Because veterinary medicine is less (oppressively) regulated than human medicine, animals are benefiting from stem cell therapies that are safe enough for human use but nonetheless still illegal to commercially develop in the US: “In a very unusual breakthrough, a stem cell treatment for racehorses is ready to be tried … on you. British scientists pioneered a technique in horses where an individuals’ own stem cells are grown outside the body, then injected into the damaged tendon. There will be a clinical trial in the UK in which 24 human patients will undergo this radical new stem cell treatment for similar tendon injuries. We’ll tell you about the proven benefits in racehorses so you’ll understand the possible benefits in people. The test subjects who join the clinical trial will be in the unique position of enjoying a medical procedure that is years behind the veterinary equivalent. If human beings have the same barely believable 80% recovery rate, this will be a leap forward for sports medicine. … The reason animals can get commercial drugs and treatments faster than people in the US and other Western countries is simple: there is enormous oversight in human medical research. Veterinary research is comparably simple. According to the FDA, bringing a new drug to market for humans requires pre-clinical laboratory tests, animal tests, and human clinical trials. Each one of those steps costs money, lots and lots of it. Approval for veterinary drugs is simpler, requiring a single study that proves the drug is safe and effective. Because of regulatory difference, progress on animal medical research can move very quickly compared to human research.”

Link: http://singularityhub.com/2011/03/10/uk-stem-cell-company-cures-race-horse-tendons-humans-next/

I notice that Science Progress has thoughtfully posted an overview of a book that, like so many, passed beneath my distracted field of vision. It’s a good overview, and in reading it I’m struck by just how greatly modern fields of intellectual study have devolved into the title of this post – efforts to find smart ways to say profoundly stupid things. This isn’t the aim and goal at the outset, of course, but with postmodernism leading the way, there is a well defined sort of style that accompanies the ability of a community of intellectuals to cut themselves off from rationality and evidence in order to build castles in the sky. Up becomes down and left becomes right, and all sorts of nonsense rises to rule the roost. The end result is a core of stupidity well wrapped by a tremendous expenditure of earnest intellectual effort: a sort of Emperor’s new clothes situation wherein few parties involved have any incentive to point out the obvious.

Outside of theology and the worst reaches of postmodernism, this disconnect from reality is perhaps most evident in modern macroeconomics – largely an effort to convince the world against all the evidence that up is down and black is white – and the various fields of ethics, such as bioethics. The bioethics community in particular long ago lost its way.

But back to some examples from that Science Progress piece:

When I say that here, too, Agar builds his argument on an appeal to nature, I have in mind his foundational premise regarding what he calls “species relativism.” The “relativism” part of that label might at first sound like a rejection of anything resembling an appeal to nature. But Agar holds that there is something good, something worth preserving, about the way members of our species typically or naturally find happiness. As he puts it, “Experiences typical of the ways in which humans live and love are the particular focus of my species-relativism” (pg.15).

So for an enhancement to count as moderate on Agar’s account, it has to be “relative” to our species. As distinct from a radical or “purported” enhancement, a moderate one has to enhance a way of being that is typical of homo sapiens.

…

He argues that, while it is indeed reasonable to want more of “a recognizably human life,” it is not reasonable to want a form of life without the sorts of experiences that are typical for members of our species. As he says, there are some Galapagos tortoises that live up to 150 years, and they no doubt enjoy experiences that are pleasurable for members of their species, but no human being would trade our “distinctively human varieties of pleasure” for distinctively tortoise varieties of pleasure. Because, however, he grants the respect in which that example is unfair – becoming a tortoise would entail diminished cognition and radical life extension would not – he needs to say more.

