We can understand aging as being an accumulation of damage - of various types - to the biological machinery in and between our cells. This proceeds in an accelerating fashion as it passes various thresholds, and prompts evolved systems and feedback loops in our biology to flail, try to compensate, or fail in cascades. But in the very late stages of aging, for the oldest old, things stop being quite so easy to frame, and relationships between functional components that hold throughout the rest of live cease or change dramatically. We see some of this change of phase in aging at work in the mortality plateau of flies - the risk of death per unit time in very old flies simply stops increasing, which poses interesting questions given that they are still alive and therefore presumably still accumulating biological damage. There are some signs that this late-life plateau of mortality rate might also exist in humans - but by no means enough data to be confident in that.

Here are a couple of papers from the Rejuvenation Research advance publication queue that also point towards the interesting nature of the late stages of aging. The first one is eye-opening, given everything we know about the effects of exercise at all other stages of life.

Physical Activity and Cardiac Function in the Oldest Old

The relationship of physical activity (PA) and cardiac function in the oldest old remains unclear. The objective of this study was to evaluate the relationship between PA and cardiac structure and function, in the oldest old. Subjects were recruited from the Jerusalem Longitudinal Cohort Study that was initiated in 1990 and has followed an age homogeneous cohort of Jerusalem residents born in 1920-1921. ... After adjusting for sex, education, diabetes, ischemic heart disease, hypertension, dependence in activities of daily living, and body mass index (BMI), no significant associations were found between systolic or diastolic function, or left ventricular structure and PA. Gender-specific analyses yielded similar findings. Our study of the oldest old did not demonstrate an association between PA and cardiac structure or function.

Paradoxical Physiological Transitions from Aging to Late Life in Drosophila

In a variety of organisms, adulthood is divided into aging and late life, where aging is a period of exponentially increasing mortality rates and late life is a period of roughly plateaued mortality rates. In this study we used 57,600 Drosophila melanogaster from six replicate populations to examine the physiological transitions from aging to late life in four functional characters that decline during aging: desiccation resistance, starvation resistance, time spent in motion, and negative geotaxis. Time spent in motion and desiccation resistance declined less quickly in late life compared to their patterns of decline during aging. Negative geotaxis declined at a faster rate in late life compared to its rate of decline during aging.

These results yield two key findings: (1) Late-life physiology is distinct from the physiology of aging, in that there is not simply a continuation of the physiological trends which characterize aging; and (2) late life physiology is complex, in that physiological characters vary with respect to their stabilization, deceleration, or acceleration in the transition from aging to late life. These findings imply that a correct understanding of adulthood requires identifying and appropriately characterizing physiology during properly delimited late-life periods as well as aging periods.

I would like to see the advent of a world in which this sort of knowledge is a mere curio, as no-one ever experiences the final stages of degenerative aging, nor indeed does anyone even become what we'd now call old, aged, over the hill. Long lives, but no decline in vigor or health. That is a world in which the SENS research program has succeeded, and everyone has the opportunity to undergo periodic repair of metabolism, mitochondria, stem cells, and removal of harmful aggregates - no more remarkable than flu shots today.

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

SAT Reading Tutor in Richmond

I am a magna cum laude college graduate with a BA in history and a VA secondary social studies teaching license. Though I am not certified to teach English, I have extensive experience as a paid writing tutor, and my Middle School English Praxis II scores qualify me to teach English under certain conditions. More importantly than the above qualifications, I really love working with kids, both on an academic level and informally. As a tutor, my preliminary goal is, of course, to improve my students' understanding of the material in order to improve their grades. However, I find little lasting value in improved grades if there is not a corresponding increase in self confidence/perseverance and intellectual curiosity. Of course, few students love every subject they study. I have never loved math and always found it hard to earn good grades in such classes. However, I have learned to appreciate its intrinsic value and through my struggles with it, I have gained greater confidence and learned perseverance. I hope to teach my students about the intrinsic value of English and history and about the great value in setting and achieving difficult goals. I want to do this by genuinely getting to know my students — understanding how they think, what motivates and interests them, and who they are as individuals inside and outside the classroom. I believe that if I can understand your student as a person, not just as a GPA or learning disability (for example), then I can point them to the ways in which English and history can be important to them as an individual. I also believe that tutors should learn as much from their students as they teach. This requires patience, humility, and a listening ear, as well as good preparation and a thorough knowledge base, all of which are qualities that I will strive to have as a tutor for your student.

