25th Annual TED Conference
posted on February 9, 2009
I spent most of Friday hanging around the 25th annual TED Conference (Technology, Entertainment, Design).
The conference brings together the world's most fascinating thinkers and doers, who are challenged to give the talk of their lives (in 18 minutes). It defines its mission as "ideas worth spreading". The lectures, also called TED Talks, cover a broad set of topics including science, arts and design, politics, culture, business, global issues, technology and development and entertainment. Speakers have included luminaries as former U.S. president Bill Clinton, Nobel laureates James D. Watson, Murray Gell-Mann, Al Gore, and internet entrepreneur Jimmy Wales and Google co-founders Sergey Brin and Larry Page. This year, Bill Gates opened the show.
The conference is a magnet for some of the key movers and shakers in science, technology and business. Hollywood superstars have also been known to attend some of the sessions, which this year included discussions about reframing and reconnecting the world around us, as well as a Segway tour of the Long Beach area and meditation classes.
Until now, the conference has been held in Monterey, California.
Approximately 370 TED talks are provided for free viewing online. As of January 2009, talks were viewed over 90 million times by more than 15 million people.
You can access the talks after the conference at www.TED.com, be among the 1500 people who pay $6000 to attend if you can get an invitation or if your application is accepted (2010 is already sold out), buy a new BMW and find a set of the TED Conference DVDs in your glove box, spend $1000 for a live feed in Palm Springs¦ or you can do what I did. You can go to one of the surrounding hotels and join a group of futurists, and watch a live feed.
Ryan Kaltman, a new but already close friend, invited me to a hospitality suite a block or two from the live event, generously hosted by Ken Rutkowski www.kenradio.com. The difference between watching it from home later and being in the area live is being able to meet some of the most interesting people on the planet. The attendees as a group are just as bright, progressive and successful as the speakers. I got to meet and hang out with some of them Fri afternoon and at a Fri eve party.
Nearly everyone there had a passionate interest in extreme life extension. These are the people who are making a positive future happen for you, the ones who are taking up the biggest challenges that our future presents, the challenges we™re going to need to respond to if we plan on living for a very long time.
The only negative things about the day were that it ended way too soon for me, and how stupid some of these geniuses made me feel.
If you want to get a real intellectual boost, if you want a megadose of optimism, or if you just want to let your hair down for a few days with kindred spirits, go to Long Beach, CA next February.
By the way, the TED Prize was introduced in 2005. Each year, three individuals are each given $100,000 and granted a "wish to change the world", which they unveil at TED.
So go to www.TED.com as soon as you finish this letter to pick and choose your favorite speakers and topics. Then plan on joining me at this hot event next year.
WHY WE NEED A WAR ON AGING “ From Reason
"Billions of dollars have been spent preparing for a flu epidemic. The Spanish flu killed 20 million people. Aging kills 30 million every year. It is the most under-researched cause of death and suffering relative to its significance. Whatever breakthroughs occur in medicine or health care generally, at the moment we face the inevitability of aging. That might not be necessary."
Gene Expression Signatures of Aging (February 06 2009) http://pmid.us/19189975
An interesting paper from the owner of senescence.info and collegues: "Numerous microarray studies of aging have been conducted, yet given the noisy nature of gene expression changes with age, elucidating the transcriptional features of aging and how these relate to physiological, biochemical, and pathological changes remains a critical problem. We performed a meta-analysis of age-related gene expression profiles using 27 datasets from mice, rats, and humans. Our results reveal several common signatures of aging, including 56 genes consistently overexpressed with age, the most significant of which was APOD, and 17 genes underexpressed with age. We characterized the biological processes associated with these signatures and found that age-related gene expression changes most notably involve an overexpression of inflammation and immune response genes and of genes associated with the lysosome. An underexpression of collagen genes and of genes associated with energy metabolism, particularly mitochondrial genes, as well as alterations in the expression of genes related to apoptosis, cell cycle, and cellular senescence biomarkers, were also observed. We suggest these molecular signatures reflect a combination of degenerative processes but also transcriptional responses to the process of aging." Supplementary data is available over at senescence.info.
