrahippocampal microinjections of (1) amyloid-beta25-35 (1.6 nmol/1 microl), (2) an aqueous molecule-colloidal solution of C60 (0.46 nmol/1 microl) and (3) an aqueous molecule-colloidal solution of C60 before amyloid-beta25-35 administration were analysed in rats. This model allowed us to study the role of amyloid-beta25-35 in the pathogenesis of Alzheimers disease and to test anti-amyloid substances. Methods of fluorescent (acridine orange) and brightfield (cresyl violet and immunohistochemistry) microscopy were used. Acridine orange staining indicated changes in protein synthesis intensity due to alterations in the rRNA state of neuron ribosomes. One day after administration of amyloid-beta25-35, the intensity of protein synthesis in the population of morphologically intact cells decreased by 45%. By day 14, degeneration occurred in the majority of pyramidal cells, and amyloid-beta25-35 deposits were observed in the neuronal cytoplasm. In necrotic cells, acridine orange staining of the cytoplasm was drastically increased as a result of RNA degradation rather than due to an increase in protein synthesis. Because amyloid-beta25-35 administration provoked oxidative stress, we assumed that an aqueous molecule-colloidal solution of C60 administered before amyloid-beta25-35 prevented protein synthesis changes on day 1, while acting as an antioxidant, and by day 14 it inhibited neurodegeneration and amyloid-beta25-35 accumulation. Based on the data that an aqueous molecule-colloidal solution of C60 prevented amyloid-beta25-35 aggregation in in vitro experiments and based on our present evidence on the antitoxicity of an aqueous molecule-colloidal solution of C60, we suggest that functionalised C60 prevents/diminishes amyloid-beta25-35 aggregation in vivo as well. Thus, an aqueous molecule-colloidal solution of C60 administered at a low concentration before amyloid-beta2-35, prevented disturbances in protein synthesis, neurodegeneration and formation amyloid-beta25-35 deposits in hippocampal pyramidal neurons in vivo. This evidence gives promise that functionalised C60 can be used to develop anti-amyloid drugs combining antioxidant and anti-aggregative properties.

The 2012 publication [Antiamyloid properties of fullerene C60 derivatives]reports A comparative estimation of the ability of complexes of fullerene C60 with polyvinylpyrrolidone and fullerene C60 derivatives (the sodium salt of the polycarboxylic derivative of fullerene C60, sodium fullerenolate), has been carried out. The fullerenes destroyed amyloid fibrils of the Abeta(1-42) peptide of the brain and the muscle X-protein. A study of the effect of fullerenes on muscle actin showed that complexes of fullerene C60 with polyvinylpyrrolidone and sodium fullerenolate did not prevent the filament formation of actin, nor did they destroy its filaments in vitro. Conversely, sodium salt of the polycarboxylic derivative of fullerene C60 destroyed actin filaments and prevented their formation. It was concluded that sodium fullerenolate and complexes of fullerene C60 with polyvinylpyrrolidone are the most effective antiamyloid compounds among the fullerenes examined.

Fullerenes may enable new anticancer therapies via various mechanisms: one is as a carrier for conventional anticancer drugs; another is enhancing cytotoxic effects of chemotherapy drugs; another yet is based on the anti-cancer activities of the fullerene molecules themselves.

With respect to the first role, as a potential carrier of conventional anti-cancer drugs, the new (November 2012) publication Water-Dispersible Fullerene Aggregates as a Targeted Anticancer Prodrug with both Chemo- and Photodynamic Therapeutic Actions reports Prodrug therapy is one strategy to deliver anticancer drugs in a less reactive manner to reduce nonspecific cytotoxicity. A new multifunctional anticancer prodrug system based on water-dispersible fullerene (C60) aggregates is introduced; this prodrug system demonstrates active targeting, pH-responsive chemotherapy, and photodynamic therapeutic (PDT) properties. Incorporating (via a cleavable bond) an anticancer drug, which is doxorubicin (DOX) in this study, and a targeting ligand (folic acid) onto fullerene while maintaining an overall size of approximately 135 nm produces a more specific anticancer prodrug. This prodrug can enter folate receptor (FR)-positive cancer cells and kill the cells via intracellular release of the active drug form. Moreover, the fullerene aggregate carrier exhibits PDT action; the cytotoxicity of the system towards FR-positive cancer cells is increased in response to light irradiation. As the DOX drug molecules are conjugated onto fullerene, the DOX fluorescence is significantly quenched by the strong electron-accepting capability of fullerene. The fluorescence restores upon release from fullerene, so this fluorescence quenching-restoring feature can be used to track intracellular DOX release. The combined effect of chemotherapy and PDT increases the therapeutic efficacy of the DOX-fullerene aggregate prodrug. This study provides useful insights into designing and improving the applicability of fullerene for other targeted cancer prodrug systems.