Contact me

Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

Better maintenance means a longer life, as illustrated by the importance of autophagy in calorie restriction (CR). Researchers are now branching out beyond CR to find other ways of influencing metabolism to better maintain cells: "The conserved insulin-signaling pathway has drawn a significant amount of attention over the past few years as a major lifespan determining signaling network. In many systems, impairing this pathway impedes the ability of caloric restriction (CR) to enhance lifespan, suggesting that nutrient sensing is key to CR. ... the Titorenko laboratory [tested] the hypothesis that networks exist within cells that are not inducible, but act constitutively to extend the lifespan of cells regardless of nutrient availability ... [the study] presents an original screen designed to isolate molecules that further lengthen the life span of yeast under calorie restriction rather than imitating this effect. ... Among the chemical compounds identified, the authors focus on one group representing 6 bile acids compounds, the most efficient of them being lithocholic acid (LCA). Bile acids are mildly toxic oxidized derivatives of cholesterol that play important roles in lipid uptake by the intestine."

View the Article Under Discussion: http://www.impactaging.com/papers/v2/n7/full/100173.html

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

Neurodegeneration has an inflammatory component, and some research groups use that as a starting point for treatment: "Neurodegenerative diseases like Alzheimer's and Parkinson's are partly attributable to brain inflammation. Researchers [now] demonstrate [that] a well-known family of enzymes can prevent the inflammation and thus constitute a potential target for drugs. Research suggests that microglial cells - the nerve system's primary immune cells - play a critical part in neurodegenerative diseases, such as Alzheimer's and Parkinson's. The over-activation of these cells in the brain can cause inflammation, resulting in neuronal death. Scientists [have] now found a way to prevent the activation of the microglia and consequently the inflammation they cause. The key is the blocking of enzymes called caspases, which the team has shown control microglial activation. ... By studying cell cultures and mice, the researchers show that certain caspases (3, 7 and 8) activate rather than kill microglial cells, which triggers an inflammatory reaction. Mice given caspase inhibitors displayed fewer activated microglia and less inflammation and cell death in the surrounding neurons."

Link: http://ki.se/ki/jsp/polopoly.jsp?d=130&a=118749&l=en&newsdep=130

Via EurekAlert!: "For years, researchers seeking new therapies for traumatic brain injury have been tantalized by the results of animal experiments with stem cells. In numerous studies, stem cell implantation has substantially improved brain function in experimental animals with brain trauma. But just how these improvements occur has remained a mystery. Now, an important part of this puzzle has been pieced together by researchers ... In experiments with both laboratory rats and an apparatus that enabled them to simulate the impact of trauma on human neurons, they identified key molecular mechanisms by which implanted human neural stem cells - stem cells that are in the process of developing into neurons but have not yet taken their final form - aid recovery from traumatic axonal injury. A significant component of traumatic brain injury, traumatic axonal injury involves damage to axons and dendrites, the filaments that extend out from the bodies of the neurons. The damage continues after the initial trauma, since the axons and dendrites respond to injury by withdrawing back to the bodies of the neurons. ... Axons and dendrites are the basis of neuron-to-neuron communication, and when they are lost, neuron function is lost. In this study, we found that our stem cell transplantation both prevents further axonal injury and promotes axonal regrowth, through a number of previously unknown molecular mechanisms. ... We identified about 400 proteins that respond differently after injury and after grafting with neural stem cells. ... a group of cytoskeleton proteins was being changed, and in particular one called alpha-smooth muscle actin, which had never been reported in the neurons before.""

Link: http://www.eurekalert.org/pub_releases/2012-01/uotm-slh011212.php

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

From Singularity Hub: "In order to work in the human body, an artificial cornea has to meet some rather stringent requirements. First, it has to bond to the human eye around its edge, but stay unclouded by cells in its center. To that end, [researchers] took a widely used opthalmological polymer (found often in intraocular lenses) and adapted it with other special polymers around the edges. Combined with the application of a growth factor protein, the modified edge promoted cell growth around the periphery of the implant and secured it in place using the body's own cells. The center of the artificial cornea, however, does not promote cell growth and remains clear so that it can be seen through. The artificial cornea also has to move freely with the eyelid and balance moisture on its faces. The polymer [researchers] chose is hydrophobic, allowing tears to lubricate the surface and provide the correct moisture on both of its sides. ... The artificial cornea has passed clinical trials and is ready to see expanded use in patients this year."

