FIGHT AGING! NEWSLETTER
October 29th 2012
The Fight Aging! Newsletter is a weekly email containing news, opinions, and happenings for people interested in aging science and engineered longevity: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives. This newsletter is published under the Creative Commons Attribution 3.0 license. In short, this means that you are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!
- Breaking the Wheel of Time
- What Happened to Protofection?
- Broadening Study of Mitochondrially Targeted Compounds
- Latest Headlines from Fight Aging!
- Gut Microbes in Aging
- The Cost of Smoking
- Reporting on the 2012 Singularity Summit
- A Report from the Alcor-40 Conference
- Persistent Infection Harms Long Term Health and Life Expectancy
- Simulating the Grandmother Effect
- Generating Cells to Treat Vascular Disease
- Exercise Beneficial for the Aging Brain
- More on Establishing an Australian Cryonics Provider
- Debates in the Mainstream of Aging Research
BREAKING THE WHEEL OF TIME
Mortality determines society. By this I mean that the function describing mortality rate by age in humans acts as a filter to determine the sort of societies that can exist and support themselves. A high mortality rate reduces the range of societies that can exist. The mechanisms at play in this relationship are economic in the broadest sense: a mix of population growth, division of labor, effectiveness in recording and transmitting knowledge, time preference, establishment of sufficient capital for more than just subsistence living. Consider the difference between the late paleolithic era and classical Greek civilization, for example, and think on why they are different.
In terms of mortality, the immediately noticeable difference between the classical era and prehistory is an upsurge in the number of people who reached old age - a reduction in the omnipresent violence between small groups, and a marginal improvement in medicine. As a general rule you don't find the bones of old people in early human archaeology: so few of them made it past 40 as to be close to absent entirely as a class. Mortality rates in classical Greek and early Roman times were horrific by modern standards, but enormously improved over those of prehistory.
Thus as a consequence there were both old people and a certain expectation of reaching old age - which means a rise in planning ahead and an increase in available capital. A longer vision breaks through destructive cycles of economic behavior that take place on shorter timescales. As one example, people cultivate their property more effectively if they think that it must last for longer under their stewardship, more readily resisting short-term gains that come at the cost of long-term gains. This incentive has operated throughout human history, whenever average life spans rose. A later example can be seen in the simultaneous rise of life span and economic well-being in 17th and 18th century England:
"If life cycle inspiration was present in rural England in the 18th century, farmers who were becoming aware that old people were gradually living for longer periods must have been more concerned about their own means of subsistence in the future. This may have been an important stimulus to reduce consumption, increase savings and take into account longer horizons."
Various destructive cycles of poverty to wealth to poverty exist for all time scales of human behavior and all population densities. A greater expected span of life doesn't make them go away entirely, but it does mean that more people will be around to suffer the consequences of ill-thought action - and as a result, endeavor to understand and avoid the acts that lead to suffering they see in others. Don't eat your own seed corn; be the ant rather than the grasshopper; don't cut down the whole forest; engage in trade rather than slavery; shun destruction in favor of construction; allow the merchant class to exist; and so forth. You might see the commonality here: it is restraining the urge to obtain short-term gains that harm the prospects for long-term gain.
One important thing to note is that all historical progress in expanding the range of possible human societies has come about without greatly altering the maximum human life span. It was possible to live to more than a century without modern medicine and in the presence of pervasive disease and violence - that outcome was just enormously unlikely for any given individual. Improved mortality rates led to a growth in the number of old people and their influence.
I submit that this largely unchanged outer limit to life span is why we can look back on thousands of years of politics to see the same patterns repeated over and again. Regions rise and fall. Empires form and decline. Countries become wealthy and then poor. Democracies slide into authoritarianism. Currencies are steadily debased and destroyed. Known and enumerated forms of governance arise over and again, and fail in the same ways each time. The patterns repeat because throughout history expectations regarding the outer limits of personal stewardship and responsibility remained set at something less than a century. It is that span of time that drives choices made between cultivating future growth versus squandering it for present advantage - and even drives whatever incentive exists to understand that you are taking one of those paths rather than the other.