He begins by suggesting that de Grey’s “Strategies for Engineered Negligible Senescence” (SENS) might create an obsessive fear of death, which might come to completely dominate the lives of those who adopted such strategies. Agar worries that, because negligibly senescent people would have more years of life to lose if they failed in one of their projects, they would have a strong reason not to take any risks at all (pg. 116). Indeed, at this point he invokes the concern that later in the book he will call its central theme: the concern about alienation, about becoming separated from the kinds of, here, risky experiences that constitute human lives as we know them. According to Agar, de Grey’s ambition to radically extend our lives “is likely to alienate us from the things and people who currently give our lives meaning” (pg. 122).

Agar allows that there may appear to be a way around the obsessive fear of death that SENS could bring about. To get around the risks associated with going out into the real world, he allows, negligibly senescent people could use technologies to have virtual experiences instead. But the problem with that strategy, he says, is that it fails to appreciate the extent to which human beings want “direct” contact with the “real” world. It fails to appreciate that “We think differently about these kinds of indirect contact [with the real world] than we do about ‘being there.’” No one, he suggests, thinks that “seeing a Discovery Channel documentary filmed on Mount Everest substitutes for actually climbing it” (pg. 123).

Castles in the sky, and straw ones at that. I would hope that little needs to be said in response to this sort of thing – it is so self-evidently hollow, a gut feel trying to cover itself in words and failing, that it falls apart at a glance.

A recent early stage trial demonstrated that first generation autologous stem cell transplants should be beneficial even if provided long after a serious damage has occurred. Large numbers of transplanted stem cells, grown over a period of weeks from a patient’s own cells, can spur the body to heal injuries that would normally linger:

Heart Damage Improves, Reverses After Stem Cell Injections in a Preliminary Human Trial:

Researchers have shown for the first time that stem cells injected into enlarged hearts reduced heart size, reduced scar tissue and improved function to injured heart areas … while this research is in the early stages, the findings are promising for the more than five million Americans who have enlarged hearts due to damage sustained from heart attacks. These patients can suffer premature death, have major disability and experience frequent hospitalizations. Options for treatment are limited to lifelong medications and major medical interventions, such as heart transplantation

…

Using catheters, researchers injected stem cells derived from the patient’s own bone marrow into the hearts of eight men (average age 57) with chronically enlarged, low-functioning hearts.

“The injections first improved function in the damaged area of the heart and then led to a reduction in the size of the heart. This was associated with a reduction in scar size. The effects lasted for a year after the injections, which was the full duration of the study,”

…

“This therapy improved even old cardiac injuries. [Some] of the patients had damage to their hearts from heart attacks as long as 11 years before treatment.”

This is generally good news for people who presently bear injuries and damage – or expect to suffer damage in the years between now and when stem cell medicine is in its prime. The most plausible future outcome looks to be that even the early stage and comparatively crude transplant therapies will provide significant benefits above and beyond any present form of medicine.

Of course, they would arrive far more rapidly and be far less costly in a world absent the FDA – but there is always medical tourism. A range of stem cell therapies that are presently forbidden from commercial development in the US have been available for several years elsewhere in the world:

The FDA forbids the development of new medical technologies long past the point at which any sane person would consider them a good risk, and in the process makes these technologies vastly more expensive. Medical tourism is a sane response to heavy-handed and unaccountable government employees: “Gregg Victor is one of the 1.5 million Americans who traveled abroad to get medical treatments last year. … More than a few were pursuing new stem-cell-based treatments unavailable in the States … ‘I am not waiting for the FDA to rule to get treatments,’ says Gregg Victor, who chose her clinic in Germany after spending a year and a half looking into stem cell treatments available all over the world. … Jordan happened upon TheraVitae, a Bangkok-headquartered biotechnology company that markets ‘VesCell stem cell treatments’ via licensing agreements with four clinics in Thailand … Thai doctors injected 25 million of his own stem cells into Jordan’s heart. Twenty thousand miles, 22 days, a cardiac arrest and $43,000 later, he came home to his wife with an ejection fraction between 30% and 35%. Even Jordan’s doctor had to admit he was happy with the results.” Results are mixed, much as you’d expect. Caveat emptor, and do your research – but a great many people are materially benefiting from technologies still forbidden by their own governments.