View the Article Under Discussion: http://singularityhub.com/2010/06/02/germanys-artificial-cornea-getting-ready-to-restore-sight-to-thousands/

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

From BusinessWeek: "Patients blinded in one or both eyes by chemical burns regained their vision after healthy stem cells were extracted from their eyes and reimplanted ... The tissue was drawn from the limbus, an area at the junction of the cornea and white part of the eye. It was grown on a fibrous tissue, then layered onto the damaged eyes. The cells grew into healthy corneal tissue, transforming disfigured, opaque eyes into functioning ones with normal appearance and color ... The stem-cell treatment restored sight to more than three-quarters of the 112 patients treated. ... The key to success is to be certain that when the stem cells extracted from the limbus are grown in culture they have the right mix of stem cells and the differentiated cells that form the corneal tissue ... If there are too few stem cells in the transplant, the improvement won't last because there will be no reservoir to form the new corneal cells needed with the normal recycling of cells over time. ... Depending on the depth of the injury, some patients regained sight in as little as two months. ... Others with deeper injuries needed a second procedure and waited a year before sight was restored."

View the Article Under Discussion: http://www.businessweek.com/news/2010-06-18/stem-cells-from-own-eyes-restore-vision-to-blinded-patients.html

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

One day, it will be possible to replace nerves with entirely artificial conduits. This is a branch of medical technology that will compete with regenerative medicine, and ultimately lead to more effective and resilient body parts. But today, the foundations are still being designed. A long road lies ahead. Here, the New Scientist looks at early work: "Schiefer is describing an experiment in which pulses of electricity are used to control the muscles of an unconscious patient, as if they were a marionette. It represents the beginnings of a new generation of devices that he hopes will allow people with paralysed legs to regain control of their muscles and so be able to stand, or even walk again. His is one of a raft of gadgets being developed that plug into the network of nerves that normally relay commands from the spinal cord to the muscles, but fall silent when a spinal injury breaks the chain. New ways to connect wires to nerves [allow] artificial messages to be injected to selectively control muscles just as if the signal had originated in the brain. Limbs that might otherwise never again be controlled by their owners can be brought back to life. ... Nerves contain tens of thousands of axons, each capable of being controlled by the ultimate puppeteer: the brain. Learning to pull even a few of those strings, though, could restore partial function to a person's limb, restoring some control to an arm or leg that was previously paralysed."

View the Article Under Discussion: http://www.newscientist.com/article/mg20627546.200-paralysed-limbs-revived-by-hacking-into-nerves.html?full=true

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

The DAF-16 gene in nematode worms such as C. elegans is thought to be the fulcrum of a metabolic feedback loop that switches between long-lived stress resistant and short-lived reproduction focused states. "Ageing is a process that all organisms experience, but at very different rates. We know that, even between closely related species, average lifespans can vary enormously. We wanted to find out how normal ageing is being governed by genes and what effect these genes have on other traits, such as immunity. To do that, we looked at a gene that we already knew to be involved in the ageing process, called DAF-16, to see how it may determine the different rates of ageing in different species. ... Researchers compared longevity, stress resistance and immunity in four related species of worm. ... They also looked for differences in the activity of DAF-16 in each of the four species and found that they were all quite distinct in this respect. And, importantly, the differences in DAF-16 corresponded to differences in longevity, stress resistance and immunity between the four species - in general higher levels of DAF-16 activity correlated with longer life, increased stress resistance and better immunity against some infections."

