From the Technology Review: "I was observing an intimate demonstration of how stem-cell technologies may one day combine with personal genomics and personal medicine. I was the first journalist to undergo experiments designed to see if the four-year-old process that creates induced pluripotent stem (iPS) cells can yield insight into the functioning and fate of a healthy individual's heart cells. Similar tests could be run on lab-grown brain and liver cells, or eventually on any of the more than 200 cell types found in humans. ... This is the next step in personalized medicine: being able to test drugs and other factors on different cell types. ... the cardiomyocytes derived from iPS cells are a huge improvement over the cadaver cells sometimes used to test potential drug compounds. Unlike the cadaver cells, IPS-­generated cells beat realistically and can be supplied in large quantities on demand. What's more, iPS-generated cells can have the same genetic makeup as the patients they came from, which is a huge advantage in tailoring drugs and treatments to individuals. ... Virtually everything about iPS cells is overhyped. But for the purpose of testing drug candidates, I think the possibilities are considerable, and we and lots of other people are pursuing this. There are lots of problems. Are iPS cells really normal? How do you get enough pure differentiated cells? But the potential is definitely there."

Link: http://www.technologyreview.com/biomedicine/38348/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Researchers are spending a fair amount of time on understanding why regeneration in mammals differs from - and is much worse than - regeneration in lower animals like salamanders. A salamander can grow back a limb any time it needs to, a mouse or a human not so much. But we can do the full regeneration trick to a far lesser degree, as humans and mice can both regrow the tip of a finger or toe when very young or very lucky, for example. You might also recall the MRL mice, an engineered species that can regenerate much more effectively than is normal for most mice.

One of the questions that researchers aim to answer is whether the mechanisms for salamander-like regeneration lie buried in mammalian biology, perhaps turned off for reasons involving cancer suppression. If they are there, perhaps they can be restored via drugs or genetic engineering for long enough to regrow major damage to limbs and organs. That's all speculative at this point, and looking more so after this latest research publication:

Tissue-specific adult stem cells are responsible for the ability of mammals to re-grow the tips of fingers or toes lost to trauma or surgery, say researchers at the Stanford University School of Medicine. The finding discredits a popular theory that holds that previously specialized cells regress, or dedifferentiate, in response to injury to form a pluripotent repair structure called a blastema.

"We've shown conclusively that what was thought to be a blastema is instead simply resident stem cells that are already committed to become specific tissue types," said Irving Weissman, MD, director of Stanford's Institute for Stem Cell Biology and Regenerative Medicine. "The controversy about limb regeneration in mammals should be over."

If you want to take the glass half full view, this might mean that it will be a shorter path to pushing these stem cells into doing more with less - rather than the alternative and longer path of trying to recreate salamander-like blastema behavior in mammals. But it's anyone's guess as to how much regeneration these cells are capable of if manipulated; no doubt less than we'd all like.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Good news from the dental research community: scientists "have developed a revolutionary new way to treat the first signs of tooth decay. Their solution is to arm dentists with a peptide-based fluid that is literally painted onto the tooth's surface. The peptide technology is based on knowledge of how the tooth forms in the first place and stimulates regeneration of the tooth defect. ... This may sound too good to be true, but we are essentially helping acid-damaged teeth to regenerate themselves. It is a totally natural non-surgical repair process and is entirely pain-free too. ... It contains a peptide known as P 11-4 that -- under certain conditions - will assemble together into fibres. In practice, this means that when applied to the tooth, the fluid seeps into the micro-pores caused by acid attack and then spontaneously forms a gel. This gel then provides a 'scaffold' or framework that attracts calcium and regenerates the tooth's mineral from within, providing a natural and pain-free repair. The technique was recently taken out of the laboratory and tested on a small group of adults whose dentist had spotted the initial signs of tooth decay. The results from this small trial have shown that P 11-4 can indeed reverse the damage and regenerate the tooth tissue. ... If these results can be repeated on a larger patient group, then I have no doubt whatsoever that in two to three years time this technique will be available for dentists to use in their daily practice."