After all, economics as a professional body of knowledge and theory only really evolved into the forms we'd recognize today in the wake of 17th to 18th century gains in longevity, after the rise and fall of physiocracy as a flawed means to explain the wealth or poverty of nations and how that related to human behavior.
Just as paleolithic hunter-gatherer groups were stuck in their own limited range of sustainable human societies, their choices and cultural evolution over time driven by high mortality rates at all ages and the near absence of elders, so are we also stuck in our own, larger range of possible societies. Our present span of life limits us to what we see. Where wealth, freedom, and the rule of law necessary to create wealth arise, they corrode over time as successive generations forget how and why their good fortune came about: they eat their own seed corn. We can see this happening in the US, somewhere past the mid-point of the process, and all somewhat analogous to the decline of the Roman Republic, at least insofar as root causes are considered: successful republics have a way of falling into empire and authoritarian rule, accompanied by massive military and welfare spending. Bread, circuses, and the legions.
All humans of our maximum life span and adult mortality rates low enough to allow for societies of cities and writing have found themselves trapped within the wheel of time I described above: the rise and fall of polities that takes place over centuries, poverty to wealth to poverty, or tribes to civilization to tribes. It is the consequence of our dominant short-termisms; where our time preference fails the test; where we squander our own potential.
The human condition has been bounded in this way for a very long time indeed, since the first cities arose more than 6,000 years ago, but it will not continue for much longer. In this age of biotechnology the transition from age-bounded life spans of a century to accident-bounded life spans of thousands of years will happen in the course of mere decades. Entire populations will stop dying as therapies capable of repairing the cellular and molecular damage of aging become widely available. Degenerative aging will become a controlled medical condition, warded and defeated like smallpox and others in the past century.
The wheel of time will be broken. Those who stand at the beginning and the height of empire will be the very same individuals who must also stand at its decline: their horizons will extend, and so the shape of empire will be quite different, if it comes about at all. How will this play out, this grand restructuring of all the incentives that lurk at the base of human societies? What new forms of society will emerge as possibilities given widespread radical life extension? These are open questions: the changes to human life span that lie ahead are dramatically different in character to those that have occurred in the past. The gulf in mortality and life span that likely lies between us and the humanity of the 22nd century is far greater than that separating paleolithic hunter-gatherers from the classical Greeks. Further, it will occur in a comparative eyeblink - a single generation will stand with one foot in each world.
Yet the wheel of time will be broken, and this seems to me to be a good thing.
WHAT HAPPENED TO PROTOFECTION?
Mitochondria are a roving herd of power plants that exist in every cell, storing energy in chemical form for use in powering cellular processes. They are the remnants of symbiotic bacteria-like organisms, and so bear their own DNA that encodes much of the protein machinery needed for their operation. Unfortunately, this mitochondrial DNA (usually abbreviated as mtDNA) sits right next to processes that generate reactive byproducts, and is far less protected than the DNA in the cell nucleus. It becomes damaged over time in ways that spiral out to harm the cell, harm surrounding tissue, and ultimately cause some fraction of degenerative aging.
Thus fixing mitochondrial DNA damage is an important line item for any future rejuvenation toolkit. Seven years ago, there was an unofficial claim of the ability to replace mitochondrial DNA in a laboratory animal using a methodology known as protofection. There has not been a great deal of progress on this front since then however: to the best of my knowledge, no-one else has managed to replicate that result. Yet that research group and others continue to work on the mechanisms used: so what's going on here?
At its heart, protofection is a cargo delivery method, and the cargo consists of gene sequences to be inserted into mitochondria - such as extra copies of important genes that tend to get damaged, causing mitochondrial dysfunction. The delivery mechanism is a protein assembled of various parts that enable it to (a) cross cell membranes, (b) be transported into the interior of mitochondria within the cell, and (c) participate in the normal processes of DNA replication. Thus a cargo of mitochondrial genes attached to this basic assembly will be carried to mitochondria and then added to the mitochondrial DNA that is already present.
