Longer Healthier Lifespans
posted on April 28, 2009
You are invited to the Party of the Century!
It™s a œCome as You Will Be Party.
In 2068, I will be 125 years old. Who, where and what will you be in 2068? If you want to take a peek into, and celebrate the future, then join the fun as the person you will be 59 years from now at my 125th birthday party on Saturday evening, May 23rd in Huntington Beach, CA.
Here™s the deal:
- First, even though some people think I look it, I™m not nearly 125¦ yet.
- We are going to project ourselves to 2068 at the party.
- You will act and speak as though it is 59 years from now. In fact, if you don™t agree to spend around two hours œin character, then stay home and let everyone else have the fun. There will be no 2009 discussions here unless you™re reminiscing. Come ready to talk about what you™ve done and accomplished from 2009-2068, where you™ve been, what you™ve become, what changes the world saw in the past 59 years, what you are doing now, what your plans are for the future and anything else you might come up with. What planet did you spend your last vacation on? Tell us about the miracle age-reversing drug you invented. How about your new warp speed family space ship? What about your new enhancements? Be creative.
- If you violate #3, you will be deposited into a worm hole in the basement which will immediately transport you back to where you came from on May 23rd, 2009.
- You will have up to five uninterrupted minutes to tell your personal story to the group if you™d like.
- Bring props if you want, including your futuristic wardrobe.
- You must deliver unto me an outrageously expensive birthday present (just kidding J).
- But do bring healthy food and drink. Remember, you won™t make it to 2068 by scarfing down pizza, cake, chips and soft drinks.
Everything will be quite different 59 years from now. Most people would tend to compare today with 59 years ago, 1950, and then project forward. If you™re tempted to do that, think again. Since the power of our technology is doubling every year now with no end in sight (at least over the next 50 years or so), our tools will be over 1000 times more powerful in only ten years. If this doubling holds up over the next 59 years, that means our technologies, particularly our computational power, will be a billion billion times more powerful. Yes, that™s a quintillion, or 1 followed by 18 zeros.
Whoa, I don™t know about you, but I can™t wrap my head around that number. It™s way too abstract for me. And I can™t even start to guess what those implications would be. I don™t know anyone who can make an accurate prediction. So let™s get down to a manageable number. Let™s call it a billion, OK? Nearly all serious scientists and futurists would agree this is conservative. So use your own imagination as to what life will be like in 59 years. Imagine what America will be like, the world, the solar system. Aging? In my humble opinion, that solution will be a slam dunk. I believe we would have solved aging well before then and will have moved on to bigger challenges.
We™ll have a wide variety of outlooks as to what we and the world will be in 2068. Some opinions on the future will be extremely aggressive, while others will be more conservative. We™ll have a mix of thought leaders, lay persons and those in between. Most of the attendees will be well schooled in extreme life extension possibilities as well as having a good handle on the basics as they apply to future technologies and their implications.
So what do you say? Are you up to spending part of Memorial Day weekend stretching your brain in Huntington Beach?
If so, RSVP email@example.com. You™ll get all the details and directions.
LATEST HEALTHY LIFE EXTENSION HEADLINES
An Interesting View of Calorie Restriction (April 24 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4175
Here is an interesting open access paper at PLoS ONE: "We generated microarray gene expression data from livers of male mice fed high calorie or [calorie restriction] CR diets, and we find that CR significantly changes the expression of over 3,000 genes, many between 10- and 50-fold. We compare our data to the GenAge database of known aging-related genes and to prior microarray expression data of genes expressed differently between male and female mice. CR generally feminizes gene expression and many of the most significantly changed individual genes are involved in aging, hormone signaling, and p53-associated regulation of the cell cycle and apoptosis. Among the genes showing the largest and most statistically significant CR-induced expression differences are Ddit4, a key regulator of the TOR pathway, and Nnmt, a regulator of lifespan linked to the sirtuin pathway. Our data show that CR induces widespread gene expression changes and acts through highly evolutionarily conserved pathways, from microorganisms to mammals, and that its life-extension effects might arise partly from a shift toward a gene expression profile more typical of females." So yet another theory to add to the many on the cause of longevity differences by gender.
Targeted Reprogramming of Cancer Cells (April 24 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4174
A good example of the sort of cellular hacking going on in the laboratory and early trials these days via EurekAlert!: researchers "have developed a nanoparticle - about one thousandth smaller than a printed period - that can travel through the blood stream. 'Decorated' with a tumor-targeting antibody, the nanoparticle is able to locate primary and hidden metastatic tumor cells and deliver its payload: a fully functioning copy of the P53 tumor suppressor gene. Normal cells have two copies of the functioning P53 gene. The protein produced by the P53 gene is activated to either coordinate the repair process in cells or induce cell suicide. In earlier work using animal models, [researchers] delivered functional p53 genes to tumor cells and tumor metastases in 16 different types of cancer, including prostate, pancreatic, melanoma, breast cancer and head and neck cancer. The presence of the replacement genes dramatically improved the efficacy of conventional cancer therapy. When the job of reinstating a normal P53 suppressor gene is done, the nanoparticle - essentially a little fat droplet wrapped around the gene - simply melts away, unlike non-biodegradable delivery systems. Clinical trials are now underway. The trial already has enrolled six patients with various cancers and anticipates a total of 14."