Link: http://www.sciencedaily.com/releases/2011/08/110823115402.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Researchers here outline one possible mechanism for the known association between chronic stress and biomarkers of health: "While the human mind and body are built to respond to stress - the well-known "fight or flight" response, which lasts only a few minutes and raises heart rate and blood glucose levels - the response itself can cause significant damage if maintained over long periods of time. When stress becomes chronic, this natural response can lead to a number of disease-related symptoms, including peptic ulcers and cardiovascular disorders. To make matters worse, evidence indicates that chronic stress eventually leads to DNA damage, which in turn can result in various neuropsychiatric conditions, miscarriages, cancer, and even aging itself. ... The newly uncovered mechanism involves ?-arrestin-1 proteins, ?2-adrenoreceptors (?2ARs), and the catecholamines, the classic fight-or-flight hormones released during times of stress - adrenaline, noradrenaline, and dopamine. Arrestin proteins are involved in modifying the cell's response to neurotransmitters, hormones, and sensory signals; adrenoceptors respond to the catecholamines noradrenaline and adrenaline. Under stress, the hormone adrenaline stimulates ?2ARs expressed throughout the body, including sex cells and embryos. Through a series of complex chemical reactions, the activated receptors recruit ?-arrestin-1, creating a signaling pathway that leads to catecholamine-induced degradation of the tumor suppressor protein p53, sometimes described as "the guardian of the genome." The new findings also suggest that this degradation of p53 leads to chromosome rearrangement and a build-up of DNA damage both in normal and sex cells." p53 is very important in a range of core cellular processes - anything touching on it usually turns out to be influential.

Link: http://www.kurzweilai.net/how-stress-causes-dna-damage

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

So far research on cellular reprogramming has largely focused on manipulation of cells outside the body. Here a researcher suggests that the future of medicine will involve achieving much the same thing inside the body: "To date, somatic cell reprogramming has been achieved in vitro. It would be of great importance to explore whether the anti-aging agents, e.g. rapamycin, could function to enhance stem cell function, protect stem cell pluripotency and even promote reprogramming in vivo. It is also very interesting to verify whether some or all adult organs/tissues do possess some significant regenerative capacity due to the suspected in vivo reprogramming. Furthermore, it has been reported that agents which effectively function for a common human disease by enhancing self-renewal could lose efficacy in older individuals due to the age-associated decline of replication. Thus understanding and realization of in vivo cell reprogramming is not only a fundamental theoretical question but also a very promising strategy for anti-aging and regenerative medicine. Reprogramming of somatic cells has been enthusiastically hoped to become an arsenal to against aging as it would leads to personalized stem-cell-based rejuvenation therapies. What we learn from research of stem cell and reprogramming could help us to develop two potential anti-aging approaches in adult and older: i) to protect, ameliorate or reverse the age-associated loss function of stem cell in vivo and ii) to replace the lost stem cells by reprogrammed pluripotent cells."

Link: http://impactaging.com/papers/v3/n8/full/100364.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Mitochondria in your cells damage themselves in the course of their vital, life-sustaining operations, and these damaged mitochondria contribute to aging. It's a progressive and complicated process of many steps, by which incidents of atomic-scale damage in the power plants of your cells steadily overwhelm evolved countermeasures and repair systems, corrupting a fraction of your cells and blossoming into a flow of damaged molecules throughout the body. That in turn produces the roots of atherosclerosis and many other age-related forms of degeneration and malfunction.

We would like to be able to do something about this - by hook or by crook restore the damage state of an old person's mitochondria to the way things were when he was young. There are many possible paths forward, most understood in some detail at this time, and which will either be be shown to fail or succeed within the next decade or two. The work proceeds, but very, very slowly. It's not a broad and well populated field of research, sad to say.