This delivery protein is known of late as recombinant human mitochondrial transcription factor A (rhTFAM) ... In recent years, it seems that the core protofection research group has dropped the use of rhTFAM as a carrier and are instead focused on exploring how it might be used in and of itself, without any cargo, as a therapy for mitochondrial conditions. It so happens that rhTFAM boosts mitochondrial activity in some ways, and progressive mitochondrial dysfunction is implicated in a range of age-related conditions, especially in the brain. Even marginal therapies here could have meaningful market value.
You might look on this as one of the more subtle ways in which the present US regulatory structure for medical research and development distorts the undertaking of science. The FDA only permits clinical applications for specific named conditions, and thus anything other than the development of treatments for late-stage disease becomes either too expensive or outright forbidden. Treatment of aging falls into the latter category, as aging is not recognized as a medical condition that should be treated. So research efforts that might have some application to aging are sidelined into the development of marginal therapies for one specific disease, often type 2 diabetes, rather than what are arguably far more important applications.
BROADENING STUDY OF MITOCHONDRIALLY TARGETED COMPOUNDS
Mitochondria, the cell's herd of bacteria-like power plants, occupy an important position in processes of aging, metabolism, and many age-related conditions. Mitochondria produce damaging reactive oxidative molecules as a side-effect of their operation, and these can cause all sorts of havoc - such as by damaging mitochondrial DNA in ways that can propagate throughout the mitochondrial population of a cell, causing it to run awry and harm surrounding tissue. This happens ever more often as we age, and is one of the principle contributions to degenerative aging.
It is worth noting that a greater ability of mitochondria to resist this sort of self-inflicted oxidative damage is theorized to explain much of the longevity of many species that are unusually long-lived for their size - such as bats, naked mole-rats, and so forth.
Thus the researcher community is increasingly interested in finding ways to target therapies to mitochondria: to slow oxidative damage, fix that damage, repair other issues such as genetic disorders in mitochondrial DNA, or alter mitochondrial operation as a way of manipulating cellular behavior and metabolic processes. Building such a therapy usually means attaching a payload molecule to a delivery molecule or particle that will be (a) taken up by a cell, passing through the cell membrane, and then (b) swallowed by a mitochondrion within the cell, passing through that mitochondrion's membranes.
A range of different research groups are working on varied forms of delivery technology. Compare, for example, the repurposed protein machinery of rhTFAM with various plastinquione compounds or polymer nanoparticles. Or, more deviously, genetic engineering that makes a cell nucleus produce and export proteins to that cell's mitochondria. There are many others.
Diversity is a good thing - though of course not all of these strategies are equal in the sort of interventions that they can support. There is a world of difference between introducing more antioxidants into the mitochondria so as to blunt their creation of damaging, reactive byproducts and introducing new genes to repair damage to mitochondrial DNA. The former only gently slows the inevitable, while the latter reverses and repairs the harm done.
The highlights and headlines from the past week follow below. Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!
LATEST HEADLINES FROM FIGHT AGING!
GUT MICROBES IN AGING
Friday, October 26, 2012
Microbes in the digestive system seem to have some influence on aging, insofar as they interact with the immune system, epigenetic regulation of nearby tissues, and so forth. In effect they act almost like an additional organ or biological system. Researchers are very much in the early stages of trying to understand how microbial life in the body fits in to the bigger picture of metabolism and aging - which is already very complex, and likely to become more so: "The ageing process affects the human gut microbiota phylogenetic composition and its interaction with the immune system. Age-related gut microbiota modifications are associated with immunosenescence and inflamm-ageing in a sort of self-sustaining loop, which allows the placement of gut microbiota unbalances among both the causes and the effects of the inflamm-ageing process. Even if, up to now, the link between gut microbiota and the ageing process is only partially understood, the gut ecosystem shows the potential to become a promising target for strategies able to contribute to the health status of older people. In this context, the consumption of pro/prebiotics may be useful in both prevention and treatment of age-related pathophysiological conditions, such as recovery and promotion of immune functions ... Moreover, being involved in different mechanisms which concur in counteracting inflammation, such as down-regulation of inflammation-associated genes and improvement of colonic mucosa conditions, probiotics have the potentiality to be involved in the promotion of longevity."
