Man himself, at the very least, is music, a brave theme that makes music also of its vast accompaniment, its matrix of storms and stars. Man himself in his degree is eternally a beauty in the eternal form of things. It is very good to have been man. And so we may go forward together with laughter in our hearts, and peace, thankful for the past, and for our own courage. For we shall make after all a fair conclusion to this brief music that is man.
Last and First Men
W. Olaf Stapeldon
The life of the universe appears to place a natural physical limit on immortality, although David Deutsch in his, The Fabric of Reality, makes a compelling case for the personal experience of immortality through a virtual experience of unending time.
Some of his thoughts may have changed, with the shift in physics and cosmology currently making a big crunch less likely than an infinite cosmological expansion driven by the effects of dark matter and dark energy.
All of these questions come to play when we think about immortality.
Immortality, grounded in science rather than myth and religion, can mean a number of different things, including:
Biological immortality maintaining a unique consciousness.
Immortality of consciousness separated from biology, but yet physically constituted.
Immortality of consciousness separated from biology, but virtually constituted.
One can think of all of these in their “strong” (analogous to the use of “strong” in “strong artificial intelligence”) form:
Physically based mechanisms enabling at minimum complete or even enhanced sensory experience, which we would recognize as existence;
Consciousness with the ability to interact and understand the physical world or some virtual equivalent of it (this might include the ability to reproduce); and
Vitality, vibrant health, or peak functioning.
Accidents can happen. A sun could go super nova. Some unforeseen or unforeseeable cosmic scaled event could blink everything out of existence. Any such event could cancel any of the proposed versions of immortality.
This leads us to a slightly weaker form of immortality, just a step down from the “strong” form.
This modified strong form would simply eliminate a physical (biological or mechanical) or virtual vehicle’s inherent constraints on immortality.
Knowledge and its application have measurably lengthened average human life span in developing countries. Only the sharing of this knowledge and the wealth to apply it constrains the same increases across the entire human population.
Still, knowledge and its application have not extended the length of life reached by the furthest outliers on the longevity distribution. Humans have an empirically observed limit of roughly 125 years.
Science and medicine have made us healthier for longer. Follow these advances and they have natural conclusions on at least three paths:
Healthier life to the full current limit (125 years).
Extending the limit.
Reversing the accumulated degenerative affects of aging.
Ray Kurzweil, Aubrey de Grey, and others have thought deeply about these questions and about how science can and will likely address these problems.
Much of medicine already does much of this. Researchers and clinicians work everyday to make life better and longer. Continue what they already do and medicine must approach the current limit.
When science and medicine reach a point where they can extend average life expectancy by one year every year, humans will have an average life expectancy rapidly approaching the current limit of 125 years.
A number of technologies seek to identify the cause of the limit and to extend it. Science has already reversed the accumulated degenerative affects of aging in mice. It has made mice functionally younger by all critical measures of aging: body mass index, metabolism, appearance, even reversing gray hair/fur.
When science and medicine reach a point where they can extend the limit by one year every year, we will all have for all practical purposes achieved biological immortality.
Would so changing or enhancing our biology change our consciousness? Perhaps. What might it mean?
I don’t want to be human. I want to see gamma rays, I want to hear X-rays, and I want to smell dark matter. Do you see the absurdity of what I am? I can’t even express these things properly, because I have to - I have to conceptualize complex ideas in this stupid, limiting spoken language, but I know I want to reach out with something other than these prehensile paws, and feel the solar wind of a supernova flowing over me. I’m a machine, and I can know much more.
John Cavil, Cylon Model Number One,
Battle Star Galactica, No Exit
A few resources:
Precautionary principle http://en.wikipedia.org/wiki/Precautionary_principle
Proactionary principle http://en.wikipedia.org/wiki/Proactionary_principle
Working in collaboration with Dr. Michael Kjaer and his research group at the Institute of Sports Medicine and Centre of Healthy Aging at the University of Copenhagen in Denmark, the UC Berkeley researchers compared samples of muscle tissue from nearly 30 healthy men who participated in an exercise physiology study. The young subjects ranged from age 21 to 24 and averaged 22.6 years of age, while the old study participants averaged 71.3 years, with a span of 68 to 74 years of age.
In experiments conducted by Dr. Charlotte Suetta, a post-doctoral researcher in Kjaer's lab, muscle biopsies were taken from the quadriceps of all the subjects at the beginning of the study. The men then had the leg from which the muscle tissue was taken immobilized in a cast for two weeks to simulate muscle atrophy. After the cast was removed, the study participants exercised with weights to regain muscle mass in their newly freed legs. Additional samples of muscle tissue for each subject were taken at three days and again at four weeks after cast removal, and then sent to UC Berkeley for analysis.