The importance of mitochondria is one of the reasons that autophagy is also important when it comes to the progression of aging. Autophagy is the name given to a collection of varied recycling machinery and processes that operate within cells, destroying damaged components - such as mitochondria. It shouldn't be a great leap to think that improving the recycling mechanisms might also improve the situation vis a vis malfunctioning mitochondria. This is probably the case, based on what researchers know of mitophagy, the processes of autophagy concerned with removing damaging mitochondria.

Insofar as the bottom line of health and longevity goes, there is plenty of evidence to suggest that dialing up autophagy extends life, and a further array of evidence to suggest that known life-extending techniques such as calorie restriction depend heavily on autophagy as a principle mechanism of action.

Based on what's coming out of the labs in recent years, I think the research community isn't too far away from conducting studies that will definitively show - or definitively disprove, which would be unexpected - benefits to longevity from improved mitoautophagy alone. Take this, for example:

[Researchers] have defined a specific protein complex that allows cells to rid themselves of damaged mitochondria, which are the energy producing machines of the cell. ... The study highlights the interaction between Hsp90-Cdc37 and Ulk1, a kinase that the authors show is required for the degradation and elimination of damaged mitochondria. Hsp90-Cdc37 stabilizes and activates Ulk1, which in turn phosphorylates its substrate Atg13, which is then released from the complex. Atg13 then eliminates damaged mitochondria via the autophagy pathway. Thus, the study links Hsp90-Cdc37-Ulk1-Atg13 in a direct pathway that is essential for efficient mitochondrial clearance.

"The new study shows that the key regulatory mechanism of this process is the Hsp90-Cdc37 chaperone, which functions as an on-off switch that is critical for the correct functioning of the Ulk1 kinase," Cleveland said. "Thus, if we can control this switch, we can significantly improve the therapeutic window."

Meaning this is a target for designed drug compounds to boost autophagy specifically aimed at clearing out more of the damaged mitochondria than would otherwise be the case. How far would this get us? A good guess would be in the same ballpark as calorie restriction mimetics: it's a similar mechanism. So in other words this may do good things for health in humans, but don't expect spectacular results when it comes to life span.

The problem with attacking mitochondria by boosting autophagy is that we already know that certain forms of mitochondrial damage manage to elude autophagic processes: that's how we end up in the bad place. So boosting autophagy just slows things down, and does't solve the underlying problem. A different type of approach is needed for a real solution, one based on repair rather than slowing existing processes of damage - and as it happens making progress along the paths towards mitochondrial repair shouldn't be any harder than safely and effectively adjusting the processes of autophagy.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A study conducted by a team of researchers from the University of Lausanne found that a diet rich in whey protein can reduce the amount of fat in the liver.

Researchers from the University of Lausanne found out that the supplementation of whey protein in a person’s diet can lower the risk of developing fatty liver disease in obese women by reducing the amount of fat in liver cells. The study was published in an issue of Clinical Nutrition. They also found that whey protein was able to improve the study participants’ blood lipid profile which is important in promoting a healthier heart. The participants were asked to take the whey protein supplements for a period of four weeks.

Lead researcher Murielle Bortolotti said that their study was uncontrolled and preliminary but it strongly suggests that whey protein supplementation helps reduce the risk of fatty liver disease and promotes cardiovascular health as a long-term benefit. The researchers gathered a group of obese patients with an average BMI of 37.6 and IHCL concentrations between 1.9 to 20.5 percent. The participants were also recorded to have noticeable resistance to insulin with an average insulin sensitivity score of 2.77. The researchers observed that, after four weeks of whey protein supplementation, the study participants’ average IHCL dropped by 21 percent while their plasma triglyceride levels also went down by 15 percent. Their overall plasma cholesterol concentration was down by more than 7 percent after about a month of taking whey protein supplements. Researchers said that the result of the study indicates that whey protein has the potential to improve triglyceride profiles and IHCL.

The Liver and Fatty Liver Disease

The liver is the largest and heaviest glandular organ in the human body with an average weight of 1.36 kilograms. It is divided into four lobes which are unequal in size and shape. It is located at the right part of the abdominal cavity and just below the diaphragm. The portal vein and hepatic artery are responsible for carrying nutrients from the small intestines and oxygen-rich blood to the liver, respectively.