THE COST OF SMOKING
Friday, October 26, 2012
There are numerous ways in which lifestyle choices can damage long-term health and lower life expectancy, but smoking remains one of the more effective, on a par with becoming obese: "The Life Span Study (LSS) was initiated in 1950 to investigate the effects of radiation, tracking over 100,000 people. However, most received minimal radiation exposure, and can therefore provide useful information about other risk factors. Surveys carried out later obtained smoking information for 68,000 men and women, who have now been followed for an average of 23 years to relate smoking habits to survival. The younger a person was when they started smoking the higher the risk in later life. Older generations did not usually start to smoke until well into adult life, and usually smoked only a few cigarettes per day. In contrast, Japanese born more recently (1920-45) usually started to smoke in early adult life, much as smokers in Britain and the USA. These differences in smoking habits are reflected in the mortality patterns. Smokers born before 1920 lost just a few years. In contrast, men born later (1920-45) who started to smoke before age 20 lost nearly a decade of life expectancy, and had more than double the death rate of lifelong non-smokers, suggesting that more than half of these smokers will eventually die from their habit. Results on the few women who had smoked since before age 20 were similar. In addition to studying the risk of smoking, the researchers were able to examine the benefits of stopping. As elsewhere, those who stopped smoking before age 35 avoided almost all the excess risk among continuing smokers, and even those who stopped around age 40 avoided most of it."
REPORTING ON THE 2012 SINGULARITY SUMMIT
Thursday, October 25, 2012
Videos of the presentations given at this year's Singularity Summit have yet to emerge online, but while we're waiting here is a report on the event: "Kurzweil took the stage on Saturday afternoon to deliver the summit's keynote address. "The singularity is near," he began quietly, a grin slowly spreading across his face. "No, it isn't here yet, but it's getting nearer," he said to laughs and applause. He spoke extemporaneously for over an hour, his presentation a mix of statistics, time series graphs, personal anecdotes, and predictions. Computing ability and technological innovation have been increasing exponentially over the past few decades, he argued, alongside similar increases in life expectancy and income. "All progress stems from the law of accelerating returns," he proclaimed. He discussed his latest project - an attempt to reverse-engineer the human brain. "Intelligence is at the root of our greatest innovations: genetics, nanotechnology, and robotics. Once we master artificial intelligence, unimaginable new frontiers will open up." After his talk, a man stood up and looked Kurzweil in the eye. "I'm in my 60s like you," he said, his voice faltering. "Do you think we'll make it?" It took me a few seconds to realize they were talking about immortality and I felt chills in that moment. "Life expectancy tables are based on what happened in the past," responded Kurzweil without skipping a beat. "In 25 years, we'll be able to add one year of life for every year that passes. We have a very good chance of making it through."" I should note that I believe Kurzweil's timelines for rejuvenation biotechnology are only possible if $300 million or more in dedicated research funding turns up at the SENS Foundation's front door tomorrow, thereby ensuring a good shot at demonstrating rejuvenation in old laboratory mice by the mid-2020s. As things stand progress towards the necessary technologies is far slower - not because it cannot be done, but because there is comparatively little interest in doing it, and therefore little funding. One of the deep puzzles of our age is how a multi-billion-dollar "anti-aging" industry, full of enthusiasm but providing nothing that significantly impacts aging, can exist alongside the near absence of interest in funding research that will produce therapies capable of reversing the progression of aging. There are strange tides at work in the psychology surrounding aging and longevity.
