|
|
| Are you new to healthy life extension? Click here to find out more about living a longer, healthier life. More >> |
|
|
|
|
| Sign up for our weekly newsletter! It contains news, opinions, and commentary for people interested in healthy life extension: making use of diet, lifestyle choices, technology, and proven medical advances to live longer, healthier lives. |
|
|
|
|
|
You can help to make therapies for aging and life extension medicine a reality. Click here to participate in improving your future health and longevity!
|
|
|
|
|
Place our comments, news and links on your website, or subscribe to our RSS feed. Click here to see how easy it is.
|
|
|
|
|
We help you stay up to date with the most interesting news in medicine, politics and the healthy life extension community. You can help us by contacting us when you see interesting items online. You can search past news postings through Google by using the form to the right.
|
|
|
|
|
| Excess fat tissue in your body actively works to change your metabolism, and largely for the worse. Here's a reminder of that fact: "Scientists are reporting new evidence that the fat tissue - far from being a dormant storage depot for surplus calories - is an active organ that sends chemical signals to other parts of the body, perhaps increasing the risk of heart attacks, cancer, and other diseases. They are reporting discovery of 20 new hormones and other substances not previously known to be secreted into the blood by human fat cells and verification that fat secretes dozens of hormones and other chemical messengers. ... [Researchers] note that excess body fat can contribute to heart disease, diabetes, cancer and other diseases. Many people once thought that fat cells were inert storage depots for surplus calories. But studies have established that fat cells can secrete certain hormones and other substances much like other organs in the body. Among those hormones is leptin, which controls appetite, and adiponectin, which makes the body more sensitive to insulin and controls blood sugar levels. However, little is known about most of the proteins produced by the billions of fat cells in the adult body." |
| The mainstream press notices sarcopenia: "Bears emerge from months of hibernation with their muscles largely intact. Not so for people, who, if bedridden that long, would lose so much muscle they would have trouble standing. Why muscles wither with age is captivating a growing number of scientists, drug and food companies ... Comparisons between age groups underline the muscle disparity: An 80-year-old might have 30 percent less muscle mass than a 20-year-old. And strength declines even more than mass. Weight-lifting records for 60-year-old men are 30 percent lower than for 30-year-olds; for women the drop-off is 50 percent. With interest high among the aging, the market potential for maintaining and rebuilding muscle mass seems boundless. Drug companies already are trying to develop drugs that can build muscles or forestall their weakening ... In addition, geriatric specialists, in particular, are now trying to establish the age-related loss of muscles as a medical condition under the name sarcopenia. ... But with sarcopenia still not established as a treatable condition, 'there is no real defined regulatory path as to how one would get approved in this area.'" When you live under a regime in which all that is not permitted is forbidden, it should be no surprise that progress is slow and expensive. One of the best things that could happen for medicine in this modern age is to tear down the FDA and other similar regulatory bodies. |
|
|
|
|
| The mainstream view of aging in the adaptive immune system is that too many memory T cells exist, uselessly specialized and using up limited resources that should be devoted to the naive T cells needed to tackle new threats. An alternative (and not mutually exclusive) theory is presented in this paper: that memory cell populations are failing in old age, meaning that acquired immunity vanishes. "Evidence is accumulating that old individuals are more susceptible to infection with organisms to which they were previously immune, indicating that there might be a limit to the persistence of immune memory. The prevailing concept is that defects in memory T-cell populations result from inexorable end-stage differentiation as a result of repeated lifelong antigenic challenge. We discuss here mechanisms that might constrain the persistence of memory T cells and consider whether humans will suffer from memory T-cell exhaustion as life expectancy increases." Whether or not this in fact occurs, the proposed therapies would look much the same as for other immune system issues known to occur with aging: destroy the old, misconfigured, damaged immune cells and replace them with new cells grown from the patient's stem cells. |
