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| A good article from Singularity Hub examines an entrepreneurial medical practice in Colorado that offers stem cell therapies in defiance of the FDA. More of this sort of proactive civil disobedience is needed, but it has a way of ending badly for those involved, sadly. FDA bureaucrats have have not hesitated in the past to destroy legitimate and responsible businesses for failing to tow the line. From the article: "RSI provides its patients with the Regenexx procedure, an adult stem cell transplant that uses your own cells (autologous) to treat joint injuries and bone damage. There’s no surgery needed. A needle extracts bone marrow, RSI isolates the stem cells and cultures them in your own blood, and then these cells are injected into the area where they are needed. They've treated 348+ patients with 800+ injections and show no signs of slowing down. According to RSI's own surveys, 89% of their knee patients showed marked improvement, as did 75% of their hip patients! Within months some patients can walk or run in ways they haven't been able to in years. We've seen these kinds of results from stem cell treatments before, but only in horses and dogs. That's because human stem cell therapies like this one aren't approved by the FDA. How can [RSI] flaunt the lack of federal approval? They claim that Regenexx is solely used as a part of their medical practice, only within the state of Colorado, and as such is no more regulated by the FDA than it would be by the FAA or the Department of Motor Vehicles." |
| Via ScienceDaily: "Coronary arteries can become blocked with plaque, leading to a decrease in the supply of blood and oxygen to the heart. Over time this blockage can lead to debilitating chest pain or heart attack. Severe blockages in multiple major vessels may require coronary artery bypass graft surgery, a major invasive surgery. ... Successfully growing new arteries could provide a biological option for patients facing bypass surgery ... In the past, researchers used growth factors -- proteins that stimulate the growth of cells -- to grow new arteries, but this method was unsuccessful. [Researchers] studied mice and zebrafish to see if they could simulate arterial formation by switching on and off two signaling pathways -- ERK1/2 and P13K. ... We found that there is a cross-talk between the two signaling pathways. One half of the signaling pathway inhibits the other. When we inhibit this mechanism, we are able to grow arteries. Instead of using growth factors, we stopped the inhibitor mechanism by using a drug that targets a particular enzyme called P13-kinase inhibitor. Because we've located this inhibitory pathway, it opens the possibility of developing a new class of medication to grow new arteries. The next step is to test this finding in a human clinical trial." |
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| Almost nothing in biology is entirely immune to a good argument for altering what is presently thought of as cause and effect. Here, for example, a researcher argues that the metabolic syndrome we presently ascribe to excess fat, caused by eating too much, is in fact a direct consequence of that high calorie intake, not the fat. It is an intriguing view, but one that needs more evidence before being taken seriously, I think. From the release: "obesity is the body's way of storing lipids where they belong, in fat tissue, in an effort to protect our other organs from lipids' toxic effects. It's when the surplus of calories coming in gets to be too much for our fat tissue to handle that those lipids wind up in other places they shouldn't be, and the cascade of symptoms known as metabolic syndrome sets in. ... There is some disagreement in the field about whether insulin resistance is a primary cause of metabolic syndrome or just one of its features ... Insulin resistance is not the cause of metabolic syndrome, [according to this theory], it is a 'passive byproduct' of fat deposition in the liver and muscle once storage in fat cells begins to fail. ... Based on the genes they carry, some people will be better able to sustain lipid storage in fat and can get away with being overweight, even obese, without the other symptoms. Eventually, though, the need to cut calories is something all of us will face. ... Once you reach a certain age, almost everybody is leptin resistant. Nature stops protecting you once you pass the reproductive years." |
| A great deal of work is presently taking place to develop targeted nanoparticles to kill very specific types of cell with no side-effects or collateral damage. This is good, as the applications of this technology range far beyond cancer: the aging immune system, for example, or cases of autoimmune disease could benefit from killing off malfunctioning immune cells. Many other potential uses exist. Here is another example of work in progress: "researchers synthesized nanoparticles - shaped something like a dumbbell - made of gold sandwiched between two pieces of iron oxide. They then attached antibodies, which target a molecule found only in colorectal cancer cells, to the particles. Once bound, the nanoparticles are engulfed by the cancer cells. To kill the cells, the researchers use a near-infrared laser, which is a wavelength that doesn't harm normal tissue at the levels used, but the radiation is absorbed by the gold in the nanoparticles. This causes the cancer cells to heat up and die. ... This is a so-called 'smart' therapy. To be a smart therapy, it should be targeted, and it should have some ability to be activated only when it's there and then kills just the cancer cells." |