A REPORT FROM THE ALCOR-40 CONFERENCE
Thursday, October 25, 2012
Members of the cryonics community gathered for the Alcor-40 conference last week. Here is a report on the event: "I was expecting some excellent talks on the current state of cryonics technology, from the particulars of preservation via vitrification with powerful cryoprotectants, to the pragmatics of transitioning a recently deceased body from the site of death to Alcor's facilities. And the talks on these topics were indeed worthwhile, giving me faith that, in spite of quite limited funding for research and operations, Alcor is steadily improving all dimensions of their practice. Alcor's new CEO Max More started in the position fairly recently, and from what I can tell he's been doing a very professional job. What surprised me was the depth of the talks on longevity science and neuroscience. One definitely got the feeling that cryonics is not nearly as marginalized as it was a decade ago or even five years ago, and is now accepted as a reasonable pursuit by a rapidly increasing subset of the scientific community. Of course, this is part of a larger trend of the gradual mainstreaming of transhumanist technologies. AGI and nanotechnology, for example, were laughed at by most academics in relevant fields just 10-20 years ago. Now they are much more broadly acknowledged as valid and important pursuits, though there are still differences in vision between the maverick advocates and the interested folks in the academic mainstream."
PERSISTENT INFECTION HARMS LONG TERM HEALTH AND LIFE EXPECTANCY
Wednesday, October 24, 2012
The decline of the immune system is an important component of aging, and one of the causes of that decline is persistent infection by common herpesviruses such as cytomegalovirus (CMV). This is near harmless in the short term, but over time more and more of the limited repertoire of immune cells are devoted to the futile attempt to clear out CMV - and ever less are left free to tackle other threats. One possible solution is to destroy the CMV-specialized immune cells to free up space. This is a very plausible goal, given advances in targeted cell killing technologies emerging from the cancer research community. But here, scientists measure the cost of CMV infection in laboratory animals - more motivation for research groups that might be trying to build a therapy: "Persistent CMV infection has been associated with immune senescence. To address the causal impact of lifelong persistent viral infection on immune homeostasis and defense, we infected young mice systemically with HSV-1, murine CMV, or both viruses and studied their
SIMULATING THE GRANDMOTHER EFFECT
Wednesday, October 24, 2012
We humans are long-lived for our size when compared with other mammals. One possible explanation is the grandmother hypothesis, suggesting that evolutionary selection favored survival to increasing age because older members of a social group can increase the survival chances of their grandchildren. As for all hypotheses there are arguments against it, but here researchers have created simulations to support the concept: "The simulations indicate that with only a little bit of grandmothering -- and without any assumptions about human brain size - animals with chimpanzee lifespans evolve in less than 60,000 years so they have a human lifespan. Female chimps rarely live past child-bearing years, usually into their 30s and sometimes their 40s. Human females often live decades past their child-bearing years. The findings showed that from the time adulthood is reached, the simulated creatures lived another 25 years like chimps, yet after 24,000 to 60,000 years of grandmothers caring for grandchildren, the creatures who reached adulthood lived another 49 years - as do human hunter-gatherers. Based on earlier research, the simulation assumed that any newborn had a 5 percent chance of a gene mutation that could lead to either a shorter or a longer lifespan. The simulation begins with only 1 percent of women living to grandmother age and able to care for grandchildren, but by the end of the 24,000 to 60,000 simulated years, the results are similar to those seen in human hunter-gatherer populations: about 43 percent of adult women are grandmothers. The new study found that from adulthood, additional years of life doubled from 25 years to 49 years over the simulated 24,000 to 60,000 years. The competing "hunting hypothesis" holds that as resources dried up for human ancestors in Africa, hunting became better than foraging for finding food, and that led to natural selection for bigger brains capable of learning better hunting methods and clever use of hunting weapons. Women formed "pair bonds" with men who brought home meat. Many anthropologists argue that increasing brain size in our ape-like ancestors was the major factor in humans developing lifespans different from apes. But the new computer simulation ignored brain size, hunting and pair bonding, and showed that even a weak grandmother effect can make the simulated creatures evolve from chimp-like longevity to human longevity."