| As researchers peer more deeply, the accelerated aging condition progeria continues to look very much like one aspect of "normal" aging run amok: "Children with Hutchinson-Gilford progeria syndrome (HGPS) exhibit dramatically accelerated cardiovascular disease (CVD), causing death from myocardial infarction or stroke between the ages of 7 and 20 years. We undertook the first histological comparative evaluation between genetically confirmed HGPS and the CVD of aging. ... We present structural and immunohistological analysis of cardiovascular tissues from 2 children with HGPS who died of myocardial infarction. Both had features classically associated with the atherosclerosis of aging, as well as arteriolosclerosis of small vessels. In addition, vessels exhibited prominent adventitial fibrosis, a previously undescribed feature of HGPS. Importantly, although progerin was detected at higher rates in the HGPS coronary arteries, it was also present in non-HGPS individuals. Between the ages of 1 month and 97 years, progerin staining increased an average of 3.34% per year in coronary arteries. ... Vascular progerin generation in young non-HGPS individuals, which significantly increases throughout life, strongly suggests that progerin has a role in the cardiovascular aging of the general population." |
|
|
|
|
| One consequence of the success of calorie restriction research is that scientists are now more closely investigating the biochemistry of exercise - and its potential to slow aging. For example: "Brain aging is a period of decreasing functional capacity and increasing vulnerability, which reflect a reduction in morphological organization and perhaps degeneration. Since life is ultimately dependent upon the ability to maintain cellular organization through metabolism, this review explores evidence for a decline in neural metabolic support during aging, which includes a reduction in whole brain cerebral blood flow, and cellular metabolic capacity. Capillary density may also decrease with age, although the results are less clear. Exercise may be a highly effective intervention for brain aging, because it improves the cardiovascular system as a whole, and increases regional capillary density and neuronal metabolic capacity. Although the evidence is strongest for motor regions, more work may yield additional evidence for exercise-related improvement in metabolic support in non-motor regions. The protective effects of exercise may be specific to brain region and the type of insult. For example, exercise protects striatal cells from ischemia, but it produces mixed results after hippocampal seizures. Exercise can improve metabolic support and bioenergetic capacity in adult animals, but it remains to be determined whether it has similar effects in aging animals. What is clear is that exercise can influence the multiple levels of support necessary for maintaining optimal neuronal function." |
| An example of the next generation of targeted cancer therapies: "Since last April, 19 cancer patients whose liver tumors hadn't responded to chemotherapy have taken an experimental drug. Within weeks of the first dose, it appeared to work, by preventing tumors from making proteins they need to survive. The results are preliminary yet encouraging. With a slight redesign, the drug might work for hundreds of diseases, fulfilling the promise that wonder cures like stem cells and gene therapy have failed to deliver. ... We can turn off any one of 20,000 genes with RNAi. The challenge has been to get a drug into only the desired cells and not harm others. ... Researchers have worried that a drug might disrupt normal protein production in a healthy cell, or that the immune system will destroy the drug before it reaches its target. [Scientists] overcame both concerns by packaging the drug in a fatty envelope that is absorbed primarily by the liver. This allowed doctors to administer the drug through the blood, rather than by an injection to one spot, which improves results by ensuring that the entire liver receives an even dose. The technique's ability to attack single genes could lead to drugs for the 75 percent of cancer genes that lack any specific treatment, as well as for other illnesses. [Researchers are] already testing RNAi therapy for Huntington's disease and high cholesterol in cell cultures; other researchers are tackling macular degeneration, muscular dystrophy and HIV. The potential has driven nearly every major pharmaceutical company to start an RNAi program." |
|
|
|
|