Morgan Carlson and Michael Conboy, researchers at UC Berkeley, found that before the legs were immobilized, the adult stem cells responsible for muscle repair and regeneration were only half as numerous in the old muscle as they were in young tissue. That difference increased even more during the exercise phase, with younger tissue having four times more regenerative cells that were actively repairing worn tissue compared with the old muscle, in which muscle stem cells remained inactive. The researchers also observed that old muscle showed signs of inflammatory response and scar formation during immobility and again four weeks after the cast was removed.
"Two weeks of immobilization only mildly affected young muscle, in terms of tissue maintenance and functionality, whereas old muscle began to atrophy and manifest signs of rapid tissue deterioration," said Carlson, the study's first author and a UC Berkeley post-doctoral scholar funded in part by CIRM. "The old muscle also didn't recover as well with exercise. This emphasizes the importance of older populations staying active because the evidence is that for their muscle, long periods of disuse may irrevocably worsen the stem cells' regenerative environment."
At the same time, the researchers warned that in the elderly, too rigorous an exercise program after immobility may also cause replacement of functional muscle by scarring and inflammation. "It's like a Catch-22," said Conboy.
The researchers further examined the response of the human muscle to biochemical signals. They learned from previous studies that adult muscle stem cells have a receptor called Notch, which triggers growth when activated. Those stem cells also have a receptor for the protein TGF-beta that, when excessively activated, sets off a chain reaction that ultimately inhibits a cell's ability to divide.
The researchers said that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells' capacity to effectively rebuild the body.
This study revealed that the same pathways are at play in human muscle, but also showed for the first time that mitogen-activated protein (MAP) kinase was an important positive regulator of Notch activity essential for human muscle repair, and that it was rendered inactive in old tissue. MAP kinase (MAPK) is familiar to developmental biologists since it is an important enzyme for organ formation in such diverse species as nematodes, fruit flies and mice.
For old human muscle, MAPK levels are low, so the Notch pathway is not activated and the stem cells no longer perform their muscle regeneration jobs properly, the researchers said.
When levels of MAPK were experimentally inhibited, young human muscle was no longer able to regenerate. The reverse was true when the researchers cultured old human muscle in a solution where activation of MAPK had been forced. In that case, the regenerative ability of the old muscle was significantly enhanced.
"The fact that this MAPK pathway has been conserved throughout evolution, from worms to flies to humans, shows that it is important," said Conboy. "Now we know that it plays a key role in regulation and aging of human tissue regeneration. In practical terms, we now know that to enhance regeneration of old human muscle and restore tissue health, we can either target the MAPK or the Notch pathways. The ultimate goal, of course, is to move this research toward clinical trials."
The NY Times just ran a short piece on a new treatment for tennis elbow: PhysEd: A New Treatment for Tennis Elbow .
“There’s a growing body of research showing that eccentric exercises are quite effective in treating Achilles tendonosis” and other tendon problems, Tyler says.
One of those studies was a well-designed 2007 experiment centered on tennis elbow. Conducted in Belgium, it found that eccentric exercises provided considerable relief. But the exercises had to be performed on expensive machines under medical supervision during repeated office visits. “We looked at those results and thought, there has to be an easier, more cost-effective way,” Tyler says.
Which is how they arrived at the rubber bar technique. He and his colleagues realized that a single, unhurried exercise using a tensile bar that looks like an oversized licorice stick could create an eccentric contraction all along the forearm. In the exercise, a person holds the bar upright at his or her side using the hand connected to the sore elbow, then grasps it near the top with the good hand. The top hand twists as the bar is brought around in front of the body and positioned perpendicular to the ground; the sore hand then takes over, slowly untwisting the bar by flexing the wrist. “Afterward, you should be sore,” Tyler says. “That’s how we know it’s effective.”
Eccentric contractions require the muscle to work against a force, in this case the coiled bar. “You can load a tendon so much more eccentrically” than with concentric exercises, Tyler says. “So we think the process may be remodeling the tendon.” Ultrasound studies by other researchers, including the group in Belgium, have shown that damaged tendons typically become less thick, indicating they are less damaged, after a course of strenuous eccentric exercise.
The article has an instructional video, also available on YouTube Isolated eccentrics with flexbar:
I ordered a flexbar at Amazon. $17.17 + shipping. Given the tendonitis I've worked around for years, it seems like a bargain.
Can we get some CrossFitters or other trainers to apply this idea of "isolated eccentrics" to other tendons?
The NY Times has an article out today with the intriguing title: Can Your Brain Fight Fatigue?:
Recently, researchers in England discovered that simply rinsing your mouth with a sports drink may fight fatigue. In the experiment which was published online in February in the Journal of Physiology, eight well-trained cyclists completed a strenuous, all-out time trial on stationary bicycles in a lab. The riders were hooked up to machines that measured their heart rate and power output. Throughout the ride, the cyclists swished various liquids in their mouths but did not swallow. Some of the drinks contained carbohydrates, the primary fuel used during exercise. The other drinks were just flavored, sugar-free water.