The human liver serves numerous functions including the production of enzymes that break down fats and produce glycogen from glucose. It is also responsible for producing urea and certain amino acids, storing of vitamins like vitamins B12, K, D, A and some minerals. The liver also produces 80 percent of the cholesterol in the body. The common disorders of the liver are liver cirrhosis, liver cancer, hepatitis and Wilson’s disease. The most harmful habit that affects the proper function of the liver is the excessive drinking of alcohol which can potentially alter the metabolic processes in the organ.

The root cause of fatty liver disease remains to be unknown. But medical experts are looking at patients’ resistance to insulin as the primary cause of the condition. Insulin resistance is a metabolic disorder where the cells are no longer responding properly to insulin in order to metabolize glucose.  In other words, insulin is no longer capable of performing its natural task of regulating sugar levels in the body. Nonalcoholic fatty liver disease is characterized by the accumulation of fat in the liver without the presence of alcohol. It refers to a wide spectrum of liver diseases from steatosis or simple fatty liver, cirrhosis or the irreversible and advanced scarring of the liver, to nonalcoholic steatohepatitis. Fatty liver disease is common throughout any age group; children can start developing fatty liver disease at the age of 10.

Natural Ways to Promote Liver Health

The liver is a very important organ in the body. Though minor health conditions concerning the liver are often very treatable, it is still necessary to keep the liver functioning properly to promote overall health.

• Diet plays a very important role in keeping the liver in tiptop shape. Ignoring hunger pangs or sudden and unscheduled eating can literally surprise the liver. Every time this happens, the liver exerts effort to produce the necessary enzymes to digest and metabolize the food properly. Eating at different hours of the day will overwork the liver and cause it to become exhausted. When struck with a sudden desire to eat, choosing foods that are not too heavy to the stomach like salads and fruits is recommended. And it is also a good way of maintaining a healthy body weight.

• Drinking plenty of water helps in washing away impurities and toxins out of the kidneys and liver. But drinking too much water while eating can interrupt the normal digestive process. So remember to observe proper pacing.

• The body has a limited requirement for sugars. Eating too much sweet foods can be dangerous to the liver and the human body. Sweets, especially those made or composed of refined sugar, will result to the excessive accumulation of fats in certain body parts like the buttocks, abdomen, thighs and the liver. Too much refined sugar will also result to the production of more triglycerides in the blood which, in turn, can increase the risk of developing cardiovascular disease. Some artificial sweeteners had been found by different studies to be poisonous to the body and result to fatigue and hypoglycemia. Eating fruits or blackstrap molasses when you want to eat something sweet are excellent alternatives to artificial sweeteners, especially for individuals with diabetes.

• Foods rich in protein like eggs, chicken, whole grains and legumes can help promote better liver health by helping it maintain a normal protein level in the body since the liver is responsible for producing protein. Low levels of protein can be a strong indication of kidney and liver disease. Eating natural and organic foods that are free of artificial sweeteners, colors, flavors and preservatives can also help in keeping the liver healthy.

• Some disease-causing bacteria can breed in the intestines. These organisms can cause permanent damage to the liver. So it is important to keep the intestines clean by drinking enough liquids and foods rich in dietary fiber.

• Eating less to lose weight can result to an insufficiency of nutrients supplied to the body. This makes the liver weak and incapable of producing enzymes that are needed in the proper digestion of food. Stop worrying too much about gaining weight and instead direct your attention to the foods that you eat to keep your liver and body healthy. As a reward, your liver will be able to better digest food and contribute in managing your weight.

Sources
nutraingredients.com
gicare.com
medicinenet.com
fitness.ygoy.com

Discuss this post in Frank Mangano’s forum!