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| The Daily Bruin looks at the work of the Gerontology Research Group and Supercentenarian Research Foundation: "UCLA's Department of Pathology and Laboratory Medicine recently autopsied 115-year-old Gertrude Baines, formerly the oldest person in the world. Baines was one of the current 77 validated living supercentenarians in the world, a group including any person aged 110 years or older. She died Sept. 11, 2009 from Senile Systemic Amyloidosis ... Supercentenarians appear to escape from the common diseases that kill ordinary people, such as heart disease, cancer, stroke and diabetes, but there's another form of the grim reaper waiting in the wings ... Senile Systemic Amyloidosis is a common cause of death among supercentenarians. The mechanism involves a slow process in which a native protein called Transthyretin, which transports thyroid hormones to the body, becomes increasingly unstable. As humans age, the carrier protein begins to unravel and misfold, sticking to the inside of blood vessels and restricting blood flow. As a result, the heart undergoes hypertrophy, growing and working harder in an attempt to compensate ... The consequence of this process includes the symptoms of congestive heart failure, but without an autopsy, the attending physician would never know the underlying cause. ... Now that we've started this research, we can draw attention to Senile Systemic Amyloidosis and we can try to find a cure for this disease. Maybe supercentenarians could live healthy even longer." |
| I see that the Campaign for Aging Research has started a blog, populating it with fairly middle of the road posts on aging research. For example, this one on fat and diabetes risk: "It is thought that the increased chance of developing type 2 diabetes as a person ages is related to increasing insulin resistance. In an interesting study comparing insulin sensitivity between different groups of individuals, no difference was identified in insulin sensitivity between old and young athletes, between older and younger normal weight individuals, or between older and younger obese subjects. The athletes demonstrated the highest insulin sensitivity, followed by the normal weight individuals, with obese subjects having the lowest sensitivity to insulin. The authors concluded that aging alone cannot account for insulin resistance, but that the decreased physical activity and obesity that can occur with aging can be responsible for age-related insulin insensitivity. An increasing amount of research has been devoted to studying the relationship between physical activity, obesity and diabetes. It is now generally accepted that the presence of abdominal fat increases the risk for diabetes and cardiovascular disease." |
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| Here, researchers identify another piece of the molecular machineries of metabolism that help to determine life span: "a protein called Sestrin [serves] as a natural inhibitor of aging and age-related pathologies in fruit flies. ... Sestrins are highly conserved small proteins that are produced in high amounts when cells experience stress. Sestrin function, however, remained puzzling until [researchers] found that these proteins function as activators of AMP-dependent protein kinase (AMPK), and inhibitors of the Target of Rapamycin (TOR). AMPK and TOR are two protein kinases that serve as key components of a signaling pathway shown to be the central regulator of aging and metabolism. ... AMPK is activated in response to caloric restriction, a condition that slows down aging, whereas TOR is activated in response to over-nutrition, a condition that accelerates aging. Activation of AMPK inhibits TOR, and drugs that activate AMPK or inhibit TOR can delay aging in several different model organisms including mammals. But how the body keeps the activity of these two protein kinases in balance to prevent premature aging was unknown. ... In future work, [researchers plan] to examine whether the mammalian Sestrins also control aging and metabolism, and whether defects in proper Sestrin expression will provide the explanation to some of the currently unexplainable degenerative diseases associated with old age." |
| Biogerontologist Aubrey de Grey is amongst the speakers scheduled for a transhumanist community conference to be held in London in April. "How will accelerating technological change affect human mental and physical capabilities as well as the environment in which we live? Humanity+ UK2010, a one-day conference in London on 24 April 2010, gathers together some of the leading thinkers to discuss these and many other topics. ... Over the last year, the regular Saturday meetings of the UK Transhumanist Association have attracted larger and larger crowds eager to listen to and debate with speakers seeking to answer these vital questions. ... Inspired by the increasing popularity of these regular meetings, this one-day conference [gathers] together some of the leading thinkers in nanotechnology, biotechnology, cognitive science and their real-world implications. ... With 9 speaker sessions and two panel discussions confronting the big issues of tech change, this is your opportunity to engage in some of the big debates that will shape our future." I see that David Pearce will be speaking also: "In 1995, he wrote an online manifesto, The Hedonistic Imperative, advocating the use of biotechnology to abolish suffering throughout the living world." The Hedonistic Imperative - the urge to engineer paradise through technology - is an important contribution to transhumanist thinking, especially for those of us interested in engineering away the horrific, worldwide suffering caused by degenerative aging. |