Another publication, dated 2013, related to use of fullerenes for anti-cancer drug delivery is PEI-derivatized fullerene drug delivery using folate as a homing device targeting to tumor.You can also see (1007) Nanotubes, Nanorods, Nanofibers and Fullerenes for Nanoscale Drug Delivery.

C60 compounds are also promising as delivery vehicles for drugs.

For example, related to myocardial treatments the 2010 publicationThe C60-fullerene porphyrin adducts for prevention of the doxorubicin-induced acute cardiotoxicity in rat myocardial cellsreports: This is a fullerene-based low toxic nanocationite designed for targeted delivery of the paramagnetic stable isotope of magnesium to the doxorubicin (DXR)-induced damaged heart muscle providing a prominent effect close to about 80% recovery of the tissue hypoxia symptoms in less than 24 hrs after a single injection (0.03 0.1 LD50). Magnesium magnetic isotope effect selectively stimulates the ATP formation in the oxygen-depleted cells due to a creatine kinase (CK) and mitochondrial respiratory chain-focusing attack of 25Mg2+ released by nanoparticles. These smart nanoparticles with membranotropic properties release the overactivating cations only in response to the intracellular acidosis. The resulting positive changes in the energy metabolism of heart cell may help to prevent local myocardial hypoxic (ischemic) disorders and, hence, to protect the heart muscle from a serious damage in a vast variety of the hypoxia-induced clinical situations including DXR side effects.

C60 can enhance the cytotoxic action of chemotherapeutic agents against cancer through autophagy.

The 2009 publication Autophagy-mediated chemosensitization in cancer cells by fullerene C60 nanocrystalreports: Autophagy may represent a common cellular response to nanomaterials, and modulation of autophagy holds great promise for improving the efficacy of cancer therapy. Fullerene C60 possesses potent anti-cancer activities, but its considerable toxicity towards normal cells may hinder its practical applications. It has been reported that fullerene C60 induces certain hallmarks of autophagy in cancer cells. Here we show that the water-dispersed nanocrystal of underivatized fullerene C60 (Nano-C60) at noncytotoxic concentrations caused authentic autophagy and sensitized chemotherapeutic killing of both normal and drug-resistant cancer cells in a reactive oxygen species (ROS)-dependent and photo-enhanced fashion. We further demonstrated that the chemosensitization effect of Nano-C60 was autophagy-mediated and required a functional Atg5, a key gene in the autophagy signaling pathway. Our results revealed a novel biological function for Nano-C60 in enhancing the cytotoxic action of chemotherapeutic agents through autophagy modulation and may point to the potential application of Nano-C60 in adjunct chemotherapy.

C60 protects against radiation-induced cell damage

The 2010 publication Dendro[C(60)]fullerene DF-1 provides radioprotection to radiosensitive mammalian cells reports: In this study, the ability of the C(60) fullerene derivative DF-1 to protect radiosensitive cells from the effects of high doses of gamma irradiation was examined. Earlier reports of DF-1s lack of toxicity in these cells were confirmed, and DF-1 was also observed to protect both human lymphocytes and rat intestinal crypt cells against radiation-induced cell death. We determined that DF-1 protected both cell types against radiation-induced DNA damage, as measured by inhibition of micronucleus formation. DF-1 also reduced the levels of reactive oxygen species in the crypt cells, a unique capability of fullerenes because of their enhanced reactivity toward electron-rich species. The ability of DF-1 to protect against the cytotoxic effects of radiation was comparable to that of amifostine, another ROS-scavenging radioprotector. Interestingly, localization of fluorescently labeled DF-1 in fibroblast was observed throughout the cell. Taken together, these results suggest that DF-1 provides powerful protection against several deleterious cellular consequences of irradiation in mammalian systems including oxidative stress, DNA damage, and cell death.

See also the 2010 publication The polyhydroxylated fullerene derivative C60(OH)24 protects mice from ionizing-radiation-induced immune and mitochondrial dysfunction.