A recent open access paper from a Spanish research group outlines yet another methodology to add to the growing list of ways to increase healthy life span in mice. Progress is signified by diversity these days; there are, I think, more than twenty different demonstrated methods of bringing about meaningful extension of life in mice as of today.

RasGrf1 deficiency delays aging in mice:

We observed that mice deficient for RasGrf1-/- display an increase in average and most importantly, in maximal lifespan (20% higher than controls). This was not due to the role of Ras in cancer because tumor-free survival was also enhanced in these animals.

Aged RasGrf1-/- displayed better motor coordination than control mice. Protection against oxidative stress was similarly preserved in old RasGrf1-/-. IGF-I levels were lower in RasGrf1-/- than in controls. Furthermore, SIRT1 expression was increased in RasGrf1-/- animals. Consistent with this, the blood metabolomic profiles of RasGrf1-deficient mice resembled those observed in calorie-restricted animals.

...

Our observations link Ras signaling to lifespan and suggest that RasGrf1 is an evolutionary conserved gene which could be targeted for the development of therapies to delay age-related processes.

The results are similar to those noted for PAPP-A knockout mice - both longer lives and less cancer. At this stage it's anyone's guess as to whether many of these methodologies in fact operate through the same thicket of connections and mechanisms in mammalian biochemistry. Time, and further research, will tell.

RasGrf1 was mentioned here last year in connection with the intriguing bi-maternal mice:

mice artificially produced with two sets of female genomes have an increased average lifespan of 28%. Moreover, these animals exhibit a smaller body size, a trait also observed in several other long-lived mouse models. One hypothesis is that alterations in the expression of paternally methylated imprinted genes are responsible for the life-extension of bi-maternal mice. Considering the similarities in postnatal growth retardation between mice with mutations in the Rasgrf1 imprinted gene and bi-maternal mice, Rasgrf1 is the most likely culprit for the low body weight and extended lifespan of bi-maternal mice.

This latest work adds weight to the supposition quoted above.

The modest goals of the mainstream longevity science community are outlined by one of its members in this article - to enable everyone to age as slowly as only some people presently do. No radical life extension or rejuvenation, as would be enabled by the damage repair approach to longevity science, but rather just a gentle slowing of aging, enabled by technologies that would probably not emerge in time to benefit those of us in middle age today. "It is the aging of our cells that causes us to develop most diseases, says Dr. Nir Barzilai, professor of medicine and genetics at the Albert Einstein College of Medicine in New York. 'We know this, paradoxically, because of the amazing success we have had in treating heart disease. We have been able to save people from heart attacks with stents and bypass surgery - only to find that within a year or two they develop Alzheimer's, diabetes or cancer at an alarming rate. Why? Because we have never treated the underlying aging of their cells. We have simply treated the disease manifestation.' So, explains Barzilai, if we can find the processes in the body that control aging and find a way to treat them, we will be able to protect people from the diseases of aging. Barzilai heads a unique longevity study of more than 500 people who have reached the age of 100. The LonGenity study is looking at the genetic makeup of centenarians to identify the biological markers that explain why they live so long and so well. Because the remarkable thing about these people is not simply that they live to the age of 100, it is that they live to 100 in pretty good health. Just why they live that long without getting sick and dying is what Barzilai wanted to find out."