By the end of the time trials, the cyclists who had rinsed with the carbohydrate drinks — and spit them out — finished significantly faster than the water group. Their heart rates and power output were also higher. But when rating the difficulty of the ride, on a numerical scale, their feelings about the effort involved matched those for the water group.
In a separate portion of the experiment, the scientists, using a functional M.R.I., found that areas within the brain that are associated with reward, motivation and emotion were activated when subjects swished a carbohydrate drink. It seems that the brains of the riders getting the carbohydrate-containing drinks sensed that the riders were about to get more fuel (in the form of calories), which appears to have allowed their muscles to work harder even though they never swallowed the liquid.
I wonder how soon they'll start to market carbhydrate laden mouth washes to the low-carb set? Interesting stuff!
Most people training for a race or sport focus on adding more miles, workouts or weight training to improve their fitness. But new research suggests that simply getting more sleep can improve athletic performance.
The small study included five members of the Stanford women’s tennis team. For two to three weeks, the athletes maintained their regular schedules, sleeping and working out as usual. They took part in sprinting and hitting drills to measure their performance. Then the players were told to extend their sleep to 10 hours a night for five to six weeks.
After increasing sleep, the athletes performed better on all the drills. Sprinting drill times dropped on average to 17.56 seconds from 19.12 seconds. Hitting accuracy, measured by valid serves, improved to 15.61 serves, up from 12.6 serves, and a hitting depth drill improved to 15.45 hits, up from 10.85 hits.Nice to see these ideas hitting the mainstream press.
Objective: This study was designed to study the effect of vitamin C on training efficiency in rats and in humans.
Design: The human study was double-blind and randomized. Fourteen men (27–36 y old) were trained for 8 wk. Five of the men were supplemented daily with an oral dose of 1 g vitamin C. In the animal study, 24 male Wistar rats were exercised under 2 different protocols for 3 and 6 wk. Twelve of the rats were treated with a daily dose of vitamin C (0.24 mg/cm2 body surface area).
Results: The administration of vitamin C significantly (P = 0.014) hampered endurance capacity. The adverse effects of vitamin C may result from its capacity to reduce the exercise-induced expression of key transcription factors involved in mitochondrial biogenesis. These factors are peroxisome proliferator–activated receptor co-activator 1, nuclear respiratory factor 1, and mitochondrial transcription factor A. Vitamin C also prevented the exercise-induced expression of cytochrome C (a marker of mitochondrial content) and of the antioxidant enzymes superoxide dismutase and glutathione peroxidase.
The "Discussion" section continues:
When supplementing with vitamin C, there is the possibility that it may act as a prooxidant in vivo. These prooxidative reactions of vitamin C readily occur in vitro, and it has been shown that they also may have relevance in vivo (30). A high intake of iron along with ascorbic acid could increase in vivo lipid peroxidation of LDL and therefore could increase the risk of atherosclerosis (31). However, another study showed that, in iron-overloaded plasma, ascorbic acid acts as an antioxidant and prevents oxidative damage to lipids in vivo (32). In the present study, we measured different variables of oxidative stress, eg, blood glutathione oxidation and plasma malondialdehyde, in rats and men (data not shown); we did not find an indication of an in vivo prooxidant effect of vitamin C in any of the experimental groups.
Free radicals as signals in muscle cell metabolism: potential interference by antioxidant vitamins
It is important to consider that free radicals are not always damaging to cells; in many cases, they serve as signals to adapt muscle cells to exercise via modulation of gene expression (9, 33). We have found that training causes an increase in 2 major antioxidant enzymes (Mn-SOD and GPx) in skeletal muscle. We were surprised to see that vitamin C prevents these beneficial effects of training. On the basis of the paradigm that enzymatic antioxidant systems such as Mn-SOD and GPx provide a first-line defense against ROS, it is expected that exercise may induce these protective mechanisms. Moderate exercise increases life span and decreases disability in rats (12) and humans (15). We report here that exercise training causes an increase in the expression of antioxidant enzymes, which is prevented by the administration of vitamin C.
Moderate exercise as an antioxidant
A major conclusion that can be drawn from our experiments is that exercise itself is an antioxidant, because training increases the expression of 2 antioxidant enzymes related with longevity—namely, SOD and GPx. We provide evidence that the continuous presence of small stimuli, such as low concentrations of ROS, in fact induces the expression of antioxidant enzymes as a defense mechanism. Low concentrations of radicals may be considered to be beneficial, because they act as signals to enhance defenses, rather than being deleterious, as they can be when they are at higher concentrations.
If this holds up it should cause many of us to rethink supplementation (or at least certain supplements). Any counter science out there?