C60 fullerenes have anti-viral properties and might be useful for preventing or delaying the onset of AIDS.

From (2007) Medicinal applications of fullerenes:Compounds with antiviral activity are generally of great medical interest and different modes of pharmaceutical actions have been described. Replication of the human immunodeficiency virus (HIV) can be suppressed by several antiviral compounds, which are effective in preventing or delaying the onset of acquired immunodeficiency syndrome (AIDS). Fullerenes (C60) and their derivatives have potential antiviral activity, which has strong implications on the treatment of HIV-infection. The antiviral activity of fullerene derivatives is based on several biological properties including their unique molecular architecture and antioxidant activity. It has been shown that fullerenes derivatives can inhibit and make complex with HIV protease (HIV-P) (Friedman et al 1993; Sijbesma et al 1993). Dendrofullerene 1 (Figure 1) has shown the highest anti-protease activity (Brettreich and Hirsch 1998; Schuster et al 2000). Derivative 2, the trans-2 isomer (Figure 1), is a strong inhibitor of HIV-1 replication. The study suggests that relative position (trans-2) of substituents on fullerenes and positive charges near to fullerenes cage provide an antiviral structural activity. Also Amino acid derivatives of fullerene C60 (ADF) are found to inhibit HIV and human cytomegalovirus replication (Kotelnikova et al 2003).

Fullerenes inhibit the allergic response

The 2007 publication Fullerene nanomaterials inhibit the allergic response reports Fullerenes are a class of novel carbon allotropes that may have practical applications in biotechnology and medicine. Human mast cells (MC) and peripheral blood basophils are critical cells involved in the initiation and propagation of several inflammatory conditions, mainly type I hypersensitivity. We report an unanticipated role of fullerenes as a negative regulator of allergic mediator release that suppresses Ag-driven type I hypersensitivity. Human MC and peripheral blood basophils exhibited a significant inhibition of IgE dependent mediator release when preincubated with C(60) fullerenes. Protein microarray demonstrated that inhibition of mediator release involves profound reductions in the activation of signaling molecules involved in mediator release and oxidative stress. Follow-up studies demonstrated that the tyrosine phosphorylation of Syk was dramatically inhibited in Ag-challenged cells first incubated with fullerenes. In addition, fullerene preincubation significantly inhibited IgE-induced elevation in cytoplasmic reactive oxygen species levels. Furthermore, fullerenes prevented the in vivo release of histamine and drop in core body temperature in vivo using a MC-dependent model of anaphylaxis. These findings identify a new biological function for fullerenes and may represent a novel way to control MC-dependent diseases including asthma, inflammatory arthritis, heart disease, and multiple sclerosis.

C60 fullerenes exercise immunomodulary effects.

The 2012 publication [The condition of lipid peroxidation in mice and the effect of fullerene C60 during immune response] reports: The aim of this study was to assess the influence of fullerene C60 on lipid peroxidation (POL) and antioxidant protection during the induction of the immune response to heteroantigen. Balb/c mice were immunized intraperitoneal (i.p.) with sheep erythrocytes for the primary immunization. Water dispersion of fullerene C60 was injected i.p. once at the dose 50 ng to mice on first, third and sixth days after immunization. During immune response, the increment ofmalonic dialdehide (MDA) was enhanced in liver, kidneys and heart tissues. Fullerene C60 induced POL during the latent phase of immune response, but inhibited this process during progression of immune response. Activities of superoxide dismutase (SOD) and catalase in liver and spleen tissues were induced after injection of fullerene C60 to intact mice. After immunization, high level of activity of antioxidant enzymes and low level of organs mass factor were determined. Injection of fullerene C60 reduced the activities of SOD and catalase in spleen tissues. The results of our study indicate that fullerene C60 can display positive effect on POL processes and antioxidant enzymes activity which is probably due to membranes stabilization action or the ability of fullerene C60 to bind free radicals independently.

Another 2012 publication that demonstrates anti-arthritis immunomodulatory activity in rats is [Fullerene C60 exhibits immunomodulatory activity during adjuvant-induced arthritis in rats].The effect of fullerene C60 (FC60) on the immune processes during experimental adjuvant-induced arthritis (AA) in rats has been studied. The results indicate the inhibitory action of FN60 during AA on cellular splenocyte proliferation, neutrophil phagocytic and oxygen-stimulatory activities in the NBT test, and humoral immune mechanisms involved in the production of antinuclear antibodies, formation of circulating immune complexes, and restoration of morphological structure of spleen. Taken together, these results allow FC60 to be considered as a new potential pharmacological agent that can realize its effects mainly through anti-inflammatory and immunomodulatory activity.