View the Article Under Discussion: http://www.bbsrc.ac.uk/media/releases/2010/100401-ageing-gene-found-to-govern-lifespan.aspx

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

From Life Extension Magazine: "the name 'regenerative medicine' came from Bill Haseltine, then of Human Genome Sciences, one of the early leaders in genomics and DNA technology. Back in the 1990s, Bill learned that researchers in aging were making important progress on turning back the clock of aging in human cells through cloning, and then creating young cells that could potentially regenerate or repair all the tissues of the aged human body. And so, upon hearing of that realistic prospect, he christened the field 'regenerative medicine' in the belief that it would one day become a major part of medical practice. So, based on its origins, I would define regenerative medicine as that collection of technologies that utilizes embryonic pluripotent stem cells and their derivatives to regenerate tissues in the body ravaged from disease, primarily degenerative disorders associated with aging. ... The problem with human biology is that the immortal reproductive cells that built you and me develop into differentiated cells within our bodies and as a result, lose the capacity to proliferate (divide) forever. So, the cells of the body are mortal, meaning they have a finite life span, and as our tissues age, or deteriorate from disease, our body has a finite capacity to regenerate and repair those tissues. As a result, we suffer progressive declines in function that lead to our death." There is more to aging than this, however.

View the Article Under Discussion: http://www.lef.org/magazine/mag2010/jun2010_Immortal-Stem-Cells-for-Anti-Aging-Therapies_01.htm

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

Vitamin K Sources Have Cancer Preventive Properties

German researchers find link between low consumption of vitamin K2 and cancer (lung cancer, specifically).

All the rage these days in the health world is the importance of getting a daily dose of vitamin D in your diet, whether it’s through the foods you fix or the sun you soak.  As a result, other vitamins have been given short shrift.

Well what better way to reacquaint oneself with other vitamins than with a study that says increasing one’s vitamin K intake can lower cancer risk?

Now, before I get into the guts of the study, this is not to suggest that eating cabbage with every meal will somehow prevent cancer.  But what the study does suggest is that certain sources of vitamin K are more cancer preventive than others.

About a year ago, I wrote about the differences between vitamin K1 and vitamin K2. I wrote about vitamin K2 being a more nutritious form of vitamin K than it’s partner in nutrition, vitamin K1, but at that point vitamin K2 was being hailed for its link to bone and cartilage development.  So, runners and people battling arthritis were encouraged to eat sources of vitamin K2.

This time, however, vitamin K2 is being hailed for its cancer-prevention prowess.

Researchers from the German Cancer Research Center in Heidelberg, Germany discovered its cancer-fighting effects after analyzing the results of a 10-year study that involved approximately 24,300 adults.  All of the adults – between the ages of 35 and 64 – were cancer free at the outset.

That fact changed 10 years later.  By the end of the study, approximately 1,800 men and women were diagnosed with cancers of various kinds, with just less than one-fourth of them dying from their disease.

But when researchers looked at the decedents’ dieting patterns, as well as those who remained cancer free throughout the study period, they saw some patterns.

For instance, among those who ate vitamin K2 rich foods, they were 28 percent less likely to be among those who died of cancer.  But when researchers looked at people who had the lowest vitamin K2 intake, they were almost 50 percent more likely to have been diagnosed with lung cancer (the most commonly diagnosed cancer there is, by the way).

Comparatively, those who had the highest vitamin K2 intake, they were less than half a percent more likely to have lung cancer.

Findings were similar among other commonly diagnosed cancers (e.g. prostate):  the more vitamin K2 eaten, the less likely they were to develop cancer.

Coincidence?  Perhaps.  The researchers are loath to suggest definitively that it’s the vitamin K2 that did it because most of the participants who ate lots of vitamin K2 got it from cheese primarily.  Thus, it could another aspect of cheese that makes it so cancer friendly.

The study is published in the American Journal of Clinical Nutrition.

Now, as most of you know, I’m not an extremist when it comes to nutrition.  Virtually everything high in calories can be enjoyed so long as it’s in moderation.

Thus, while cheese is pretty high in saturated fat and cholesterol, there are enough good things in cheese to make it a healthful food when eaten in moderation.

But there are other healthy sources of vitamin K2 that you don’t have to scrimp on.  One of them is natto, which, like cheese, is a fermented food (vitamin K2 primarily comes from fermented foods).  I’ve never eaten natto, but seeing as how the Japanese have eaten it for well over a thousand years—a culture that is known for its long lifespan and healthy dieting habits—it’s clearly a food worth trying.