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

Another hit in the search for compounds that extend life in lower animals: "Basic Yellow 1, a dye used in neuroscience laboratories around the world to detect damaged protein in Alzheimer's disease - [also] known as Thioflavin T, (ThT) - extended lifespan in healthy nematode worms by more than 50 percent and slowed the disease process in worms bred to mimic aspects of Alzheimer's. The research, conducted at the Buck Institute for Research on Aging, could open new ways to intervene in aging and age-related disease. The study highlights a process called protein homeostasis - the ability of an organism to maintain the proper structure and balance of its proteins, which are the building blocks of life. Genetic studies have long indicated that protein homeostasis is a major contributor to longevity in complex animals. Many degenerative diseases have been linked to a breakdown in the process. ... this study points to the use of compounds to support protein homeostasis, something that ThT, did as the worms aged. ThT works as a marker of neurodegenerative diseases because it binds amyloid plaques - the toxic aggregated protein fragments associated with Alzheimer's. In the nematodes ThT's ability to not only bind, but also slow the clumping of toxic protein fragments, may be key to the compound's ability to extend lifespan ... We have been looking for compounds that slow aging for more than ten years and ThT is the best we have seen so far. But more exciting is the discovery that ThT so dramatically improves nematode models of disease-related pathology as well. ThT allows us to manipulate the aging process, it has the potential to be active in multiple disease states and it enhances the animal's innate ability to deal with changes in its proteins."

Link: http://www.eurekalert.org/pub_releases/2011-03/bifa-nss032411.php

While we're on the subject of the importance of the brain to engineered longevity, here is news of an infrastructural advance from EurekAlert!: "The Allen Institute for Brain Science announced today that it has launched the Allen Human Brain Atlas, a publicly available online atlas charting genes at work throughout the human brain. The data provided in this initial data release represent the most extensive and detailed body of information about gene activity in the human brain to date, documenting which genes are expressed, or 'turned on' where. In the coming years, the Atlas will be expanded with more data and more sophisticated search, analysis and visualization tools to create a comprehensive resource useful to an increasingly wide range of scientists and research programs worldwide. The Allen Human Brain Atlas, available at http://www.brain-map.org, is a unique multi-modal atlas of the human brain that integrates anatomic and genomic information to create a searchable, three-dimensional map of gene activity in the brain. Data modalities in this resource include magnetic resonance imaging (MRI), diffusion tensor imaging (DTI) and histology - providing information about gross neuroanatomy, pathways of neural connections, and microscopic anatomy, respectively - as well as gene expression data derived from multiple approaches."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-05/aifb-aif052410.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

The differences in a nutshell: "Calorie restriction (CR) is the only paradigm that has consistently increased lifespan in a wide variety of model organisms. Many hypotheses have been proposed as the underlying mechanism, including a reduction in body size and adiposity, which is commonly observed in calorie-restricted animals. This has led to investigations as to whether similar changes in body composition produced by increasing energy expenditure via exercise can replace or enhance the benefits of reducing energy intake. ... In rodents, the data clearly show that exercise, regardless of body weight changes, can improve health and survival, but unlike CR, fails to extend lifespan. In humans, short-term weight loss studies show that exercise and CR produce similar improvements in disease risk factors and biomarkers of aging, while some parameters clearly benefit more with exercise. Epidemiologic evidence in humans supports exercise as a strategy to reduce the risk of morbidity and mortality, but not to extend lifespan. It is unknown whether CR can extend human lifespan, but the metabolic profile of humans engaged in long-term CR shares many similarities with calorie restricted rodents and nonhuman primates. In conclusion, like CR, exercise can limit weight gain and adiposity, but only CR can extend lifespan. Therefore, in rodents, the ability of CR to slow aging is apparently more dependent on decreasing nutrient flux, rather than changes in energy balance and body composition."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20703061

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Aubrey de Grey of the SENS Foundation presented at TEDxChicago 2012 a month ago or so, and video of the event recently made its way to YouTube:

Dr. Aubrey de Grey is a biomedical gerontologist. As the Chief Science Officer of the SENS Foundation (a foundation working to develop widespread access to rejuvenation biotechnologies), author of numerous journal articles and books, and board member of a handful of editorial and scientific advisory boards, it is incontestable that Dr. Aubrey de Grey has dedicated his life to the science of combating the aging process. He received his BA and Ph.D. from the University of Cambridge, however, his original field was computer science.? Dr. de Grey is a Fellow of both the Gerontological Society of America and the American Aging Association and sits on the editorial and scientific advisory boards of numerous journals and organisations. He has appeared on countless shows, was even featured in the Max Wexler documentary, How to Live Forever, and has also spoken at a number of world-renowned events, including TED.