GENERATING CELLS TO TREAT VASCULAR DISEASE
Tuesday, October 23, 2012
Much of the stem cell research community is engaged in determining the recipes needed to create large numbers of specific types of cell for specific therapeutic uses. There are a few hundred different types of cell in the human body, so you'll periodically see announcements such as this as successes are achieved: "A new approach for generating large numbers of circulatory system cells, known as vascular endothelial cells (VECs), from human amniotic-fluid-derived cells (ACs) is reported ... The strategy, which shows promise in mice, opens the door to establishing a vast inventory of VECs for promoting organ regeneration and treating diverse vascular disorders. VECs line the entire circulatory system, including the heart and blood vessels, and they help to control blood pressure, promote the formation of new blood vessels, and support the regeneration and repair of injured organs. A wide range of vascular diseases stem from dysfunctions in VECs, so generating healthy cells for transplantation in patients would represent an attractive treatment strategy. But past stem cell strategies have fallen short: VECs derived from stem cells are unstable and tend to convert to nonvascular cells, and they do not increase rapidly in number, limiting their potential for clinical use. To overcome these limitations, [researchers] developed a safe approach for producing a large number of stable VECs from amniotic cells, which are extracted during routine amniocentesis procedures and thus represent a steady source of cells. To reprogram amniotic cells into mature and functional VECs, called rAC-VECs, the researchers turned specific genes on and off using members of the E-twenty-six family of transcription factors - proteins that bind DNA and are important for VEC development. The rAC-VECs resembled human adult VECs in that they expressed the normal set of vascular-specific genes. When rAC-VECs were transplanted into the regenerating livers of mice, they formed stable, normal, and functional blood vessels."
EXERCISE BENEFICIAL FOR THE AGING BRAIN
Tuesday, October 23, 2012
Regular exercise, much like calorie restriction, has a beneficial effect on near all measures of aging in humans - though unlike calorie restriction it doesn't increase maximum life span in laboratory animals. Here is a reminder that decline in brain function is slowed by exercise: "The new research included about 700 people living in the United Kingdom who all had brain scans when they reached the age of 73. Three years earlier, at age 70, the study participants were questioned about the leisure and physical activities they engaged in. People in the study who reported being the most physically active tended to have larger brain volumes of gray and normal white matter, and physical activity was linked to less brain atrophy. Regular exercise also appeared to protect against the formation of white matter lesions, which are linked to thinking and memory decline. [In another study, researchers] recruited 120 older inactive adults with no evidence of dementia. ... Half began a modest exercise routine that included walking at a moderate pace for 30 to 45 minutes, three times a week. The other half did stretching and toning exercises. A year later, MRI brain scans showed that a key region of the brain involved with memory, known as the hippocampus, was slightly larger in the walking group, while it has shrunk slightly in the non-aerobic stretching group. "The old view is that as we get older our brains become less malleable and less able to change. The new view is that it remains plastic even very late in life. We were able to show positive change after just one year of moderate-intensity physical activity.""