C60 fullerenes appear to affect the innate immune system

An august 2012 publication Effect of buckminsterfullerenes o cells of the innate and adaptive immune system: an in vitro study with human peripheral blood mononuclear cellsreported: C60 nanoparticles, the so-called buckminsterfullerenes, have attracted great attention for medical applications as carriers, enzyme inhibitors or radical scavengers. However, publications evaluating their immunological mechanisms are still rather limited. Therefore, we aimed to analyze systematically the in vitro influence of polyhydroxy-C60 (poly-C60) and N-ethyl-polyamino-C60 (nepo-C60) on peripheral blood mononuclear cells (PBMC) from healthy individuals, angling their effect on proliferation, expression of surface markers, and cytokine production. We isolated PBMC from 20 healthy subjects and incubated them in a first step only with poly-C60 or nepo-C60, and in a second step together with recall antigens (purified protein derivative, tetanus toxoid, bacillus Calmette-Gurin). Proliferation was determined by (3)H-thymidine incorporation, activation of PBMC-subpopulations by flow cytometry by measurement of the activation marker CD69, and secretion of T helper cell type 1 (TH1)- (interferon-gamma [IFN-], tumor necrosis factor beta [TNF-]), TH2- (interleukin-5 [IL-5], -13, -10) and macrophage/monocyte-related cytokines (IL-1, IL-6, TNF-) into the supernatants by enzyme-linked immunosorbent assay. Both fullerenes did not influence T cell reactivity, with no enhanced expression of CD69 and production of T cell cytokines observed, the CD4/CD8 ratio remaining unaffected. In contrast, they significantly enhanced the release of IL-6 and CD69-expression by CD56 positive natural killer cells. PBMC, which had been cultured together with the three recall antigens were not affected by both fullerenes at all. These data indicate that fullerenes do not interact with T cell reactivity but may activate cells of the innate immune system. Furthermore, they seem to act only on nave cells, which have not been prestimulated with recall antigens, there are however, large inter individual differences.

C60 may affect platelet aggregation

A 2012 Russian publicationEffects of fullerene C60 nanocomposites on human platelet aggregationREPORTS: The effects of fullerene C(60) nanocomposites on human platelet aggregation induced by ADP, ristocetin, and collagen were studied. The nanocomposite containing fullerene C(60) in polyvinyl pyrrolidone solution did not change platelet aggregation, while fullerene C(60) in crown ether and Twin-80 solutions inhibited ADP-induced platelet aggregation by 20 and 30%, respectively. I do not know if the study was controlled to take account the effects of the solvents used.

Fullerenes can potentiate hair growth

The 2009 publicationFullerene nanomaterials potentiate hair growthreports Hair loss is a common symptom resulting from a wide range of disease processes and can lead to stress in affected individuals. The purpose of this study was to examine the effect of fullerene nanomaterials on hair growth. We used shaved mice as well as SKH-1 bald mice to determine if fullerene-based compounds could affect hair growth and hair follicle numbers. In shaved mice, fullerenes increase the rate of hair growth as compared with mice receiving vehicle only. In SKH-1 hairless mice fullerene derivatives given topically or subdermally markedly increased hair growth. This was paralleled by a significant increase in the number of hair follicles in fullerene-treated mice as compared with those mice treated with vehicle only. The fullerenes also increased hair growth in human skin sections maintained in culture. These studies have wide-ranging implications for those conditions leading to hair loss, including alopecia, chemotherapy, and reactions to various chemicals.

Less perspective be lost, it is important to keep in mind that the major interests in C60 relate to developing new structural materials and electronic applications.

For these reasons C60 is currently being manufactured in industrial quantities measured in tons and there has been considerable concern about the biological impact of C60 and other fullerenes being released into the environment.

Literature related to the toxicity of C60 comes to mixed conclusions. One the one hand, there has been much general concern about toxicities and long-term biological impacts of fullerenes. And theoretical studies strongly suggest toxic actions of C60 against DNA and other cell components. On the other hand, specific studies of C60 show few or no toxic effects on whole animals. Researchers caution against possible yet-unobserved long-term effects.