Link: http://www2.macleans.ca/2011/03/17/living-like-a-centenarian/

Via EurekAlert!: "A gene therapy called NLX-P101 dramatically reduces movement impairment in Parkinson's patients, according to results of a Phase 2 study ... The approach introduces a gene into the brain to normalize chemical signaling. ... The study is the first successful randomized, double-blind clinical trial of a gene therapy for Parkinson's or any neurologic disorder ... Half of patients receiving gene therapy achieved dramatic symptom improvements, compared with just 14 percent in the control group. Overall, patients receiving gene therapy had a 23.1 percent improvement in motor score, compared to a 12.7 percent improvement in the control group. ... Improved motor control was seen at one month and continued virtually unchanged throughout the six-month study period. ... Gene therapy is the use of a gene to change the function of cells or organs to improve or prevent disease. To transfer genes into cells, an inert virus is used to deliver the gene into a target cell. In this case, the glutamic acid decarboxylase (GAD) gene was used because GAD makes a chemical called GABA, a major inhibitory neurotransmitter in the brain that helps 'quiet' excessive neuronal firing related to Parkinson's disease. ... In Parkinson's disease, not only do patients lose many dopamine-producing brain cells, but they also develop substantial reductions in the activity and amount of GABA in their brains. This causes a dysfunction in brain circuitry responsible for coordinating movement."

Link: http://www.eurekalert.org/pub_releases/2011-03/nyph-gtr031411.php

Via EurekAlert!: "A gene therapy called NLX-P101 dramatically reduces movement impairment in Parkinson's patients, according to results of a Phase 2 study ... The approach introduces a gene into the brain to normalize chemical signaling. ... The study is the first successful randomized, double-blind clinical trial of a gene therapy for Parkinson's or any neurologic disorder ... Half of patients receiving gene therapy achieved dramatic symptom improvements, compared with just 14 percent in the control group. Overall, patients receiving gene therapy had a 23.1 percent improvement in motor score, compared to a 12.7 percent improvement in the control group. ... Improved motor control was seen at one month and continued virtually unchanged throughout the six-month study period. ... Gene therapy is the use of a gene to change the function of cells or organs to improve or prevent disease. To transfer genes into cells, an inert virus is used to deliver the gene into a target cell. In this case, the glutamic acid decarboxylase (GAD) gene was used because GAD makes a chemical called GABA, a major inhibitory neurotransmitter in the brain that helps 'quiet' excessive neuronal firing related to Parkinson's disease. ... In Parkinson's disease, not only do patients lose many dopamine-producing brain cells, but they also develop substantial reductions in the activity and amount of GABA in their brains. This causes a dysfunction in brain circuitry responsible for coordinating movement."

Link: http://www.eurekalert.org/pub_releases/2011-03/nyph-gtr031411.php

A recent early stage trial demonstrated that first generation autologous stem cell transplants should be beneficial even if provided long after a serious damage has occurred. Large numbers of transplanted stem cells, grown over a period of weeks from a patient's own cells, can spur the body to heal injuries that would normally linger:

Heart Damage Improves, Reverses After Stem Cell Injections in a Preliminary Human Trial:

Researchers have shown for the first time that stem cells injected into enlarged hearts reduced heart size, reduced scar tissue and improved function to injured heart areas ... while this research is in the early stages, the findings are promising for the more than five million Americans who have enlarged hearts due to damage sustained from heart attacks. These patients can suffer premature death, have major disability and experience frequent hospitalizations. Options for treatment are limited to lifelong medications and major medical interventions, such as heart transplantation

...

Using catheters, researchers injected stem cells derived from the patient's own bone marrow into the hearts of eight men (average age 57) with chronically enlarged, low-functioning hearts.

"The injections first improved function in the damaged area of the heart and then led to a reduction in the size of the heart. This was associated with a reduction in scar size. The effects lasted for a year after the injections, which was the full duration of the study,"

...

"This therapy improved even old cardiac injuries. [Some] of the patients had damage to their hearts from heart attacks as long as 11 years before treatment."

This is generally good news for people who presently bear injuries and damage - or expect to suffer damage in the years between now and when stem cell medicine is in its prime. The most plausible future outcome looks to be that even the early stage and comparatively crude transplant therapies will provide significant benefits above and beyond any present form of medicine.