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| Something to think about from EurekAlert!: "IGF-I is a protein hormone similar in structure to insulin and is regulated in the body by growth hormone (GH). Levels of GH and IGF-I decline progressively with age in both men and women and this drop is thought to be related to deteriorating health conditions found with advanced age. In an attempt to combat aging some people use GH as its actions elevate IGF-1. This study however showed that older men who had higher levels of IGF-I were more likely to die from a cancer-related cause in the following 18 years than men with lower levels. ... This is the first population-based study to show an association of higher IGF-I levels with increased risk of a cancer-related death in older men. Although the design of this study does not explicitly show that the higher IGF-I levels caused the cancer death, it does encourage more study as well as a reexamination of the use of IGF-I enhancing therapies as an anti-aging strategy. ... researchers used data on 633 men aged 50 and older from the Rancho Bernardo Study, a population-based study of healthy aging. ... In this study, the increased risk of cancer death for older men with high levels of IGF-I was not explained by differences in age, body size, lifestyle or cancer history." You might compare this with other findings on IGF-1 levels in long-lived humans. |
| From the IEET Blog: "When I was in undergrad, a professor asked our whole class a strange question. ... 'Lets say that I have in my hand, right now, a pill. This pill, if you take it, will make you ageless. [If] you would take this pill, raise your hand.' ... His point was not that people want to age and die but that we naturally distrust such offers. It simply sounds too good to be true. ... Our brains are trained, over time, to understand what a reasonably possible benefit can exist for a given price. A free pill that has no side-effects and no Twilight Zone caveats (you have to be alive, can't die so are tortured, etc) seems more impossible than the idea of anti-aging itself. The problem is that this protective aspect of our mind can become over excited, so we stop believing certain solutions are ever possible. To cure, or even significantly reduce the damages caused by aging, are such an epic benefit that it seems our minds will actively manufacture problems, because the benefit must have some sort of epic cost associated. So we tell ourselves curing aging will cause too many problems and that aging has a lot of natural beauty to it and creates a lot of meaning and that all of that is good." |
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| It is good that more new theories on the mechanisms of Alzheimer's disease are emerging, such as this, via EurekAlert! One thing you don't want to see in an advancing field of science is a monoculture of ideas. "For years we thought that A-beta was just metabolic garbage produced as a byproduct of other processes within the brain, but these data suggest it is a normal component of the brain's innate immune system. It looks like factors that trigger hyperactivity of the innate immune system - not only infection but also traumatic brain injury and stroke, which are already known to increase the risk for Alzheimer's - could cause excessive deposition of A-beta. ... The researchers suggest that chronic activation of the innate immune system in response to either a persistent or transient infection of the central nervous system might lead to excess production and accumulation of A-beta. Known Alzheimer's risk factors – such as stroke, head injury and exposure to certain anesthetics – could also trigger the innate immune system and increase A-beta production, leading to an excessive and dangerous inflammatory response within the brain. ... Now we need to figure out what is triggering the innate immune system, particularly as we age, and what genes control A-beta's role in the innate response. If we can identify which pathogens are more likely to trigger A-beta plaque aggregation, we might develop ways to prevent or control that response, for example by immunization." |
| Over at the Immortality Institute forums, researcher John Schloendorn (who worked on LysoSENS and is now one of the driving forces behind Livly) remarks: "I have a bazillion surplus Ending Aging books sitting at my house in Mountain View, CA. If anyone has a creative use for them, I can give them out for the cost of shipping or free if you pick them up." Ending Aging is a great book, and there are some good ideas in that discussion thread as to what to do with Schloendorn's surplus copies, such as handing them out at conferences, or donating them to libraries. If you have a good idea as to what to do with the copies, or would like one yourself, jump on in and have your say. |