The rat longevity study mentioned earlier was basically conducted to measure C60 toxicity, and found little or none. Another 2012 study Sub-acute oral toxicity study with fullerene C60 in ratsreports: To obtain initial information on the possible repeated-dose oral toxicity of fullerene C60, Crl:CD(SD) rats were administered fullerene C60 by gavage once daily at 0 (vehicle: corn oil), 1, 10, 100, or 1,000 mg/kg/day for 29 days, followed by a 14-day recovery period. No deaths occurred in any groups, and there were no changes from controls in detailed clinical observations, body weights, and food consumption in any treatment groups. Moreover, no treatment-related histopathological changes were found in any organs examined at the end of the administration period and at the end of the recovery period. Blackish feces and black contents of the stomach and large intestine were observed in males and females at 1,000 mg/kg/day in the treatment group. There were no changes from controls in the liver and spleen weights at the end of the administration period, but those weights in males in the 1,000 mg/kg/day group increased at the end of the recovery period. Using liquid chromatography-tandem mass spectrometry, fullerene C60 were not detected in the liver, spleen or kidney at the end of the administration period and also at the end of the recovery period. In conclusion, the present study revealed no toxicological effects of fullerene C60; however, the slight increases in liver and spleen weights after the 14-day recovery period may be because of the influence of fullerene C60 oral administration. In the future, it will be necessary to conduct a long-term examination because the effects of fullerene C60 cannot be ruled out.

More on the cautious side is the 2009 book chapter Cytotoxicity and Genotoxicity of Carbon Nanomaterials: With the recent development in nanoscience and nanotechnology, there is a pressing demand for assessment of the potential hazards of carbon nanomaterials to humans and other biological systems. This chapter summarizes our recent in vitro cytotoxicity and genotoxicity studies on carbon nanomaterials with an emphasis on carbon nanotubes and nanodiamonds. The studies summarized in this chapter demonstrate that carbon nanomaterials exhibit material-specific and cell-specific cytotoxicity with the general trend for biocompatibility: nanodiamonds > carbon black powders > multiwalled carbon nanotubes > single-walled carbon nanotubes, with macrophages being much more sensitive to the cytotoxicity of these carbon nanomaterials than neuroblastoma cells. However, the cytotoxicity to carbon nanomaterials could be tuned by functionalizing the nanomaterials with different surface groups. Multiwalled carbon nanotubes and nanodiamonds, albeit to a less extend, can accumulate in mouse embryonic stem (ES) cells to cause DNA damage through reactive oxygen species (ROS) generation and to increase the mutation frequency in mouse ES cells. These results point out the great need for careful scrutiny of the toxicity of nanomaterials at the molecular level, or genotoxicity, even for those materials like multiwalled carbon nanotubes and nanodiamonds that have been demonstrated to cause limited or no toxicity at the cellular level.

Despite its apparent benevolence when ingested by rats, C60 and its derivatives solutions when photo-activated can produce singlet oxygen radicals which are biologically damaging.

For example, see Photo-Induced Damages of Cytoplasmic and Mitochondrial Membranes by a [C60]Fullerene Malonic Acid Derivative. On the one hand, the photo-activation properties of C60 appear to make it toxic and dangerous for some aquatic species(ref)(ref)(ref). So, there is serious concern about release of manufactured C60 into natural aquatic environments. On the other hand, there has been thought of exploiting these properties in photo-based anticancer therapies(ref). fullerenes can effectively photoinactivate either or both pathogenic microbial cells and malignant cancer cells. The mechanism appears to involve superoxide anion as well as singlet oxygen, and under the right conditions fullerenes may have advantages over clinically applied photosensitizers for mediating photodynamic therapy of certain diseases(ref). Photo-responsiveness of cells exposed to C60 can be fairly complex(ref).

I strongly suspect that a deeper biological mechanism is involved in the health and longevity-producing effects of C60 despite the prevailing wisdom. As I see it the candidates for these deeper effects of C60 are (1) effects exercised on DNA including impacts on structural configuration, epigenetic gene activation effects, histones and nuclear envelope shape, (2) effects exercised on microtubule structures in cells, (3) effects on mitochondria, and (4) epigenetic impacts such as on histones and DNA methylation.

I cannot prove this suspicion; that will require further research. However I can cite arguments that tend to confirm my suspicion.