| From The Week: "In 20 years, we will have stem cell banks like pharmacies. You will get a specific diagnosis and take a specific type of stem cell. ... Meantime, scientists are using cells to produce pig hearts, rat livers, and mice teeth that grow independently in a lab. Anthony Atala, director of the Wake Forest Institute for Regenerative Medicine, grows human bladders, and has implanted more than two dozen of them in human patients since 2006. ... Hollow organs are easier to create than solid ones, but researchers have recently made strides with livers, hearts, and even lungs. Major challenges remain. But sometime in the future, scientists hope, humans will be able to mimic the processes that enable other animals to regenerate body parts. When a salamander loses a leg, it sprouts a new one. A zebra fish can even regenerate a portion of its heart. Humans can regenerate bones and skin, but like other higher species, lost the capacity to regrow limbs and organs during the process of evolution. By manipulating specific genes, scientists may turn this miraculous power back on. ... In a world in which aging or diseased people can swap a damaged heart, liver, or other organ for a new one created from their own DNA, a majority of children alive today might live to 100 or beyond. It's hard to know how far-reaching the effects might be because we're still only at the dawning of the biological revolution. But true believers have seen enough to predict changes of historical import. ... We're beginning to understand how life is coded and how life makes things. How we make things, where we make things, is going to change on a scale similar to that of the Industrial Revolution. It's already happening." |
| Broadly, we might think that there are two types of degeneration that accompany aging: the forms that are largely preventable via lifestyle choices, and the forms that you can only slow down, even with the best tools presently available. Insulin resistance is an example of the former, and mitochondrial damage is an example of the latter. From a recent review paper: "This review addresses the question whether insulin sensitivity and mitochondrial oxidative capacity are independently affected during aging and type 2 diabetes. ... Humans with or at risk of type 2 diabetes frequently exhibit insulin resistance along with structural and functional abnormalities of muscular mitochondria. Low mitochondrial oxidative capacity causes muscular fat accumulation, which impedes insulin signaling via lipid intermediates, in turn affecting oxidative capacity. However, insulin sensitivity is not generally reduced with age, when groups are carefully matched for physical activity and body fatness. Moreover, lifestyle intervention studies revealed discordant responses of mitochondrial oxidative capacity and insulin sensitivity. ... In the elderly, low mitochondrial oxidative capacity likely results from age-related effects acquired during life span. Insulin resistance occurs independently of age mostly due to unhealthy lifestyle on top of genetic predisposition. Thus, insulin sensitivity and mitochondrial function may not be causally related, but mutually amplify each other during aging." |
|
|
|
|
| From Nature: "A model published this week questions a popular theory dubbed the 'grandmother hypothesis', which says that human females, unlike those of the other great apes, survive well past their reproductive prime because of the benefits that post-menopausal women offer to their grandchildren. ... Chimps almost never live into their forties in the wild, but most humans, if they're lucky enough to make it to adulthood, live beyond the childbearing years. ... Despite its anecdotal support and intuitive appeal, the grandmother hypothesis lacked much quantitative proof showing that it was possible for longevity to evolve from grandmothering ... [Researchers] ran a mathematical simulation to test the theory's plausibility. Their agent-based model, which simulates the actions and interactions of individuals, begins with a population of 1,000 people whose lifespans and reproductive windows are an inherited trait that mutates over time. ... After about 500 generations, the model demonstrated that the assistance of a grandmother during infancy shortened the interval between the times their daughters give birth, and led to shorter reproductive windows. However, compared with simulations in which grandmothers did not help out, the benefits never result in a change in longevity. ... In hindsight [the] result isn't as surprising at it might seem. Natural selection is strongest early in life, and its influence on a trait wanes as an organism ages. Therefore, the benefits of grandmothering would have to be enormous to extend human lifespan." |
| A post on autophagy at Metamodern: "I’d like to say a few words about one of the hottest and, in my view, most important areas in biomedicine: autophagy, a process crucial to health, disease, and aging. Autophagy research is expanding rapidly. In autophagy ('self eating'), cells engulf and digest their own macromolecules and organelles. Autophagy serves two functions: providing critical nutrients in times of scarcity, and recycling damaged cellular structures. ... It seems that lab animals and human beings fed ad-libitum do too little autophagic recycling. The resulting accumulation of damaged machinery causes a wide range of functional deficits, and accumulation of damaged mitochondria, in particular, increases the production of reactive oxygen species, accelerating further damage. In a range of organisms, dietary restriction both induces autophagy and results in wide-ranging health benefits, including the extension of healthy lifespans. Blocking autophagy blocks the most important of these effects. Rapamycin induces autophagy and extends lifespan, as does sirtuin-1. Autophagy again appears to be central to these effects. A recent review article examines genetic interventions that indicate 'tight connections between autophagy, health span and aging'." |