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| The irreverent Viceland interviews Aubrey de Grey: "Typically, today, the therapies [of regeneration] involve things like injecting stem cells into the spinal cord or the heart in the vicinity of a trauma, to stimulate rebuilding of the damaged tissue, or else wholesale surgical replacement of an organ such as the heart or bladder with one created in the laboratory by tissue engineering. But as we progress, it will broaden to include 'molecular-level' regeneration, such as injecting enzymes (or the genes encoding them, depending on the target tissue) that can break down unwanted molecular byproducts of metabolism that are accumulating in cells as 'garbage' and that eventually impair cell function. In the case of injecting genes, we're talking about the standard techniques being developed for somatic gene therapy for inherited diseases: packaging the new DNA in a virus that worms its way into cells and integrates into the chromosome. (In many cases it will be doable much more safely, however, by performing this manipulation on stem cells outside the body, which can be verified for the correct genetic alteration before being injected.) The type of damage we repair need not be restricted to sudden, trauma-derived damage either - the gradually progressive damage that comprises aging is just as legitimate a target for regenerative medicine." |
| From the New York Times: "What, I’d like to know, will persuade the majority of Americans who remain sedentary to get off their duffs and give their bodies the workout they deserve? My hope is that every new testimonial to the value of exercise will win a few more converts until everyone is doing it. ... Physical inactivity is one of the strongest predictors of unsuccessful aging for older adults and is perhaps the root cause of many unnecessary and premature admissions to long-term care. ... [It has long been] well established that higher quantities of physical activity have beneficial effects on numerous age-related conditions such as osteoarthritis, falls and hip fracture, cardiovascular disease, respiratory diseases, cancer, diabetes mellitus, osteoporosis, low fitness and obesity, and decreased functional capacity. ... exercise [produces] a significantly reduced risk of cognitive impairment after two years for participants with moderate or high physical activity [when older] than 55. ... Sedentary skeptics are fond of saying that of course exercise is associated with good health as one ages; the people who exercise are healthy to begin with. But studies in which some participants are randomly assigned to a physical activity program and others to a placebo (like simply being advised to exercise) call their bluff. Even less exacting observational studies, like the Nurses' Health Study, take into account the well-being of participants at enrollment." |
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| Cancers depend on continually lengthening telomeres to overcome limits on cell proliferation. If that process can be blocked, it would stop cancer in its tracks. This is the basis of the SENS approach to cancer, WILT, but there are other initiatives aimed at a similar goal: "It starts with the enzyme telomerase, which affects the caps, or telomeres, at the end of a chromosome. Telomeres shorten over time. But telomerase prevents this from happening, making the cell immortal. If cancer is triggered in the cell, the presence of telomerase leads to the growth of the cancer. Telomerase is kept in control by the protein TRF1, which keeps the telomeres operating correctly. But another protein, Fbx4, can bind to TRF1 and degrade it, causing the telomeres to lengthen. Now, researchers have discovered, a third protein, TIN2, can step in and override Fbx4 by binding to TRF1 first and preventing Fbx4 from attaching to it. This finding paves the way for developing a drug that acts like TIN2, keeping everything in check ... In 90 percent of cancers, no matter what caused the cancer to form, it needs telomerase activity to maintain the cell. Without telomerase, the cell will die. Our work is key to understanding a detailed mechanism for how these molecules interact and how to design a drug to block Fbx4." |
| The NetAge Project website contains a lot of interesting information, even if the user interface leaves something to be desired: "Hundreds of genes and miRNAs have been identified as being involved in the determination of longevity, aging patterns and in the development of age-related diseases (ARDs). The interplay between these genes as well as the role of miRNAs in the context of protein-protein interaction (PPI) networks has as yet been poorly addressed. This work was undertaken in order to integrate the data accumulated in the field, from a network-based perspective. The results are organized in the NetAge database-an online database and network analysis tools for biogerontological research. ... The NetAge database contains gene sets and miRNA-regulated PPI networks for longevity, ARDs and aging-associated processes, and also common signatures (overlapping networks). The database is available through the NetAge website, which provides the necessary bioinformatics tools for searching and browsing the networks, as well as showing network info and statistics. By making these resources available online, we hope to provide the scientific community with a new, network-oriented platform for biogerontological research, and encourage greater participation in the systems biology of aging." |