And who knows?  One bite may make you nutso for natto!

Sources:
newsmaxhealth.com
naturalhealthontheweb.com
gaia21.net

Discuss this post in Frank Mangano’s forum!

Make It Magnesium for Healthy Brain Function

A newly developed magnesium supplement may help boost memory.

Late last year I predicted that 2010 would be magnesium’s year.  And with the latest study on magnesium, my prediction is bearing fruit.

True, magnesium hasn’t dominated the health headlines this year like, say, vitamin D has in terms of frequency.  But in terms of import, magnesium’s time to shine is now, as a recent study suggests that this magnificent mineral helps buoy one’s memory.

Researchers from Israel’s Tel Aviv University recognized magnesium’s magnificence after supplementing two groups of rats with the same food regimen, but tinkered with one of the rat groupings by adding a new-fangled magnesium supplement that purports to better penetrate the brain than contemporary magnesium supplements.

Through brain scans and cognitive tests, researchers found that, indeed, the magnesium-supplemented group outperformed the other group both in cognitive function and brain development.

In a statement, the researchers said they were “pleased” by the findings, but they couldn’t help but be somewhat disconcerted by the findings at the same time.

Apparently when they used over the counter magnesium supplements, there was no measurable difference in cognition between the two groups.

Translation:  According to the researchers, magnesium supplements on the market today don’t help with brain function.

Now, this study should not suggest that magnesium supplements on the market don’t work period, only that they don’t seem to be effective for brain health and development.  Researchers are confident, however, that when the new and improved magnesium supplement becomes commercially available—magnesium-L-theronate, or MgT— it will help make memories magnificent.

In the meantime, increase your magnesium intake by supplementing with – you guessed it – magnesium-rich foods.

Some of the richest magnesium sources come from seeds (like pumpkin seeds), leafy greens (like spinach) and beans (like black beans).  A quarter cup of pumpkin seeds has 184 milligrams of magnesium, a cup of boiled spinach has 156 milligrams and a cup of black beans has 120 milligrams.

Not to be outdone as a solid source for magnesium is salmon.  A four-ounce serving of salmon has 138 milligrams of magnesium.  Other significant sources for magnesium in the seafaring family include halibut (4 oz.=121 mg), scallops (4 oz.=77 mg), tuna (4 oz.=72 mg) and shrimp (4 oz.=38 mg).

Adult men should be getting at least 420 milligrams of magnesium per day, while women should get about 320 milligrams per day.

Sources:
whfoods.com
newsmaxhealth.com

Discuss this post in Frank Mangano’s forum!

Whole brain emulation is the topic for today: being able to run all of the processes of a brain on some form of computing machinery other than the evolved biological structures we presently possess. Considered in the long term this is an important line of research, as radical life extension will ultimately require moving away from flesh and into some more robust form of machinery in order to better manage the risk of fatal accidents. 'Ultimately' here is a long way into the future, centuries or more, long after we have solved the basic problems of repairing our aging biology so as to attain continual youth. Some people will be satisfied with copying themselves from their biological substrate into a machine substrate and letting that machine copy continue on, but that seems to me little more than an expensive form of procreation - continuation of the self requires a slow transformation of the original, not a quick cut and paste of data to a new computing device. But this is an old and often rehashed argument between identity as pattern and identity as continuity.

Here are some past posts on whole brain emulation if you'd like to do some background reading:

• A Preliminary Roadmap to Whole Brain Emulation
• The Age of Artificial Brains

Regardless of how people decide to use the ability to host a conscious individual somewhere other than a human brain, the technologies of whole brain emulation will have to be built. They are a precursor to any program of replacing the brain's present biological machinery with something better. From where I stand, brain emulation is also the most plausible path to true artificial intelligence, which at this time looks far more likely to arise from attempts to duplicate and then improve on the operation of human brains than from efforts to improve expert systems of varying sorts.

Reasonable people differ on this, of course, as even a brief survey of publications on artificial intelligence will tell you.