Of course, they would arrive far more rapidly and be far less costly in a world absent the FDA - but there is always medical tourism. A range of stem cell therapies that are presently forbidden from commercial development in the US have been available for several years elsewhere in the world:

The FDA forbids the development of new medical technologies long past the point at which any sane person would consider them a good risk, and in the process makes these technologies vastly more expensive. Medical tourism is a sane response to heavy-handed and unaccountable government employees: "Gregg Victor is one of the 1.5 million Americans who traveled abroad to get medical treatments last year. ... More than a few were pursuing new stem-cell-based treatments unavailable in the States ... 'I am not waiting for the FDA to rule to get treatments,' says Gregg Victor, who chose her clinic in Germany after spending a year and a half looking into stem cell treatments available all over the world. ... Jordan happened upon TheraVitae, a Bangkok-headquartered biotechnology company that markets 'VesCell stem cell treatments' via licensing agreements with four clinics in Thailand ... Thai doctors injected 25 million of his own stem cells into Jordan's heart. Twenty thousand miles, 22 days, a cardiac arrest and $43,000 later, he came home to his wife with an ejection fraction between 30% and 35%. Even Jordan's doctor had to admit he was happy with the results." Results are mixed, much as you'd expect. Caveat emptor, and do your research - but a great many people are materially benefiting from technologies still forbidden by their own governments.

Researchers recently demonstrated that increased cellular housekeeping could slow neurodegeneration, and here a different group show the same outcome: "Cells, which employ a process called autophagy to clean up and reuse protein debris leftover from biological processes, were the original recyclers. A team of scientists [have] linked a molecule that stimulates autophagy with the reduction of one of Alzheimer's disease's major hallmarks, amyloid peptide. Their finding suggests a mechanism that could be used to eliminate built-up proteins in diseases such as Alzheimer's, Down syndrome, Huntingdon's and <a href="http://en.wikipedia.org/wiki/Beta_amylo&quot; the="The" molecule,="molecule," called="called" smer28,="SMER28," spurs="spurs" autophagy,="autophagy," which="which" in="in" turn="turn" eliminates="eliminates" unwanted="unwanted" materials="materials" such="such" as="as" amyloid-beta, the protein aggregates that cause Alzheimer's plaques. Increasing autophagy, either through a drug or a natural process such as diet, could improve the outcome for people with neurodegenerative diseases ... The researchers [tested] various compounds for their ability to reduce the buildup of amyloid-beta by exposing cultured cells to compounds known to activate autophagy. They then compared the effect of these compounds by removing growth factors from the culture medium, a well-established stimulant of autophagy known as 'starvation.' The researchers found that SMER28 was the most effective compound, and focused their studies on it to characterize the cellular components involved in this phenomenon. They compared the effect of SMER28 on amyloid-beta formation using normal cells or cells where the expression of genes known to be involved in autophagy was reduced or abolished. They found that three important autophagic players were involved, and one of them was essential for SMER28's effect."

Link: http://www.eurekalert.org/pub_releases/2011-03/ru-mts031611.php

The present generation of therapies for rheumatoid arthritis are based on TNF inhibition - a fairly crude manipulation of the immune system when considered in the grand scheme of what is possible, but one that is getting better. From Technology Review: "A new protein engineered to inhibit molecules that cause inflammation not only reduces symptoms of rheumatoid arthritis in mice but also may have potential to reverse the disease's course. Researchers hope the findings will point toward a new therapy for this crippling and difficult-to-treat disease, which occurs when the immune system attacks the body's own joints. Even medications that are most successful in halting joint inflammation are effective in only about half of the patients who try them. ... The new synthetic protein [appears] to target TNF in a far more specific fashion and could be produced at a small fraction of the cost [of present TNF inhibitors]. ... a protein called progranulin binds to TNF receptors and that administering the protein to mice with rheumatoid arthritis reduced or even eliminated their symptoms. Then they determined which fragments of progranulin were responsible for binding to TNF and combined those fragments to engineer a protein that works even better to suppress disease. Mice with mild arthritis appeared to be disease-free after several weeks of regular injections of the modified progranulin."