Smoking and Accelerated Aging (February 06 2009) http://www.scienceblog.com/cms/effects-smoking-linked-accelerated-aging-protein-18505.html
Aging is exactly an accumulation of biochemical damage and the resulting disarray caused by that damage. We all know that smoking is bad for you, but it seems that smoking causes some of the same effects as one of the genetic conditions that causes accelerated aging: "Smoking can accelerate the aging process and shorten the lifespan by an average of more than 10 years. We focused on what happens within the lungs because of the similar aging effects, including atherosclerotic diseases and cancer, seen in people with Werner's syndrome and people who smoke. Werner's syndrome involves a genetic mutation that causes a deficiency in what's known as Werner's syndrome protein. The protein normally helps repair DNA damage. Smoking does not appear to cause the same mutation, but our study showed that it does decrease Werner's syndrome protein. The team also applied cigarette smoke extract to cultured lung fibroblasts taken from nonsmokers. They saw that Werner's syndrome protein expression was decreased, and the cells had lost their ability to repair wounds. In contrast, when the team caused the lung fibroblasts in petri dishes to overexpress Werner's syndrome protein, it had a protective effect and helped resist the damaging effects of cigarette smoke."
Intermediate Tissue Engineering Goals (February 05 2009) http://www.sciencedaily.com/releases/2009/02/090202175327.htm
For a long development process - such as the tissue engineering of replacement organs - to run to completion, there must be profitable uses for early, intermediate progress. Profit makes the world go round, after all. This EurekAlert! release looks at what can be done with slight advances in building complex tissue from scratch: "biomedical engineers can now grow and assemble living microtissues into complex three-dimensional structures in a way that will advance the field of tissue engineering and may eventually reduce the need for certain kinds of animal research. There is a need [for] tissue models that more closely mimic natural tissue already inside the body in terms of function and architecture. We think this is one step toward using building blocks to build complex-shaped tissues that might one day be transplanted." Research using cultured tissue will in due course be far cheaper than animal studies, which means that it will be widely adopted. This in turn will help to fuel advances towards the ultimate goal of building new tissue to repair age-damaged human organs.
Simpler Induced Pluripotency (February 05 2009) http://www.eurekalert.org/pub_releases/2009-02/cp-sfc020209.php
This path to creating pluripotent stem cells is becoming simpler: "the introduction of four ingredients could transform differentiated cells taken from adult mice into 'induced pluripotent stem cells' (iPS) with the physical, growth, and genetic characteristics typical of embryonic stem cells. Subsequent studies found that the four-ingredient recipe could in some cases be pared down to just two or three essential ingredients, [and] Now we've come down to just one that is sufficient. In terms of the biology, it's really quite amazing. Adult cells could be reprogrammed by adding four factors “ specifically Oct4, Sox2, Klf4, and c-Myc.
Recently, [researchers] demonstrated that Oct4 and Klf4 are sufficient to induce pluripotency in neural stem cells. By omitting Klf4 in the new study, they have now established that Oct4 is the 'driving force' behind the conversion of the neural stem cells into iPS cells. The lone transcription factor is not only essential, but it is also sufficient to make neural stem cells pluripotent." Simpler means cheaper, and cheaper means a broader range of applications in further development.
The Complex Trait (February 04 2009) http://ouroboros.wordpress.com/2009/02/04/systems-biology-of-aging-understanding-yeast-cr-by-network-inference/
From Ouroboros: "Aging is what geneticists like to call a 'complex trait' - simply put, a trait that is controlled by a large number of genes and the interactions between them. Complex traits differ from simple traits in the following way: When one is studying a simple trait, one simply identifies a mutant in the relevant trait and, after an ingenious combination of clever crosses and muscular cloning steps, finds the defective gene - thus gaining a great deal of explanatory power about the trait in question. When one is studying a complex trait, however, approaches like a mutant screen fall short. They don't fall totally flat - one of the great innovations of the last decade or so is the realization that we can learn quite a bit by studying aging at the single-gene level - but they can't get us all the way home. Suppose you do a screen and find fifty mutants that all lengthen lifespan by forty percent (not far from the situation in worms) - or, speaking more generally about complex traits, you find fifty loci in the human genome that are associated with a higher risk of schizophrenia. What then? What have you really learned about how the system works?" This complexity is why slowing aging by metabolic manipulation is a much harder path forward than aiming to preserve the metabolism we have by repairing the known damage of aging.