|
|
|
|
| Work on artificial replacements for damaged corneas is showing promise: "A new study from researchers in Canada and Sweden has shown that biosynthetic corneas can help regenerate and repair damaged eye tissue and improve vision in humans. ... Globally, diseases that lead to clouding of the cornea represent the most common cause of blindness. More than a decade ago, [researchers] began developing biosynthetic corneas in Ottawa, Canada, using collagen produced in the laboratory and moulded into the shape of a cornea. ... Together, they initiated a clinical trial in 10 Swedish patients with advanced keratoconus or central corneal scarring. Each patient underwent surgery on one eye to remove damaged corneal tissue and replace it with the biosynthetic cornea, made from synthetically cross-linked recombinant human collagen. Over two years of follow-up, the researchers observed that cells and nerves from the patients' own corneas had grown into the implant, resulting in a 'regenerated' cornea that resembled normal, healthy tissue. Patients did not experience any rejection reaction or require long-term immune suppression, which are serious side effects associated with the use of human donor tissue. The biosynthetic corneas also became sensitive to touch and began producing normal tears to keep the eye oxygenated. Vision improved in six of the ten patients, and after contact lens fitting, vision was comparable to conventional corneal transplantation with human donor tissue." |
| Cellular reprogramming progresses: "Because liver cells (hepatocytes) cannot be grown in the laboratory, researching liver disorders is extremely difficult. However, today's new research [demonstrates] how to create diseased liver-like cells from patients suffering from a variety of liver disorders. By replicating the organ's cells, researchers can not only investigate exactly what is happening in a diseased cell, they can also test the effectiveness of new therapies to treat these conditions. It is hoped that their discovery will lead to tailored treatments for specific individuals and eventually cell-based therapy - when cells from patients with genetic diseases are 'cured' and transplanted back. Additionally, as the process could be used to model cells from other parts of the body, their findings could have implications for conditions affecting other organs. ... the scientists took skin biopsies from seven patients who suffered from a variety of inherited liver diseases and three healthy individuals (the control group). They then reprogrammed cells from the skin samples back into stem cells. These stem cells were then used to generate liver cells which mimicked a broad range of liver diseases - the first time patient-specific liver diseases have been modelled using stem cells - and to create 'healthy' liver cells from the control group. Importantly, the three diseases the scientists modelled covered a diverse range of pathological mechanisms, thereby demonstrating the potential application of their research on a wide variety of disorders." |
|
|
|
|
| Mitochondria are an important determinant of life span, demonstrated by some beneficial mutations and comparison between species. Researchers continue to investigate longevity mutations to better understand the underlying mechanisms: "The [known] Caenorhabditis elegans mitochondrial (Mit) mutants have disrupted mitochondrial electron transport chain (ETC) functionality, yet, surprisingly, they are long lived. We have previously proposed that Mit mutants supplement their energy needs by exploiting alternate energy production pathways normally used by wild-type animals only when exposed to hypoxic conditions. We have also proposed that longevity in the Mit mutants arises as a property of their new metabolic state. If longevity does arise as a function of metabolic state, we would expect to find a common metabolic signature among these animals. ... we show that long-lived clk-1(qm30) and isp-1(qm150) Mit mutants have a common metabolic profile that is distinct from that of aerobically cultured wild-type animals and, unexpectedly, wild-type animals cultured under severe oxygen deprivation. Moreover, we show that 2 short-lived mitochondrial ETC mutants, mev-1(kn1) and ucr-2.3(pk732), also share a common metabolic signature that is unique. ... Our study suggests long-lived, genetically specified Mit mutants employ a novel metabolism and that life span may well arise as a function of metabolic state." |