Link: http://technologyreview.com/biomedicine/35091/

The Global Forum for Longevity is an industry-sponsored forum taking place later this month; fairly mainstream, no talk of radical life extension or other forms of futurism that might lead to intellectual discomfort for some. I mention it because it is a symptom of the growing interest in biogerontology on the part of the vast insurance industries of the world - which should not be a surprising phenomenon. To find people likely to pay close attention to the future of longevity science, you want to look amongst the folk who stand to gain or lose a great deal of money due to changes in human life spans. Life insurance, pensions, and other forms of making money through managing statistical risks on life expectancy data are, taken together, a very big business indeed.

So here an insurance conglomerate is, as many of them are, sponsoring an event to help spread knowledge through the system: from scientists to actuaries to risk managers and other decision makers in the food chain. Building bridges and forming communities is in and of itself a form of risk management in the long term: it is a way to lower the likelihood of unpleasant surprises by trying to better understand what the scientific community believes are likely outcomes for longevity science over the decades ahead.

Some quotes from the conference site:

We are living in an era of radical change. Longevity offers us all an opportunity to make more ambitious life choices and look to the future with renewed hope. This is why it is vitally important that we move quickly to meet the challenges which it poses for our society.

Drawing on its expertise as an insurer, AXA is playing its part by creating a space to convene an exchange between decision-makers and experts working to ensure this phenomenon is better defined and fully grasped: the Global Forum for Longevity.

...

Our conviction as an insurer and observer of demographic and societal changes worldwide, is that longevity is not a fate to be endured but instead an opportunity. We need to respond quickly in order to meet the challenges which it poses to our society.

"Challenges." One thing to bear in mind here is that the big insurance groups are inextricably tied in to the unsustainable pension promises made by politicians past and present in many countries around the world - unsustainable even with modest increases in longevity, never mind what is likely to result from the biotechnology revolution. So there is a certain amount of long term public relations work being undertaken by various parties so as to avoid becoming the sacrificial goat in the end when the system of entitlements collapses. You can make your own decision as to how much of the motivation behind this conference falls into that bucket versus the knowledge transfer aims discussed above.

Empires end when an entrenched elite can spend from the public purse and take on debt without immediate consequence or forethought, destroying the value of their currency in the process. Assuming (perhaps optimistically) that present economic empires survive the next couple of decades, a combination of foolish promises and increasing human longevity will be the rock that sinks them.

Nanotechnology can be used to build assemblies of designed molecules that seek out specific cells - such as cancer cells - but an alternative approach to targeted therapies is to build machinery large enough to be controlled from outside the body, such as the microcarriers demonstrated here: "Soon, drug delivery that precisely targets cancerous cells without exposing the healthy surrounding tissue to the medication's toxic effects will no longer be an oncologist's dream but a medical reality ... sing a magnetic resonance imaging (MRI) system, [researchers] successfully guided microcarriers loaded with a dose of anti-cancer drug through the bloodstream of a living rabbit, right up to a targeted area in the liver, where the drug was successfully administered. This is a medical first that will help improve chemoembolization, a current treatment for liver cancer. ... The therapeutic magnetic microcarriers (TMMCs) [are made] from biodegradable polymer, [measure] 50 micrometers in diameter - just under the breadth of a hair - [and] encapsulate a dose of a therapeutic agent (in this case, doxorubicin) as well as magnetic nanoparticles. Essentially tiny magnets, the nanoparticles are what allow the upgraded MRI system to guide the microcarriers through the blood vessels to the targeted organ. During the experiments, the TMMCs injected into the bloodstream were guided through the hepatic artery to the targeted part of the liver where the drug was progressively released."