(1) C60 is known to bind to and have impact on DNA. While the results of modeling studies indicate toxic effects on DNA, certain effects could possibly be beneficial.

That C60 binds to and deforms DNA has been known for some time. A 2005 publication C60 binds to and deforms nucleotides reported: Atomistic molecular dynamics simulations are performed for up to 20 ns to monitor the formation and the stability of complexes composed of single- or double-strand DNA molecules and C60 in aqueous solution. Despite the hydrophobic nature of C60, our results show that fullerenes strongly bind to nucleotides. The binding energies are in the range -27 to -42 kcal/mol; by contrast, the binding energy of two fullerenes in aqueous solution is only -7.5 kcal/mol. We observe the displacement of water molecules from the region between the nucleotides and the fullerenes and we attribute the large favorable interaction energies to hydrophobic interactions. The features of the DNA-C60 complexes depend on the nature of the nucleotides: C60 binds to double-strand DNA, either at the hydrophobic ends or at the minor groove of the nucleotide. C60 binds to single-strand DNA and deforms the nucleotides significantly. Unexpectedly, when the double-strand DNA is in the A-form, fullerenes penetrate into the double helix from the end, form stable hybrids, and frustrate the hydrogen bonds between end-group basepairs in the nucleotide. When the DNA molecule is damaged (specifically, a gap was created by removing a piece of the nucleotide from one helix), fullerenes can stably occupy the damaged site. We speculate that this strong association may negatively impact the self-repairing process of the double-strand DNA. Our results clearly indicate that the association between C60 and DNA is stronger and more favorable than that between two C60 molecules in water. Therefore, our simulation results suggest that C60 molecules have potentially negative impact on the structure, stability, and biological functions of DNA molecules.

The recent 2012 publicationA large-scale association study for nanoparticle C60 uncovers mechanisms of nanotoxicity disrupting the native conformations of DNA/RNA,a modeling study, reports: Nano-scale particles have attracted a lot of attention for its potential use in medical studies, in particular for the diagnostic and therapeutic purposes. However, the toxicity and other side effects caused by the undesired interaction between nanoparticles and DNA/RNA are not clear. To address this problem, a model to evaluate the general rules governing how nanoparticles interact with DNA/RNA is demanded. Here by, use of an examination of 2254 native nucleotides with molecular dynamics simulation and thermodynamic analysis, we demonstrate how the DNA/RNA native structures are disrupted by the fullerene (C60) in a physiological condition. The nanoparticle was found to bind with the minor grooves of double-stranded DNA and trigger unwinding and disrupting of the DNA helix, which indicates C60 can potentially inhibit the DNA replication and induce potential side effects. In contrast to that of DNA, C60 only binds to the major grooves of RNA helix, which stabilizes the RNA structure or transforms the configuration from stretch to curl. This finding sheds new light on how C60 inhibits reverse transcription as HIV replicates. In addition, the binding of C60 stabilizes the structures of RNA riboswitch, indicating that C60 might regulate the gene expression. The binding energies of C60 with different genomic fragments varies in the range of -56 to -10 kcal mol(-1), which further verifies the role of nanoparticle in DNA/RNA damage. Our findings reveal a general mode by which C60 causes DNA/RNA damage or other toxic effects at a systematic level, suggesting it should be cautious to handle these nanomaterials in various medical applications.

A 2011 publication DNA Exposure to Buckminsterfullerene (C60): Toward DNA Stability, Reactivity, and Replicationconveys a somewhat different story, indicating that fullernols not only have major impacts on the structures and biological properties of DNA, but also that they can contribute remarkably to DNA stability against thermal degredation.

Buckminsterfullerene (C60) has received great research interest due to its extraordinary properties and increasing applications in manufacturing industry and biomedical technology. We recently reported C60 could enter bacterial cells and bind to DNA molecules. This study was to further determine how the DNAC60 binding affected the thermal stability and enzymatic digestion of DNA molecules, and DNA mutations. Nano-C60 aggregates and water-soluble fullerenols were synthesized and their impact on DNA biochemical and microbial activity was investigated. Our results revealed that water-soluble fullerenols could bind to lambda DNA and improve DNA stability remarkably against thermal degradation at 7085 C in a dose-dependent manner. DNase I and HindIII restriction endonuclease activities were inhibited after interacting with fullerenols at a high dose. Experimental results also showed the different influence of fullerenol and nano-C60 on their antibacterial mechanisms, where fullerenols contributed considerable impact on cell damage and mutation rate. This preliminary study indicated that the application of fullerenols results in significant changes in the physical structures and biochemical functions of DNA molecules.