| A press release from InnoCentive and the SENS Foundation announces a short-term incentive program "seeking innovative ideas to biologically reverse one of the causes of aging and age-related diseases believed to be attributed to glucosepane, a protein crosslink that reduces elasticity throughout the body. This is a Theoretical Challenge, so Solvers need to submit a detailed and thorough description of their solution. The Challenge runs for 60 days and one Solver will receive $20,000 if their solution is chosen. ... Finding an innovative solution to breaking down glucosepane, or what we call 'public enemy number one,' is our Foundation's top priority in the category of protein crosslinks, as it is the most abundant protein crosslink in aged humans. We believe there are several radical possibilities to solving this Challenge - things we haven't even thought of - and will keep an open mind to solutions we receive. Our goal is to discover solutions that can be implemented and reverse stiffening, therefore restoring youthful health and vigor to the world's population. ... Evidence suggests that glucosepane may play a role in osteoporosis, cardiovascular diseases like hypertension, inflammation and diabetes. Scientists have studied the accumulation of glucosepane for 30 years with little success, so SENS Foundation is reaching out to InnoCentive's 200,000+ Solvers for innovative solutions to find a way to break the formation of glucosepane." This seems like a good way to draw attention to aspects of the SENS program that are not greatly studied - very few groups are working seriously on crosslink breakers at the present time. |
|
|
|
|
| From the SENS Foundation: "A comprehensive suite of rejuvenation biotechnologies must include the removal of extracellular aggregates from aging cells and tissues. The most clinically-advanced such biotechnology is immunotherapy against aggregated beta-amyloid protein (Abeta), a characteristic neuropathological lesion that accumulates in the brain in Alzheimer's disease (AD) patients and as part of "normal" brain aging. ... The promise of active and passive Abeta-targeting vaccines is high, but experimental and clinical testing of such therapies have revealed some of their limitations. Immunotherapeutics currently in clinical development rely in different ways on the mobilization of the patient's immune processes. ... Therapeutic efficacy thus depends on the patient's immune response to vaccination, which notoriously declines with aging. ... An ideal Abeta immunotherapy would thus not depend on the patient's immune system for effectiveness or safety, but would have an "intrinsic" mechanism of action ... [researchers] have made significant progress with a promising novel approach to Abeta immunotherapy that promises to deliver on all of these fronts. They have identified, purified, and characterized [antibodies] with direct hydrolytic activity against these pathological aggregates." Antibodies are the weapons used by immune cells to mark and destroy their targets - but if you can regularly infuse antibodies into the body, then you don't necessarily need the immune cells to take action. |
| Cancer chemotherapy is harrowing is because it is indiscriminate. But all of the old chemotherapies can be made much better and safer when used as the payload in one of the new cell targeting nanotechnologies: researchers "have developed a nano-sized vehicle with the ability to deliver chemotherapy drugs directly into cancer cells while avoiding interaction with healthy cells, increasing the efficiency of chemotherapeutic treatment while reducing its side effects. ... Inside the nano-vehicle itself are tiny particles of chemotherapy drugs. When the delivery vehicle comes into contact with cancer cells, it releases the chemotherapeutic payload directly into the cell. ... the nanomedical device can be used to treat many different types of cancer, including lung, blood, colon, breast, ovarian, pancreatic, and even several types of brain cancers. ... The key to the drug delivery platform is the molecule used to create the outer coating of this cluster nano-vehicle, a sugar recognized by receptors on many types of cancer cells. ... When the nano-vehicle interacts with the receptor on the cancerous cell, the receptor undergoes a structural change and the chemotherapy payload is released directly into the cancer cell. [This] leads to more focused chemotherapeutic treatment against the diseased cells. ... clinical trials [should] begin in two years or less." |
|
|
|
|