Link: http://www.eurekalert.org/pub_releases/2011-03/pm-wf-031511.php

Because veterinary medicine is less (oppressively) regulated than human medicine, animals are benefiting from stem cell therapies that are safe enough for human use but nonetheless still illegal to commercially develop in the US: "In a very unusual breakthrough, a stem cell treatment for racehorses is ready to be tried ... on you. British scientists pioneered a technique in horses where an individuals' own stem cells are grown outside the body, then injected into the damaged tendon. There will be a clinical trial in the UK in which 24 human patients will undergo this radical new stem cell treatment for similar tendon injuries. We'll tell you about the proven benefits in racehorses so you'll understand the possible benefits in people. The test subjects who join the clinical trial will be in the unique position of enjoying a medical procedure that is years behind the veterinary equivalent. If human beings have the same barely believable 80% recovery rate, this will be a leap forward for sports medicine. ... The reason animals can get commercial drugs and treatments faster than people in the US and other Western countries is simple: there is enormous oversight in human medical research. Veterinary research is comparably simple. According to the FDA, bringing a new drug to market for humans requires pre-clinical laboratory tests, animal tests, and human clinical trials. Each one of those steps costs money, lots and lots of it. Approval for veterinary drugs is simpler, requiring a single study that proves the drug is safe and effective. Because of regulatory difference, progress on animal medical research can move very quickly compared to human research."

Link: http://singularityhub.com/2011/03/10/uk-stem-cell-company-cures-race-horse-tendons-humans-next/

I notice that Science Progress has thoughtfully posted an overview of a book that, like so many, passed beneath my distracted field of vision. It's a good overview, and in reading it I'm struck by just how greatly modern fields of intellectual study have devolved into the title of this post - efforts to find smart ways to say profoundly stupid things. This isn't the aim and goal at the outset, of course, but with postmodernism leading the way, there is a well defined sort of style that accompanies the ability of a community of intellectuals to cut themselves off from rationality and evidence in order to build castles in the sky. Up becomes down and left becomes right, and all sorts of nonsense rises to rule the roost. The end result is a core of stupidity well wrapped by a tremendous expenditure of earnest intellectual effort: a sort of Emperor's new clothes situation wherein few parties involved have any incentive to point out the obvious.

Outside of theology and the worst reaches of postmodernism, this disconnect from reality is perhaps most evident in modern macroeconomics - largely an effort to convince the world against all the evidence that up is down and black is white - and the various fields of ethics, such as bioethics. The bioethics community in particular long ago lost its way.

But back to some examples from that Science Progress piece:

When I say that here, too, Agar builds his argument on an appeal to nature, I have in mind his foundational premise regarding what he calls "species relativism." The "relativism" part of that label might at first sound like a rejection of anything resembling an appeal to nature. But Agar holds that there is something good, something worth preserving, about the way members of our species typically or naturally find happiness. As he puts it, "Experiences typical of the ways in which humans live and love are the particular focus of my species-relativism" (pg.15).

So for an enhancement to count as moderate on Agar's account, it has to be "relative" to our species. As distinct from a radical or "purported" enhancement, a moderate one has to enhance a way of being that is typical of homo sapiens.

...

He argues that, while it is indeed reasonable to want more of "a recognizably human life," it is not reasonable to want a form of life without the sorts of experiences that are typical for members of our species. As he says, there are some Galapagos tortoises that live up to 150 years, and they no doubt enjoy experiences that are pleasurable for members of their species, but no human being would trade our "distinctively human varieties of pleasure" for distinctively tortoise varieties of pleasure. Because, however, he grants the respect in which that example is unfair - becoming a tortoise would entail diminished cognition and radical life extension would not - he needs to say more.