A great many of de Grey's conference presentations and other appearances are archived in the depths of YouTube, as it happens. At some point when you have a spare few minutes, you might take a look at the full list. There are probably a few in there that you haven't seen, such as this presentation given earlier this year at TechFest 2012 in Bombay:

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via EurekAlert!: researchers "studied 713 women aged 70 to 79 years who took part in the Women's Health and Aging Studies. This study was designed to evaluate the causes and course of physical disability in older women living in the community. ... A number of studies have measured the positive impact of exercise and healthy eating on life expectancy, but what makes this study unique is that we looked at these two factors together. ... Researchers found that the women who were most physically active and had the highest fruit and vegetable consumption were eight times more likely to survive the five-year follow-up period than the women with the lowest rates. ... Study participants' physical activity was measured through a questionnaire that asked the amount of time the spent doing various levels of physical activity, which was then converted to the number of calories expended. The women were then followed up to establish the links between healthy eating, exercise and survival rates. Key research findings included: More than half of the 713 participants (53%) didn't do any exercise, 21% were moderately active, and the remaining 26% were in the most active group at the study's outset. During the five-year follow up, 11.5% of the participants died. Serum carotenoid levels were 12% higher in the women who survived and total physical activity was more than twice as high. Women in the most active group at baseline had a 71% lower five-year death rate than the women in the least active group. Women in the highest carotenoid group at baseline had a 46% lower five-year death rate than the women in the lowest carotenoid group. When taken together, physical activity levels and total serum carotenoids predicted better survival."

Link: http://www.eurekalert.org/pub_releases/2012-05/w-eaa053012.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The New Scientist on calorie restriction: "Dreams of eternal youth feature in many cultures throughout history, but it was only in the 20th century that research into longevity really began. Much about ageing is still mysterious - we don't even know the underlying reasons why we journey into old age. There are many lines of enquiry into how to live longer, though, with one of the most intriguing being calorie restriction: in effect, going on a lifelong diet. Calorie restriction dramatically extends not only the lifespan of laboratory animals, but also their 'healthspan' - how long they live free of disease. On the assumption that it has the same effect in people, some individuals have already adopted a restricted diet. The latest evidence suggests that while calorie restriction is indeed beneficial for humans, when it comes to lifespan extension, it may not be the whole story. The good news is that we might be able to delay ageing without cutting our food intake. ... There's a definite possibility that if you balance the diet correctly, a longer lifespan can be achieved without full food restriction. ... It is unclear why eating less should make animals live longer. While a restricted diet triggers numerous changes at the molecular and genetic levels, only some of these are common across all the species tested. However, there does seem to be a general principle that a dearth of nutrients causes organisms to divert resources away from growth and reproduction and towards basic survival functions. From an evolutionary perspective, these adaptations could help an organism survive famine."

View the Article Under Discussion: http://www.newscientist.com/article/mg20627621.100-eat-less-live-longer.html?full=true

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

An example of the way in which the machinery of cells is very intertwined, components reused by evolution in many different mechanisms: "This was certainly an unexpected finding. It is rather uncommon for one gene to have two very different and very significant functions that tie together control of aging and inflammation. The two, if not regulated properly, can eventually lead to cancer development. It's an exciting scientific find. ... For decades, the scientific community has known that inflammation, accelerated aging and cancer are somehow intertwined, but the connection between them has remained largely a mystery ... What was known [was] that a gene called AUF1 controls inflammation by turning off the inflammatory response to stop the onset of septic shock. But this finding, while significant, did not explain a connection to accelerated aging and cancer. When the researchers deleted the AUF1 gene, accelerated aging occurred, so they continued to focus their research efforts on the gene. ... The current study reveals that AUF1, a family of four related genes, not only controls the inflammatory response, but also maintains the integrity of chromosomes by activating the enzyme telomerase to repair the ends of chromosomes, thereby simultaneously reducing inflammation, preventing rapid aging and the development of cancer. ... [Researchers are now] examining human populations for specific types of genetic alterations in the AUF1 gene that are associated with the co-development of certain immune diseases, increased rates of aging and higher cancer incidence in individuals to determine exactly how the alterations manifest and present themselves clinically."