The general topic of nanopartucles binding is covered in a 2012 review publication Prospects of nanoparticleDNA binding and its implications in medical biotechnology. This remains a very new and immature area of research.

Right now it seems fair to conclude that C60 is very likely to bind to and interact with DNA/RNA, but the macroscopic outcomes of such interactions are unknown. There does seem to be contradictions between rodent studies that suggest no overall toxic effects of C60 and the molecular-chemical studies which suggest that C60 could play havoc with DNA.

(2) C60 is known to affect the formation and durability of microtubules.

First of all, a little on microtubules for those not familiar with them. Although almost never mentioned in the longevity literature they are critical to health and longevity. According to Wikipedia, Microtubules are a component of the cytoskeleton. These cylindrical polymers of tubulin can grow as long as 25 micrometers and are highly dynamic. The outer diameter of microtubule is about 25 nm. Microtubules are important for maintaining cell structure, providing platforms for intracellular transport, forming the mitotic spindle, as well as other cellular processes.[1] There are many proteins that bind to microtubules, including motor proteins such as kinesin and dynein, severing proteins like katanin, and other proteins important for regulating microtubule dynamics Microtubules are part of a structural network (the cytoskeleton) within the cells cytoplasm. The primary role of the microtubule cytoskeleton is mechanical. However, in addition to structural support, microtubules also take part in many other processes. A microtubule is capable of growing and shrinking in order to generate force, and there are also motor proteins that allow organelles and other cellular factors to be carried along a microtubule. This combination of roles makes microtubules important for organising cell layout. A notable structure involving microtubules is the mitotic spindle used by most eukaryotic cells to segregate their chromosomes correctly during cell division. The process of mitosis is facilitated by a subgroup of microtubules known as astral microtubules, defined as a microtubule originating from the centrosome that does not connect to a kinetochore. Astral microtubules develop in the actin skeleton and interact with the cell cortex to aid in spindle orientation. They are organized into radial arrays around the centrosomes. The turn-over rate of this population of microtubules is higher than that of any other population. Astral microtubules function in concert with specialized dynein motors, which are oriented with the light chain portion attached to the cell membrane and the dynamic portion attached to the microtubule. This allows for dynein contraction to pull the centrosome toward the cell membrane, thus assisting in cytokinesis. Astral microtubules are not required for the progression of mitosis, but they are required to ensure the fidelity of the process; they are required for the correct positioning and orientation of the mitotic spindle apparatus. They are also involved in determination of cell division site based on the geometry and polarity of the cells (ref).[2][3]

Image source

Microtubules and microfiliments

I first discussed microtubules in my blog entry Quantum Biology. There I pointed out how some quantum biologists argue that there is yet-another role for microtubules they are quantum computers possibly exercising command and control functions for cell processes. In fact it is known that microtubules are semiconductors as are certain arrays of fullerenes. However, the quantum computer role for microtubules remains controversial. For now, it is enough to know that microtubules are important for cell structure and are main rail lines for transport of molecules within cells.

The 2004 publication In Vitro and In Vivo Investigation of Collagen C60(OH)24 Interactionargues that fullerole affects intermolecular communications from collegen fibers through integrines and microtubules to cell nucleus.

A 2011 publication In vitro polymerization of microtubules with a fullerene derivative reports that a fullerene C60 derivative inhibits the polymerization of tubulin and therefore inhibits the formation of new microtubules. Fullerene derivative C(60)(OH)(20) inhibited microtubule polymerization at low micromolar concentrations. The inhibition was mainly attributed to the formation of hydrogen bonding between the nanoparticle and the tubulin heterodimer, the building block of the microtubule, as evidenced by docking and molecular dynamics simulations. Our circular dichroism spectroscopy measurement indicated changes in the tubulin secondary structures, while our guanosine-5-triphosphate hydrolysis assay showed hindered release of inorganic phosphate by the nanoparticle. Isothermal titration calorimetry revealed that C(60)(OH)(20) binds to tubulin at a molar ratio of 9:1 and with a binding constant of 1.3 0.16 10(6) M(-1), which was substantiated by the binding site and binding energy analysis using docking and molecular dynamics simulations. Our simulations further suggested that occupancy by the nanoparticles at the longitudinal contacts between tubulin dimers within a protofilament or at the lateral contacts of the M-loop and H5 and H12 helices of neighboring tubulins could also influence the polymerization process. This study offered a new molecular-level insight on how nanoparticles may reshape the assembly of cytoskeletal proteins, a topic of essential importance for illuminating cell response to engineered nanoparticles and for the advancement of nanomedicine. An in-vitro result, it suggests the opposite of a health-producing effect of C60 on microtubules.