He begins by suggesting that de Grey's "Strategies for Engineered Negligible Senescence" (SENS) might create an obsessive fear of death, which might come to completely dominate the lives of those who adopted such strategies. Agar worries that, because negligibly senescent people would have more years of life to lose if they failed in one of their projects, they would have a strong reason not to take any risks at all (pg. 116). Indeed, at this point he invokes the concern that later in the book he will call its central theme: the concern about alienation, about becoming separated from the kinds of, here, risky experiences that constitute human lives as we know them. According to Agar, de Grey's ambition to radically extend our lives "is likely to alienate us from the things and people who currently give our lives meaning" (pg. 122).

Agar allows that there may appear to be a way around the obsessive fear of death that SENS could bring about. To get around the risks associated with going out into the real world, he allows, negligibly senescent people could use technologies to have virtual experiences instead. But the problem with that strategy, he says, is that it fails to appreciate the extent to which human beings want "direct" contact with the "real" world. It fails to appreciate that "We think differently about these kinds of indirect contact [with the real world] than we do about 'being there.'" No one, he suggests, thinks that "seeing a Discovery Channel documentary filmed on Mount Everest substitutes for actually climbing it" (pg. 123).

Castles in the sky, and straw ones at that. I would hope that little needs to be said in response to this sort of thing - it is so self-evidently hollow, a gut feel trying to cover itself in words and failing, that it falls apart at a glance.

Are clinical trials using animal studies always valid for humans? Consider me a skeptic.

I frequently see advertisements and newsletters (even some written by physicians) that promote lab tests and treatments based entirely on studies done using rodents. These “experts” frequently draw conclusions from these studies that their lab test or product is a breakthrough of vital importance to humanity. While it may be true, all too often it’s not.

Let me give you a recent example of a study done in mice that could lead to the conclusion that every woman with breast cancer should be taking very robust doses of the adrenal hormone DHEA. This study should serve both as an encouragement and as a caution, an example of the care we must exercise when we use animal studies to draw conclusions about humans.

In this test, laboratory mice had their ovaries removed, and were given a large dose of estrogen each day.  Small pieces of human breast cancer were transferred under the skin of these laboratory mice, and permitted to grow for 9 1/2 months.  During that time, some mice received treatment with DHEA while others did not. At the end of the test period, in the non-DHEA mice the tumors had expanded to nearly ten times their original size.  By contrast, the mice that were given varied doses of DHEA had much smaller tumors.  How much smaller? Depending on the dosage, the tumors in the treated mice were anywhere from 50% to an amazing 80% smaller.  The optimum dose seemed to be about 1 milligram of DHEA daily.

Sounds compelling. But how does this translate into the DHEA dose for a human woman?  Well, let’s do some basic math:

The average laboratory mouse weighs about 20 grams.  I’ll use my wife (with her permission, of course) as a sample female human: she is a small woman, weighing about 50 kilograms (or 50,000 grams). I’m a relatively big guy at about 100 kilograms, or 100,000 grams.  This means that my small wife is about 2,500 times larger than a mouse – and I am about 5,000 times larger!

You can see the obvious problem. Just consider how much DHEA my wife would have to take to match the one milligram mouse dose – 2,500 milligrams of DHEA per day. If I were the patient I would need twice as much: 5,000 milligrams per day!  Since the average over-the-counter DHEA pill provides a 25 milligram dose, my wife would need 100 pills per day and I would have to take 200.

I’ve seen medical studies in which patients were given 100 milligrams per day of DHEA.  The negative side effects were almost nonexistent.  But no one knows what would happen if you gave a human being 2,500 milligrams of DHEA every day, and I frankly don’t know anybody crazy enough to find out. DHEA is a potent participant in the body’s intracrine system (the hormones that work inside our cells). DHEA is converted into a variety of sex hormones in virtually every tissue in the body and is also part of the neurotransmitters within the brain. No one has any idea of what would happen to a human being taking such massive doses.

Does research on rodents and other animals have value? I’m sure it does. But at Longevity Medical Clinic we strongly prefer to base our treatments on peer-reviewed studies done on human beings. That’s a sure way of making sure we’re prescribing just the right dose – for a person, not a mouse!