If you find this topic interesting, you might look at the latest issue of the International Journal of Machine Consciousness, featuring many of the usual suspects from the transhumanist community - folk who have been putting in time on AI and molecular nanotechnology research for some years. A couple of the more intriguing items:

Non-Destructive Whole-Brain Monitoring Using Nanorobots: Neural Electrical Data Rate Requirements

Neuronanorobotics, a promising future medical technology, may provide the ultimate tool for achieving comprehensive non-destructive real-time in vivo monitoring of the many information channels in the human brain. This paper focuses on the electrical information channel and employs a novel electrophysiological approach to estimate the data rate requirements, calculated to be (5.52 ± 1.13) × 10^16 bits/sec in an entire living human brain, for acquiring, transmitting, and storing single-neuron electrical information using medical nanorobots, corresponding to an estimated synaptic-processed spike rate of (4.31 ± 0.86) × 10^15 spikes/sec.

Why Uploading Will Not Work, or, the Ghosts Haunting Transhumanism

Transhumanists tend to have a commitment to materialism and naturalism but nonetheless pursue goals traditionally associated with religious ideologies, such as the quest for immortality. Some hope to achieve immortality through the application of a technology whereby the brain is scanned and the person "uploaded" to a computer. This process is typically described as "transferring" one's mind to a computer.

I argue that, while the technology may be feasible, uploading will not succeed because it in fact does not "transfer" a mind at all and will not preserve personal identity. Transhumanist hopes for such transfer ironically rely on treating the mind dualistically - and inconsistently with materialism - as the functional equivalent of a soul, as is evidenced by a carefully examination of the language used to describe and defend uploading. In this sense, transhumanist thought unwittingly contains remnants of dualistic and religious concepts.

A Framework for Approaches to Transfer of a Mind's Substrate

I outline some recent developments in the field of neural prosthesis concerning functional replacement of brain parts. Noting that functional replacement of brain parts could conceivably lead to a form of "mind-substrate transfer" (defined herein), I briefly review other proposed approaches to mind-substrate transfer then I propose a framework in which to place these approaches, classifying them along two axes: top-down versus bottom-up, and on-line versus off-line; I outline a further hypothetical approach suggested by this framework. I argue that underlying technological questions about mind-substrate transfer, there is a fundamental question which concerns our beliefs about continuity of identity.

On this last topic, present developments in neural prosthetics are well worth the time taken to investigate. Being able to replace some lesser pieces of the brain in the event of damage is on the verge of being a going concern - sometime within the next twenty years there will be a fair number of people walking around with implanted medical devices in their brains. Those devices will replace or augment the function of one or more component parts of the brain, allowing these patients to live where they would otherwise have died or suffered a lower quality of life. This is the start of the next wave of mapping the physical structure of the brain to its function, and that field of research will expand and accelerate just like all other areas of medicine, driven by the ongoing biotechnology revolution.

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

Researchers here report on another way to tell old stem cells to get back to work on maintaining muscle tissue - though not one that has immediate application, as it requires removal of an important component of immune system function. Thus this is only promising if researchers can pick apart the different functions of this component and interfere only where it suppresses stem cell activity in muscle regeneration: "Wnt signaling plays critical roles in development of various organs and pathogenesis of many diseases, and augmented Wnt signaling has recently been implicated in mammalian aging and aging-related phenotypes. We here report that complement C1q activates canonical Wnt signaling and promotes aging-associated decline in tissue regeneration. Serum C1q concentration is increased with aging, and Wnt signaling activity is augmented during aging in the serum and in multiple tissues of wild-type mice, but not in those of C1qa-deficient mice. ... Skeletal muscle regeneration in young mice is inhibited by exogenous C1q treatment, whereas aging-associated impairment of muscle regeneration is restored by C1s inhibition or C1qa gene disruption. Our findings therefore suggest the unexpected role of complement C1q in Wnt signal transduction and modulation of mammalian aging."

Link: http://www.cell.com/retrieve/pii/S0092867412005314

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

Functional Neurology with Dr. Shannon Leon
I run a neurology based practice in Long Island, NY, focused on disease prevention, nutrition, and wellness. I am committed to taking patient #39;s from acute an...