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| Intriguing research: microvesicles "are several times smaller than a normal cell and contain genetic information such as messenger ribonucleic acid (RNA), other species of RNA and protein. ... During times of cellular injury or stress, or with certain diseases like cancer, infections and cardiovascular disease, these particles are shed and then taken up by other cells in the body. The genetic information and protein in the microvesicles helps to reprogram the accepting cell to behave more like the cell from which the particle was derived. ... Our work suggests that when the lung is injured or diseased and cells within the lung are stressed or dying, they shed microvesicles. Those microvesicles are then consumed by cells within the bone marrow, including stem cells, which are present in small numbers within the circulatory system. Those bone marrow cells then turn into lung cells. ... microvesicles not only supply information to stem cells with lung injury, but this process also occurs in other organs as well, like the heart, liver and brain. ... the change in those stem cells that have consumed microvesicles made by injured lung cells is very stable - the change appears to be permanent. ... This would be relevant to any type of disease - if you want to repair damaged tissue, these microvesicles potentially provide a durable fix, and the hope is that it would be fixed forever." |
| From the Campaign Against Aging website: "Pictures have just been uploaded of Doug distributing flyers to students at a college campus. ... I had a great time distributing these flyers. I would say 70% or more of the reactions I got were positive. Under 10% of people did not take a flyer, and about 20% responded negatively. I used a few different slogans while distributing the flyers. For the most past I used 'Death sucks. We should stop it.', followed by 'Dying is bad. We shouldn't do it.', and least frequently 'Getting old sucks. We should do something about it.' I got the highest proportion of positive reactions in the same order (which is why I used 'death sucks' most frequently). I distributed about 200-300 flyers total today. ... I talked to several people and groups at length about what is involved in fighting aging. I explained that aging is not a magical process and that we do not have a clock inside our body that makes us get older. Aging is just a building up of damage over time inside our cells, and that damage can be reversed. I explained briefly a few of the different kinds of age related damage, including lipofuscin accumulation and protein cross linking." |
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| Chinese researchers here demonstrate that some forms of fetal stem cell transplant are unambiguously beneficial in mice - the absence of cancerous development is perhaps surprising. This suggests that if an individual's stem cells could be sampled, altered to look more like fetal stem cells, and returned to the body, then they could achieve the same end: a general improvement in tissue repair, bodily systems, and life expectancy. From the paper: "To determine the role of allogeneil graft of mesenchymal stem cells in mammalian longevity, mesenchymal stem cells were isolated from [mouse fetal tissue] and then were purified and amplified by adherent culture. Identified P1 mesenchymal stem cells were injected [into] the 15-month-old [mother mice] three times. The mice were evaluated ... The results showed that after transplantation, the long-term surviving stem cells were found to be located in many organ tissues ... Median life span was increased in these animals after transplantation. Skin, cardiac, lung, kidney and colon pathology development were delayed. [Amongst other markers of aging, the degeneration] of heart function was attenuated [and markers of oxidative stress] were reduced three months after transplantation. These results support the idea that longevity can be enhanced by transplantation of mesenchymal stem cells." |
| Via CryoNet, some advice to follow on from the cautionary tale of a few days ago: "There has been some discussion about relatives causing suspensions to not take place as the cryonics member gets older and how we cryonicists can protect ourselves from this happening. Suspension interference happens more then most cryonicists realize. As a retired member of of Alcor management I have seen a lot of it. ... You think your relatives will continue to honor your wishes as you grow old? A lot of them will tall you to your face that they will, but in reality they believe that cryonics is a waste of your time and your money. So they have no moral reservations about causing you to cancel your membership and have the money go to them if and when they get a chance to take over. How can you protect yourself? Make sure that your life insurance policy says that if you don't get suspended for any reason that the proceeds still go to your cryonics organization and not your relatives. So there is no financial incentive for the relatives to cause you to cancel your arrangements. Put a clause in your will that says that if you don't get suspended that all your estate goes to your cryonics company and not your relatives so that there is a financial incentive for your relatives to see that you do get suspended." |
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