Again, the interactions of C60 with cell microtubules and their creation and destruction appear to be not well understood. It seems such interactions do exist. Although modeling studies suggest that the macroscopic results of such interactions may be toxic rather than health-producing, we just dont know for sure.

(3) C60 buckballs cross cell barriers and preferentially localize themselves in mitochondria. There, they exercise powerful antioxidant effects and possibly other effects as well.

When fullerene is derivatized with polar groups, as in case of polyhydroxylated fullerenes (fullerenol) and C60 tris(malonic)acid, they become water soluble enabling them to cross the cell membrane and localize preferentially to mitochondria (Foley et al 2002; Youle and Karbowski 2005), which generate great masses of cellular oxygen free radicals. This phenomenon makes them useful for a variety of medical applications (Tsai et al 1997; Lotharius et al 1999; Bisaglia et al 2000). These radical scavengers have shown to protect cell growth from various toxins that can induce apoptotic injuries in vitro (Lin et al 1999; Lin et al 2002; Chen et al 2004) in different cell types such as neuronal cells (Dugan et al 1997; Bisaglia et al 2000), hepatoma cells (Huang et al 1998), or epithelial cells (Straface et al 1999).(ref)

Does C60 do more in the microchondria than act as a super anti-oxidant? Or does the super antioxidant power of C60 create permanent changes in the mitochondria? If the research literature is indicative, no one has so far grappled with these questions or even asked them for that matter.

Final comments

I could quote and discuss here only a small but hopefully representative sample of the unfolding literature related to C60 and its biological impacts. The rodent longevity studies are tantalizing but tiny and hopefully will be soon followed by much larger ones. There appear to be some basic contradictions and many more basic questions are raised than those answered. For rodents at least, far from being toxic pure C60 appears to be not only benevolent but life-extending. On the other hand, mostly-theoretical studies of the likely impacts of C60 on DNA and on microtubules and cell morphology suggest that C60 may generate all kinds of havoc on the cell level. Without question C60 is a powerful antioxidant. However it tends to generate permanent longevity-enhancing changes and it is not at all clear how an antioxidant could do that? How does it work to so grossly extend longevity? Are there other means through which C60 works its health and longevity benefits, and if so, what are they?

The literature references I have been able to surface seemed to focus on the lipid membrane and antioxidant and other chemical properties of C60 mostly 1990s ways of looking at biological mechanisms which are valid but limited. The research literature so far seems to be remarkably silent on certain issues that could turn out to be key: C60 and DNA methylation, impacts of C60 on histones, C60 and the DNA repair machinery, C60 as related to stem cells, C60 and siRNAs, and C60 as related to key known aging pathways. It the longevity impacts of C60 hold up, there are important layers of knowledge here yet to be revealed. If this were an archeological dig, we have so far only gone down a foot or two.

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Monday, August 6th, 2018

Healthy Body Paks

The entry level Healthy Body Paks (Start Pak, Weight Loss Pak, Blood Sugar Pak, etc. see above) are a great favorite among those new to the world of self-health through smart supplementation because they are both affordable and tailored to meet a variety of individual need. Selection is easy. Decide which one comes closest to describing the physical function you most wish to support, decide between the different flavors (tangerine, peach) and delivery formats (powder, pill, liquid) and, finally, select the one that is priced right for you.You cant go wrong. After all, Dr. Wallach has seen to it that each Healthy Body Pak delivers a foundation of all 90 nutrients essential to human health ("90 For Life") and that each Healthy Body Pak contains his built-in secret sauce. It is his secret sauce that makes everything work, that both enhances overall product performance and targets nutritional support to specific physiological function. And it is his 90 For Life foundation, a full spectrum of essential nutrients, that keeps the body supplied with everything it requires to perform optimally. Nothing is left to chance.....MORE

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