| Researchers continue to produce improvements to infrastructure technologies needed for stem cell research and development: "Human pluripotent stem cells, which can become any other kind of body cell, hold great potential to treat a wide range of ailments, including Parkinson's disease, multiple sclerosis and spinal cord injuries. However, scientists who work with such cells have had trouble growing large enough quantities to perform experiments - in particular, to be used in human studies. Furthermore, most materials now used to grow human stem cells include cells or proteins that come from mice embryos, which help stimulate stem-cell growth but would likely cause an immune reaction if injected into a human patient. To overcome those issues, MIT chemical engineers, materials scientists and biologists have devised a synthetic surface that includes no foreign animal material and allows stem cells to stay alive and continue reproducing themselves for at least three months. It's also the first synthetic material that allows single cells to form colonies of identical cells, which is necessary to identify cells with desired traits and has been difficult to achieve with existing materials." |
| From the Mayo Clinic: "researchers found that healthy young people who put on as little as 9 pounds of fat, specifically in the abdomen, are at risk for developing endothelial cell dysfunction. Endothelial cells line the blood vessels and control the ability of the vessels to expand and contract. ... [researchers] recruited 43 healthy Mayo Clinic volunteers with a mean age of 29 years. They were tested for endothelial dysfunction by measuring the blood flow through their arm arteries. The volunteers were assigned to either gain weight or maintain their weight for eight weeks, and their blood flow was tested. The weight-gainers then lost the weight and were tested again. ... Endothelial dysfunction has long been associated with an increased risk for coronary artery disease and cardiovascular events. Gaining a few pounds in college, on a cruise, or over the holidays is considered harmless, but it can have cardiovascular implications, especially if the weight is gained in the abdomen. ... Among those who gained weight in their abdomens (known as visceral fat), even though their blood pressure remained healthy, researchers found that the regulation of blood flow through their arm arteries was impaired due to endothelial dysfunction. Once the volunteers lost the weight, the blood flow recovered. Blood flow regulation was unchanged in the weight-maintainers and was less affected among those who gained weight evenly throughout their bodies." |
|
|
|
|
| This is one of several techniques shown to restore function in spinal injury using transplanted stem cells: "A UC Irvine study is the first to demonstrate that human neural stem cells can restore mobility in cases of chronic spinal cord injury, suggesting the prospect of treating a much broader population of patients. Previous breakthrough stem cell studies have focused on the acute, or early, phase of spinal cord injury, a period of up to a few weeks after the initial trauma when drug treatments can lead to some functional recovery. The UCI study [is] significant because the therapy can restore mobility during the later chronic phase, the period after spinal cord injury in which inflammation has stabilized and recovery has reached a plateau. There are no drug treatments to help restore function in such cases. ... The [team] transplanted human neural stem cells into mice 30 days after a spinal cord injury caused hind-limb paralysis. The cells then differentiated into neural tissue cells, such as oligodendrocytes and early neurons, and migrated to spinal cord injury sites. Three months after initial treatment, the mice demonstrated significant and persistent recovery of walking ability in two separate tests of motor function when compared to control groups." |
| Via PhysOrg.com: "A team of University of Michigan scientists has found that suppressing a newly discovered gene lengthens the lifespan of roundworms. Scientists who study aging have long known that significantly restricting food intake makes animals live longer. But the goal is to find less drastic ways to achieve the same effect in humans someday. ... scientists found that a gene, drr-2, is an important component in a key cellular pathway, the TOR nutrient-sensing pathway, where many scientists are looking for potential drug targets. The U-M scientists then found that when they caused the drr-2 gene to be under- or over-expressed, they could lengthen or shorten lifespan in C. elegans, a worm widely used in research. Manipulating the drr-2 gene's action produced the same effects as reducing or increasing caloric intake. ... The study also found that drr-2 appears analogous to a human gene, eIF4H, that controls similar cell functions. ... Many genes identified in C. elegans to control the speed of aging turned out to be evolutionarily conserved, meaning that you can find them in other animals, too. And many are very similar to those found in humans. ... When calories or certain nutrients are restricted, scientists detect less oxidative damage in animal cells and a slower decline in DNA repair, a decline that normally occurs with age. It's thought that limiting oxidative damage and slowing the decline in DNA repair could help postpone or avoid many age-related diseases." |
|
|
|