Theory: It's All Down To Autophagy (April 23 2009)
As I've mentioned in the past, autophagy - the process by which cells destroy and replace damaged or old components - seems to be very important in the natural longevity you are granted by the operation of your metabolism. It's required for the longevity boost given by calorie restriction, for example. Some groups would go so far as to say that most or all longevity-inducing tweaks to metabolism operate through increased autophagy: "Autophagy is involved in cellular protein and organelle degradation, which is mediated by the lysosomal pathway. [Autophagy] has a key role in cellular housekeeping by removing damaged organelles. During aging, the efficiency of autophagic degradation declines and intracellular waste products accumulate. In Caenorhabditis elegans, there is clear evidence that lifespan is linked to the capacity to regulate autophagy. Recent studies have revealed that the same signaling factors regulate both aging and autophagocytosis, thus highlighting the role of autophagy in the regulation of aging and age-related degenerative diseases. Here, we examine in detail the interactions of the signaling network involving longevity factors SIRT1, mTOR, FoxO3, NF-kappaB and p53 in the regulation of autophagy. We discuss the possibility that these well-known stress resistance and longevity factors regulate the aging process via autophagy."
NPR On the Ongoing Biotech Revolution (April 23 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4172
Times are changing, and some very interesting and transformative technologies are emerging from the life sciences. Expect biotech to look increasingly like open source software development in years ahead: "at least three major technologies are shovel-ready: the programming of tissues, the ability to engineer cells, and robots. These discoveries mean that one can write out a life code, manipulate a cell, and execute a specific desired function. It means we can convert cells into programmable manufacturing entities. But this software builds its own hardware, allowing companies to begin using bacteria to produce chemicals, fuels, medicines, textiles, data storage, or any series of organic products. A second major tsunami is our increasing ability to grow complex organic structures, such as limbs, bladders, hearts, and tracheas. All complex organisms start out as undifferentiated, pluripotent cells, meaning these cells contain an entire genome and are able to produce all body parts. Mexico's dinosaur-like axolotl salamanders naturally regrow body parts, including sections of their hearts and brains as well as whole limbs. And soon, it may be possible to do this without a full body, just some cells. As innovators begin to read, reproduce, and program life, they will change almost every industry across the globe."
Mannoheptulos as Calorie Restriction Mimetic (April 21 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4169
The success of Sirtris at enriching its founders has given further impetus to the field of calorie restriction mimetic compounds. Scientists respond to the same incentives as the rest of us, after all. Here, Science News notes one of the latest lines of investigation. Researchers "have been mining avocados [for] MH (mannoheptulose)]. It's a fairly simple sugar with a 7-carbon backbone. When fed to mice in fairly concentrated doses (roughly 300 milligrams per kilogram of an animal's body weight), it improved insulin sensitivity and the clearance of glucose from the blood. Meaning it helped overcome diabetes-like impairments to blood-sugar control. MH supplementation also improved the ability of insulin, a hormone, to get cells throughout the body to do its bidding (and that's a good thing). MH revved up the burning of fats in muscle. That's the opposite of fat deposition and something that these scientists note 'would be an expected effect of a calorie restriction mimetic.' Treated mice also lived longer - some 30 percent longer than untreated animals. Their food intake and weight matched that of untreated mice."
Growing Hair from Stem Cells (April 20 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4167
From the Daily Yomiuri, a short note on work aimed at tissue engineering new hair: a researcher "has succeeded in regenerating hair on mice using embryonic stem cells. Yamaki extracted mesenchymal stem cells taken from the teeth of mice embryos and mixed them with mice embryonic stem cells, which form the basis of skin cells. The clumps resulting from the mix were then nurtured. It was later found that about 40 percent of the 48 clumps had one or two hairs growing from them. When protein, which quickens growth, is added, the hair growth rate increased to about 60 percent. Hair growth was observed on all 12 mice that had the clumps implanted on their back muscles. Hair papilaries, which supply nourishment to the hair, also were found to have formed on the back muscle. If embryonic stem cells are combined with mesenchymal stem cells, which perform a number of other functions, a different organ can probably be created. The first thing I want to try to do is regenerate hair using human embryonic stem cells."
Regenerative Medicine for AMD (April 20 2009) http://www.longevitymeme.org/news/vnl.cfm?id=4166
From the Times Online: "scientists have developed the world's first stem cell therapy to cure the most common cause of blindness. Surgeons predict it will become a routine, one-hour procedure that will be generally available in six or seven years' time. The treatment involves replacing a layer of degenerated cells with new ones created from embryonic stem cells. The treatment will tackle age-related macular degeneration (AMD), the most common cause of blindness. Embryonic stem cells are transformed into replicas of the missing cells. They are then placed on an artificial membrane which is inserted in the back of the retina. Laboratory trials completed by the British team have demonstrated that stem cells can prevent blindness in rats with a similar disease to AMD. They have also successfully tested elements of the technology in pigs. The treatment would take 'less than an hour, so it really could be considered as an outpatient procedure. We are trying to get it out as a common therapy.' The clinical trial, due within two years, is expected to be the second in the world to use embryonic stem cells on humans. The first, on patients with spinal cord injuries, will start this year in America."