By: Dr. Shannon Leon

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Functional Neurology with Dr. Shannon Leon - Video

Advanced glycation end-products (AGEs) are implicated in aging - one of the forms of chemical gunk that accumulates in the body over time, harming the operation of intricate biomolecular machinery (in this case probably by triggering cells to respond in an undesirable way). AGEs are a part of our dietary intake as well as being generated in the body, and there is a debate over the degree to which dietary intake of AGEs is important in the pace of buildup over a lifetime - and the role of gut bacteria for that matter, given that they can independently produce AGEs as well. Here is a review paper on the subject: "Advanced glycation end products (AGEs) are a heterogeneous, complex group of compounds that are formed when reducing sugar reacts in a non-enzymatic way with amino acids in proteins and other macromolecules. This occurs both exogenously (in food) and endogenously (in humans) with greater concentrations found in older adults. While higher AGEs occur in both healthy older adults and those with chronic diseases, research is progressing to both quantify AGEs in food and in people, and to identify mechanisms that would explain why some human tissues are damaged, and others are not. In the last twenty years, there has been increased evidence that AGEs could be implicated in the development of chronic degenerative diseases of aging, such as cardiovascular disease, Alzheimer's disease and with complications of diabetes mellitus. Results of several studies in animal models and humans show that the restriction of dietary AGEs has positive effects on wound healing, insulin resistance and cardiovascular diseases. Recently, the effect of restriction in AGEs intake has been reported to increase the lifespan in animal models. This paper will summarize the work that has been published for both food AGEs and in vivo AGEs and their relation with aging, as well as provide suggestions for future research."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22254007

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

Via EurekAlert!: "Regenerative medicine, or the use of specially grown tissues and cells to treat injuries and diseases, has been successful in treating disorders of a number of organs, including heart, pancreas, and cartilage. However, efforts to treat disorders of the corneal endothelium, a single cell layer on the inner surface of the cornea, with regenerative techniques have been less effective. Now, a group of scientists has developed a method that enhances the adhesion of injected corneal endothelial cells (CECs), allowing for successful corneal transplantation to repair pathological dysfunctions. ... Previous studies demonstrated that Rho-associated kinase (ROCK) signaling interferes with adhesion. We found that transplanting cultivated CECs in combination with a low-molecular weight compound that inhibits ROCK (ROCK inhibitor Y-27632), successfully achieved the recovery of corneal transparency. ... Using rabbit cells, researchers cultivated CECs in the lab and injected them into the anterior chamber of rabbit eyes with damaged corneal endothelia. Based on the recovery of the corneal endothelial function, they found that when the cultivated cells were injected along with Y-27632, the rabbit corneas regained complete transparency 48 hours after injection. ... Since rabbit CECs are highly prolific in vivo, the scientists performed another round of experiments with monkey CECs, which are more similar to those in humans. The transplantation of CECs in these primates also achieved the recovery of long-term corneal transparency with a monolayer of hexagonal cells, suggesting that cell adhesion modified by ROCK inhibitor may be an effective treatment for human corneal endothelial disorders."

Link: http://www.eurekalert.org/pub_releases/2012-06/ehs-rcm061112.php

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

An interview with Aubrey de Grey of the SENS Foundation: "I'm interested in making sure that none of [the forms of biological damage that cause aging] are left behind. ... the main reason why we prioritize certain things over others is simply if they are not being prioritized by the rest of the world. At the moment, [in] our Research Center in Mountain View, we are working on LysoSENS, as you said, but we are also working on MitoSENS, the elimination of mitochondrial mutations in aging, and ways to make those mitochondrial mutations harmless essentially by putting copies of the mitochondrial genome into the nuclear genome. And in projects that we are funding in university labs around the country, we are doing a number of other things relating to other aspects of SENS. So yes, we are interested in focusing on all of these things in parallel. ... So at the moment, there are just a few areas within SENS that we are de-prioritizing because they are being funded quite well elsewhere. One of them is the elimination of amyloids [that] occurs in Alzheimer's disease. And even there, it's only sort of that one subset of that one deadly thing that we are not working on. So we are working on something very similar, the accumulation of a similar type of garbage outside cells that occurs predominantly in the heart. It just turns out that even though Alzheimer's work is well-funded and well respected and everything, nevertheless during the same sort of approach for other types of amyloids, other types of extracellular garbage, it is not being particularly enthusiastically pursued by other people, so we are doing our bit. Similarly, in the case of lost cells where cells die and they are not automatically replaced by other cells or by the division of other cells - that is what stem cells are for. Stem cell therapy is very real - people are working in lots of areas in that field, so of course we are not trying to duplicate that effort. But even there, we are doing one of two things. For example, we're interested in a particular type of cell loss which is the shrinkage of an organ called the thymus, which is responsible for the creation of certain types of immune cells. It turns out that restoration of the thymus to its useful size is something that not many people work on. The approaches that have been tried have not been very successful. We are looking at some more ambitious but we think more promising approaches that have not been looked at by other people."