Confirmation of FOXO3A Link to Human Longevity (February 03 2009) http://www.uni-kiel.de/aktuell/pm/2009/2009-012-langlebigkeit-e.shtml
The FOXO3A gene is linked to the web of biochemical research surrounding calorie restriction, sirtuins and calorie restriction mimetics, and the rest of the major efforts in understanding how metabolism determines longevity. It is the human version of a gene already demonstrated to influence longevity in lesser animals: "A variation in the gene FOXO3A has a positive effect on the life expectancy of humans, and is found much more often in people living to 100 and beyond - moreover, this appears to be true worldwide. A research group [has] now confirmed this assumption by comparing DNA samples taken from 388 German centenarians with those from 731 younger people. We have now eliminated that uncertainty about the connection between FOXO3A and longevity, both by our results from the German sample study and by the support from our French partners in Paris, whose research on French centenarians showed the same trend. We can now conclude that this gene is probably important as a factor in longevity throughout the world."
Alzheimer's as Brain Diabetes (February 03 2009) http://news.bbc.co.uk/2/hi/health/7866022.stm
The view of Alzheimer's disease as a form of diabetes - and thus largely as avoidable as diabetes - continues to gather strength: "The relationship between insulin and brain disease has been under scrutiny since doctors found evidence that the hormone was active there. The latest [study] looked at the effects of insulin on proteins called ADDLs, which build up in the brains of Alzheimer's patients and cause damage. ... Sensitivity to insulin can decline with aging, which presents a novel risk factor for Alzheimer's disease - our results demonstrate that bolstering insulin signaling can protect neurons from harm. Recognizing that Alzheimer's disease is a type of brain diabetes points the way to novel discoveries that may finally result in disease-modifying treatments for this devastating disease. People with diabetes are at higher risk of developing Alzheimer's. It is well known that insulin affects how the brain works, and this research adds more evidence to the possibility that Alzheimer's could be a type of brain diabetes."
State of the Art in Targeted Cancer Therapies (February 02 2009) http://www.eurekalert.org/pub_releases/2009-02/uotm-tnf013009.php
Another example of what will be in the clinics a decade from now via EurekAlert! - and would be in the clinics now if the FDA didn't exist: "Hollow gold nanospheres equipped with a targeting peptide find melanoma cells, penetrate them deeply, and then cook the tumor when bathed with near-infrared light. Active targeting of nanoparticles to tumors is the holy grail of therapeutic nanotechnology for cancer. We're getting closer to that goal. When heated with lasers, the actively targeted hollow gold nanospheres did eight times more damage to melanoma tumors in mice than did the same nanospheres that gathered less directly in the tumors. The researchers packaged hollow, spherical gold nanospheres with a peptide - a small compound composed of amino acids - that binds to the melanocortin type 1 receptor, which is overly abundant in melanoma cells. They first treated melanoma cells in culture and later injected both targeted and untargeted nanospheres into mice with melanoma, then applied near-infrared light. The targeted nanospheres were actively drawn into the cells through the cell membrane. When the researchers beamed near-infrared light onto treated cultures, most cells with targeted nanospheres died, and almost all of those left were irreparably damaged."
On Intermittent Fasting (February 02 2009) http://www.latimes.com/features/printedition/health/la-he-fasting2-2009feb02,0,7813891,full.story
The Los Angeles Times looks at the science of intermittent fasting, one approach to calorie restriction: "In normal health subjects, moderate fasting - maybe one day a week or cutting back on calories a couple of days a week - will have health benefits for most anybody. We're not good at responding to too many calories, but we're very good at responding to fasting. Fasting, in itself, is not an unhealthy process. During fasting, almost every system in the body is 'turned down.' The body changes how it uses fuel. Certain hormone levels fall. Growth stops. Reproduction becomes impossible. By the end of three weeks of fasting you are a completely different metabolic creature. It affects many, many processes - but in a somewhat predictable way that takes you toward disease prevention. Intermittent fasting appears to offer the same advantages as long-term calorie restriction - defined as eating at regular times but consuming 25% to 30% fewer calories than what is recommended for that person based on age, size and gender."