Link: http://www.sciencedaily.com/releases/2012/05/120524122851.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The Guardian talks to researcher Tom Kirkwood: "We've known for some time that ageing is extremely variable; that everybody is different and that the differences of individuals' experience of ageing are greater than differences in earlier stages of life ... And why so variable? ... Because of the nature of the ageing process. I've been involved in this field for more than 35 years and when I entered it people fondly believed that ageing was programmed; that there was a mechanism inside our bodies that determined how long we would live. It was kind of written into our genes that we would die at a certain age. What we've been able to show is that the idea of this genetically programmed ageing makes no sense at all. There is no evidence. ... But, surely, genetic influences - a family susceptibility to cardiovascular problems, for instance - play a part in determining longevity? Only to a degree. [For example] a Danish study shows that such influences only explain about a quarter of the factors determining a lifespan. ... What we now know is that the genetic factors that influence your longevity are not genes that measure out the passage of time; the reason we age and die is because, as we live our lives, our bodies accumululate a great variety of small faults in the cells, and the molecules that make up the cells in our body - so ageing is driven by this accumulation of faults. The genes that influence longevity are those that influence how well the body copes with damage, how aggressive our repair mechanisms are; they're genes that regulate the house-keeping and maintenance and repair." All the more reason to focus research on the development of biotechnologies that can do a far better job of repair.

Link: http://www.guardian.co.uk/society/2012/may/29/tom-kirkwood-research-dispels-myths-ageing

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An interesting discovery, and one more benefit of exercise: "researchers have found one more reason to exercise: working out triggers influential stem cells to become bone instead of fat, improving overall health by boosting the body's capacity to make blood. The body's mesenchymal stem cells are most likely to become fat or bone, depending on which path they follow. ... The exercising mice ran less than an hour, three times a week, enough time to have a significant impact on their blood production ... In sedentary mice, the same stem cells were more likely to become fat, impairing blood production in the marrow cavities of bones. ... The composition of cells in the bone marrow cavity has an important influence on the productivity of blood stem cells. In ideal conditions, blood stem cells create healthy blood that boosts the immune system, permits the efficient uptake of oxygen, and improves the ability to clot wounds. Bone cells improve the climate for blood stem cells to make blood. But when fat cells start to fill the bone marrow cavity - a common symptom of sedentary behavior - blood stem cells become less productive, and conditions such as anemia can result. ... Some of the impact of exercise is comparable to what we see with pharmaceutical intervention. Exercise has the ability to impact stem cell biology. It has the ability to influence how they differentiate."

Link: http://www.eurekalert.org/pub_releases/2011-09/mu-ebh090111.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Here is a study claiming a noticeable impact on mortality rates from eating red meat. Weight is considered to some degree via body mass index, but I have to wonder if this only reflects a modest association of red meat consumption with other, less healthy lifestyle choices rather than an actual red-meat-based mechanism - as an obvious candidate mechanism for that isn't also present in all meat consumption isn't springing to mind: researchers "found that red meat consumption is associated with an increased risk of total, cardiovascular, and cancer mortality. The results also showed that substituting other healthy protein sources, such as fish, poultry, nuts, and legumes, was associated with a lower risk of mortality. ... [Researchers] observed 37,698 men from the Health Professionals Follow-up Study for up to 22 years and 83,644 women in the Nurses' Health Study for up to 28 years who were free of cardiovascular disease (CVD) and cancer at baseline. Diets were assessed through questionnaires every four years. ... One daily serving of unprocessed red meat (about the size of a deck of cards) was associated with a 13% increased risk of mortality, and one daily serving of processed red meat (one hot dog or two slices of bacon) was associated with a 20% increased risk. ... These analyses took into account chronic disease risk factors such as age, body mass index, physical activity, family history of heart disease, or major cancers. ... Replacing one serving of total red meat with one serving of a healthy protein source was associated with a lower mortality risk: 7% for fish, 14% for poultry, 19% for nuts, 10% for legumes, 10% for low-fat dairy products, and 14% for whole grains. The researchers estimated that 9.3% of deaths in men and 7.6% in women could have been prevented at the end of the follow-up if all the participants had consumed less than 0.5 servings per day of red meat."