Link: http://hplusmagazine.com/2012/01/17/progress-in-therapies-for-rejuvenation-and-their-delivery/

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

I'm not a big fan of the optimization mindset when it comes to long term health and longevity. Like all forms of optimization, it makes for a great hobby - with the potential to turn into a massive sink of time and money if you head on all the way down the rabbit hole. Importantly, however, and unlike optimization hobbies that involve cars, games, and other easily measured items, you will never really know how well you are doing when it comes to your own life expectancy. It's extremely easy to get the 80/20 result: practice calorie restriction and exercise regularly. But beyond that, there's no real way to tell whether any of your more esoteric practices are helping, hindering, or doing more or less nothing. There is no meaningful scorecard for future remaining life expectancy that you can measure and check your optimization efforts against.

This may well change over the next ten years, but for now it is what it is. By all means make health your hobby - it beats some of the other options in terms of general utility - but don't for one moment imagine that you actually know how well you're doing past the 80/20 point. And if you're not practicing calorie restriction, then it doesn't much matter what else you're doing because you haven't even captured all of the easy 80%.

Anyway, that all said, here is an interesting article that looks at measuring risk and life expectancy at the small scale - which is often a prelude to optimization, given human nature.

Many risks we take don't kill you straight away: think of all the lifestyle frailties we get warned about, such as smoking, drinking, eating badly, not exercising and so on. The microlife aims to make all these chronic risks comparable by showing how much life we lose on average when we're exposed to them: a microlife is 30 minutes off your life expectancy

Life expectancy for a man aged 22 in the UK is currently about 79 years, which is an extra 57 years, or 20,800 days, or 500,000 hours, or 1 million half hours. So, a young man of 22 typically has 1,000,000 half-hours (57 years) ahead of him, the same as a 26 year-old woman. We define a microlife as a chronic risk that shortens life on average by just one of the million half hours that they have left.

Here are some things that would, on average, cost a 30-year-old man 1 microlife:

Smoking 2 cigarettes

Drinking 7 units of alcohol (eg 2 pints of strong beer)

Each day of being 5 Kg overweight

A chest X-ray will set a middle-aged person back around 2 microlives, while a whole body CT-scan would weigh in at around 180 microlives.

This falls under the general heading of "fun with population-wide statistical measures of mortality," but you should find it food for thought, even if not of immediate application. On that note, an interesting speculative calculation to run, or at least build a framework for, would be a guesstimation of the benefit in microlives gained per dollar donated to the SENS Foundation.

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

A brief overview of one of the lines of work advocated by the Science for Life Extension Foundation: "Aging biomarkers are parameters that always, and in all people, change during aging. It is possible to evaluate and improve therapies that are aimed at slowing down aging, using the biomarkers of aging. The value and changing dynamics of aging markers provides information about the intensity of aging processes in the cells of the patient. Aging biomarker monitoring allows us not only to diagnose various diseases, but also to prevent their development. Aging can be slowed down. At the moment, there are already several scientific approaches that could lead to slowing down aging, and extending life. Scientists have been able to significantly extend the lifespans of model animals. Now, it is time to apply the biogerontology knowledge in clinical practice. To understand if a given therapy is effective or not, first of all we compile data via conventional clinical tests to create the 'electronic health passport.' After that, we can perform measurements of the aging biomarkers listed in the table. The indicators will inform us if the therapy is working. Soon we will be able to look at thousands of parameters, obtained using genome and transcriptome sequencing, epigenome mapping and analysis of proteome and metabolome. The additional data will make the anti-aging therapies more precise. ... view our entire booklet that lists twenty (20) aging bio-markers."

Link: http://ieet.org/index.php/IEET/more/konovalenko20120118

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