MORE ON ESTABLISHING AN AUSTRALIAN CRYONICS PROVIDER
Monday, October 22, 2012
The small cryonics industry provides a method of low-temperature storage after death, with the aim of preserving the fine structure in brain tissue that stores the data of the mind. Cryopreserved people can wait out the development of sufficiently advanced applications of molecular nanotechnology that are capable of restoring them to active life. Over the decades since the first cryonics providers were established the industry has not grown greatly, but it is nonetheless the only option other than the grave available to the billions who will die prior to the advent of biotechnologies to reverse aging. In a better world, cryonics providers would be as commonplace as funeral homes and near everyone would be preserved. But there are only a small number of active organizations: a couple in the US, a more recently launched project in Russia, and a few others in various stages of early development. At present it looks like an initiative to launch a cryonics provider in Australia is nearing fruition. Here is a recent article on this effort: "Milton first heard about cryonics as a kid, through reading science fiction, but only became seriously interested four years ago, while researching life-extension techniques. One night he attended a meeting of the Cryonics Association of Australasia (CAA) in a cafe in the city, where he met Peter Tsolakides, a retired manager for ExxonMobil, the oil company. At the meeting, both men were disappointed to discover that there was no cryonics facility in Australia. If you wanted to get frozen, you had to go to the USA. This is not impossible - the Cryonics Institute, in Michigan, has six Australians in cryopreservation, and the Alcor Life Extension Foundation, in Arizona, has two - but it is certainly inconvenient. You either had to be aware you were on the way out and get on a plane, quickly, or wait till you had de-animated and have someone, usually an obliging member from CAA, pack you in ice and mail you over. Either way, it was a logistical nightmare, and so Milton and Tsolakides decided to start a local operation. That was in 2009. Since then, Stasis has recruited 11 investors, each of whom has agreed to put in $50,000. This money will fund the construction of the facility, which should be complete by 2014, and pay for the investors' cryonic suspension, when the time comes. Milton, who works from home, spends his time liaising with NSW Health, which has been "very supportive", and, more recently, scouting for suitable land sites. "We are currently looking for a couple of acres in regional NSW - Yass, Wagga Wagga, Goulburn ... It has to be a low-risk area for natural disasters, like bushfires, earth tremors or flooding, and it needs to be somewhere with reliable power, sealed access and liquid nitrogen delivery routes, because liquid nitrogen is essential.""
DEBATES IN THE MAINSTREAM OF AGING RESEARCH
Monday, October 22, 2012
The most important strategic debate in aging science is over how to go about producing therapies for aging. The present dominant camp believes that only minimal progress is possible in the near term, and that altering the operation of metabolism is one of the few viable methods: they are aiming to gently slow aging, such as by replicating some of the beneficial changes that occur in calorie restriction. The minority position in this debate looks to build therapies capable of true rejuvenation, reversal of aging by repairing the cellular and molecular damage that causes aging. This is a path that should prove no harder, will produce far better results, but yet remains unpopular in the research community. If we want to see meaningful progress towards engineered longevity in our lifetimes, it is the path that will have to win out, however. The mainstream position has its own internal debates over strategy, as a recent article illustrates, while taking a swipe at the repair-based approach along the way: "In the current issue of Scientific American, author Katherine Harmon takes a brief look at two schools of thought in the field of human lifespan expansion science. One group believes lifespan can be extended by limiting diseases one at a time. Focusing on the top two, cancer and heart disease, they beleive will go a long way. "If we can focus on the major causes of death - cancer, cardiovascular disease - if we can really conquer those diseases and replace parts of the body if they wear out, that is the best possible outcome," gerontologist Sarah Harper is quoted as saying. The other group believes the actual underlying aging pathway itself can be slowed. This camp is represented by Dr . S. Jay Olshanksy at the University of Chicago. He believes that even if diseases are eliminated, cells and organs will age and degenerate and people will still age and die, perhaps some number of fixed years later. Olshansky is said with colleagues to be launching a "Manahttan-style project to slow aging" whose primary goal is to extend healthy lifespan by seven years in the next decade or two. Since disease risk doubles every seven years, slowing aging by seven years will reduce diseases by half. The aim of this group is to find compounds that slow aging. No specific mention was made in the article of Dr. Aubrey de Grey and his SENS Foundation and his premise that age-related damage can be fixed and aging reversed and halted. His efforts are derided by associating one his quotes that the first person to live to 150 has already been born to "pseudoscience backwater, swamped with snake oil and short-lived hopes."" The snake oil abounds amidst the lies and frauds of the "anti-aging" market of course, but it's simple laziness to associate serious scientific efforts like SENS with snake oil salesmen just because both groups say that they want to greatly extend healthy life.