Link: http://www.sciencedaily.com/releases/2012/03/120312162746.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A look at why, in this age of biotechnology and great uncertainty over the degree to which life spans will be extended in the next few decades, it is unwise to trust your financial future to large pension and welfare institutions. Any significant progress over the present very modest baseline of incidental life extension through general advances in medicine will likely bring down much of the existing system in the years ahead - which of course suggests that big centralized pension systems should be avoided like the plague, but that won't happen. If today's politics are any guide, politicians will continue to aggressively devalue their national currencies, taking wealth from their broader population to pay for what cannot be afforded until such time as the house of cards cannot be propped up any longer. The lesson to be taken away here: expect to provide for your own financial security in later life, and act accordingly now: "Here's the issue: governments have done their analysis of the aging issue largely based on best guesses of population developments in the future. These developments include further drops in fertility and some further increase in longevity. The trouble is that in the past, longevity has been consistently and substantially underestimated. We all live much longer now than had been expected 30, 20, and even just 10 years ago. So there is a good chance in the future people will live longer than we expect now. We call this longevity risk - the risk we all live longer than anticipated. ... Why is that a risk, you may ask. We all like to live longer, healthy lives. Sure, but let's now return to those pension worries. If you retire at 65 and plan your retirement finances expecting to live another 20 years (assuming you have enough savings for at least that period), you would face a serious personal financial crisis if you actually live to 95, or - well in your 100s. You could rely on your social security system at that point, but the program is also counting on people not living much beyond their mid-80s in most countries. Your personal financial problem multiplies by the size of the population, and, for society as a whole, becomes a very large problem." An example of how the present politics and systems of wealth transfer reward irresponsibility at all levels until such time as growth in collective irresponsibility sinks the whole venture.

Link: http://www.huffingtonpost.com/erik-oppers/seven-billion-reasons-to-_b_1417749.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A mainstream press article on exercise and aging: "As we age, our bodies change in ways that challenge athletic ability. But exercise also can slow down - and in some cases even prevent - some of the physiological ravages of time. ... A lot of things that we thought were just inherent to the aging process and were going to happen no matter what don't really have to happen if you maintain an appropriate lifestyle. ... How much can exercise slow down the ravages of aging? Potentially a lot. It will partially, but not completely, prevent arterial stiffening with age and completely prevent the dysfunction of the arterial lining that develops with age ... Exercise, it turns out, is probably as powerful as any other kind of prevention strategy or treatment that has been assessed so far. ... . For 21 years, researchers at Stanford University have studied the effects of consistent exercise on 284 runners 50 and older. In a 2002 article [they] reported that - 13 years into the study - a control group of 156 similar people who exercised much less on the whole than the runners had a 3.3 times higher death rate than runners as well as higher rates of disabilities. In a 2008 [study] they reported that after 19 years, 15% of runners had died, compared with 34% of the control group. After 21 years, runners had significantly lower disability levels than non-runners; their death rates from cardiovascular events, cancer and neurologic disorders were much lower than in non-runners - 65 of the runners had died of cardiovascular, neurologic and cancer events compared with 98 deaths in the control group."

Link: http://www.latimes.com/health/la-he-aging-physiology-20110901,0,5975284.story

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm