As you may know, a range of ways to extend life in nematode worms (such as the common laboratory species Caenorhabditis elegans) involve interfering in the operation of mitochondria. This is also true in a range of other lower animals - mitochondrial operation is apparently strongly coupled to the natural range of longevity enjoyed by a given species. But what are mitochondria? They are a roving swarm of tiny power plants, present inside every cell, and inside each mitochondrion there can be found an array of intricate molecular machinery that gives rise to what is called the electron transport chain. This is a critical component in the process of building stores of chemical energy - in the form of ATP - used to power the operation of the cell. It is alterations in the operation of the electron transport chain that can alter longevity for the better in many species.

A recent open access paper digs into other mechanisms that relate to this link between electron transport chain operation and life span, outlining the discovery of a gene that is necessary for that enhanced longevity:

Mitochondria have long been associated with aging and age-related diseases. Recent research has shown that a slight dampening of mitochondrial function can dramatically increase the lifespan of a wide range of organisms, suggesting that a similar mechanism likely operates in humans. The molecular basis of this observation is largely unknown, however. Uncovering the genes that allow altered mitochondrial function to impact longevity will give us important new insights into how mitochondria affect the aging process and will pave the way for future therapeutic developments aiming to improve healthy aging and to treat age-related diseases.

Here, we used an RNAi screen in the genetic model organism C. elegans, a nematode worm, to uncover how altered mitochondrial function can modulate longevity. We found that in order for mitochondria to affect lifespan, they must communicate with several unique transcription factors in the nucleus. Notably, we discovered that the putative homeobox transcription factor CEH-23, which has not previously been implicated in longevity determination, is able to respond to changes in mitochondrial function and in turn causes an extension in lifespan. ... ceh-23 expression levels are responsive to altered METC, and enforced overexpression of ceh-23 is sufficient to extend lifespan in wild-type background.

So it looks like some form of programmed response causes the life extension in these methods, and manipulations of the electron transport chain only trigger that response - which is interesting. Not what you might expect, given all the other ways in which mitochondria touch on aging, such as through accumulated damage to their DNA.

You may recall that composition of cell membranes is strongly correlated to species longevity - the idea being that some membranes are more resistant to the damage of reactive oxygen species than others, and that damage resistance at the cellular level ultimately translates into a longer-lived animal. Here is more on that topic: "This review begins with the premise that an organism's life span is determined by the balance between two countervailing forces: (i) the sum of destabilizing effects and (ii) the sum of protective longevity-assurance processes. Against this backdrop, the role of electrophiles is discussed, both as destabilizing factors and as signals that induce protective responses. Because most biological macromolecules contain nucleophilic centers, electrophiles are particularly reactive and toxic in a biological context. The majority of cellular electrophiles are generated from polyunsaturated fatty acids by a peroxidation chain reaction that is readily triggered by oxygen-centered radicals, but propagates without further input of reactive oxygen species(ROS). Thus, the formation of lipid-derived electrophiles such as 4-hydroxynon-2-enal (4-HNE) is proposed to be relatively insensitive to the level of initiating ROS, but to depend mainly on the availability of peroxidation-susceptible fatty acids. This is consistent with numerous observations that life span is inversely correlated with membrane peroxidizability and with the hypothesis that 4-HNE may constitute the mechanistic link between high susceptibility of membrane lipids to peroxidation and shortened life span. Experimental interventions that directly alter membrane composition (and thus their peroxidizability) or modulate 4-HNE levels have the expected effects on life span, establishing that the connection is not only correlative but causal. Specific molecular mechanisms are considered, by which 4-HNE could (i) destabilize biological systems via nontargeted reactions with cellular macromolecules and (ii) modulate signaling pathways that control longevity-assurance mechanisms."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21708248

A long and fascinating post from Chronosphere details the extensive preparations that go into transporting the body of a cryonics patient for cryopreservation: "Many patients will be remote from the facility where cryoprotective perfusion will be carried out and will be transported by common carrier or private carrier over considerable geographical distances. In some cases it will be possible to move the patient using a specialized transport vehicle with on-going extracorporeal support. In other cases the distances will be sufficiently great that the only realistic option is iced-shipment in the absence of perfusion. It is often necessary to use a commercial air freight service to move the patient from one area of the United States to another (or from one country to another). ... Because of time constraints to get freight loaded rapidly, air freight is often not handled with care by airport personnel. ... Whenever possible, the Transport Technician should supervise the handling of the patient every step of the way, including on and off the aircraft. Due to recent terrorist acts it has become increasingly difficult for the Transport Technician to do this. Until quite recently it was usually easy for the Technician to get access to air freight facilities and the tarmac to supervise loading of the patient onto the aircraft. This is now all but impossible. However, it is still important to accompany the patient to the air freight depot and to emphasize that extra care should be used in handling the patient, and that every precaution should be taken against misrouting."

Link: http://chronopause.com/index.php/2011/06/28/commercial-air-transport-of-the-cryopreservation-patient/

I'm pleased to see that the Immortality Institute / Longecity has completed fundraising for their latest project, an investigation of the potential benefits of microglia transplants in the aging brain:

After months of fundraising we are now delighted to announce that the project has started! Through many donations large and small, the community has raised sufficient funds to initiate the project. Last month, we passed the 80% mark and knew that full success would only be a matter of time. Then, something amazing happened: though promoting this effort, a far sighted investor has stepped forward who can see the potential in developing this research project. The angel [committed] a substantial contribution towards a research arm that is closely aligned to the project LongeCity is funding. Thus, we have achieved something amazing together: every dollar donated to this life extension research project has not only been doubled through internal funds but multiplied manifold! Few people, especially those with very limited personal means, who want to invest in life extension would find such effective opportunities to make a real difference.

Which is good news all round. I've mentioned this effort in past months, so you can head on back into the archives for more details on the funded research. We live in an age in which a large range of meaningful early-stage work in biotechnology can be performed for comparatively little money - a few tens of thousands of dollars, or less. A single young researcher with lab access can validate theories, determine whether a line of research has promise, or make new connections in a field - and all in a matter of a few months to half a year of work, as one of a number of ongoing projects.

Most importantly, the new reality of low costs means that people of everyday means can band together in small associations to fund the research that they find important, on a project by project basis. This sort of grassroots, bottom-up organization is greatly aided by the internet, but crowdsourced philanthropy for science in detail is only just in its infancy. Projects like those undertaken by the Immortality Institute volunteers are the first signs of the true future of research funding - a detailed and glorious patchwork in which everyone can pick and choose the exact projects they wish to fund, and in doing so learn more about the science behind the causes they support.

Another sign of progress in this direction is the creation of dedicated crowdsourced scientific philanthropy initiatives like FundScience, which has actually been around for a couple of years, and will be holding a meetup on July 15th in the Bay Area:

FundScience was formed to get the public invested in science. We aim to accomplish two goals:

1. Provide a way for scientists and researchers to self fund their research by crowd funding.

2. Bring people closer to science by providing an insight into research activities done across the globe.

In addition to staying in touch with scientific activity via FundScience.org , we are launching monthly meetups to give you an opportunity to get to know your favorite researchers in person. Come find out how you can be a part of their amazing work.

I co-founded FundScience a few years ago with the hope of getting the public invested in science. We had two goals when we began. The first was to get much needed funding and guidance to young researchers. The other was to get non-scientists to interact with researchers and understand the research process. Our first round of projects was selected and posted on the site late last year. In keeping with our goal of bringing science to the masses we've decided to complement our online presence with a monthly meetup were we can get researchers to discuss their advancements and get non-scientists to come and ask questions, interact and fund some projects.

There are a fair number of philanthropic ventures that help funnel dollars from many donors to worthy causes, such as Philanthroper for example, but still very few ventures that take the next step of breaking things down into fine-grained projects. Much of the wall between the broader charitable public and the details of the work they support is, I feel, unnecessary. The faster it evaporates the better off we'll all be.

Type 2 diabetes is the poster child for an avoidable age-related condition: barring the worst of genetic bad luck, calorie restricted, well exercised people will not suffer from type 2 diabetes. But this is, undeniably, an age-related illness. Becoming ever more obese and sedentary will hasten the onset of diabetes into ever earlier years of life, but older obese and sedentary people are still far more likely to suffer type 2 diabetes than are equally overweight and sedentary younger counterparts. So while failing to take care of your health at any age is just another form of self-harm, there are other, less avoidable processes taking place at the level of cells and organs that make older people more vulnerable.

Here is an open access paper that reviews what researchers presently know of the decline of insulin-producing beta cells in the pancreas - which turns out to be not enough, as is still true of so much of our biochemistry. There are changes, cataloged and identified, but the chains of causation for those changes are poorly understood at best.

Type 2 Diabetes and the Aging Pancreatic Beta Cell

An increased incidence of diabetes is observed with age, and there are many possibly reasons for this. One of these is that the beta cell has reduced proliferative capacity and in diabetic individuals this is further confounded by higher rates of beta cell apoptosis. The currently known underlying mechanisms behind the reduction in beta cell proliferation observed with age include reduced expression of cell cycle activators, increased expression of cell cycle inhibitors, reduced pdx1 expression, and increased amylin aggregation. Studying aging in the non-diabetic rodent and human models is currently a developing field; therefore very few broad conclusions can be drawn. Further study in these areas is important as they could indicate targets for preventing or slowing the progression of diabetes with age.

I look on this as a good illustration of why the detailed, tissue by tissue, understand everything approach to repairing aging is doomed to take a very long time indeed. This is but one population of vital cells in one organ, one of the most studied forms of cell in past decades, and the research community remains far from a complete understanding as to how and why they fail with age.

Better strategies to deal with aging exist - such as SENS - and need to gain wider support and adoption. SENS-like approaches work around the challenge posed by the sheer complexity of human biochemistry by focusing on the known common mechanisms of aging, the root causes from which there is good reason to believe all other changes descend. Repairing these root causes is the fast path to the first generation of rejuvenation biotechnology, and that, in my eyes, is the only real shot at building viable interventions in the aging process that will arrive in time to help us.

Via ScienceDaily: "Even long after it is formed, a memory in rats can be enhanced or erased by increasing or decreasing the activity of a brain enzyme. ... Our study is the first to demonstrate that, in the context of a functioning brain in a behaving animal, a single molecule, PKMzeta, is both necessary and sufficient for maintaining long-term memory. ... Unlike other recently discovered approaches to memory enhancement, the PKMzeta mechanism appears to work any time. It is not dependent on exploiting time-limited windows when a memory becomes temporarily fragile and changeable - just after learning and upon retrieval - which may expire as a memory grows older. ... This pivotal mechanism could become a target for treatments to help manage debilitating emotional memories in anxiety disorders and for enhancing faltering memories in disorders of aging. ... In their earlier studies, [researchers] showed that even weeks after rats learned to associate a nauseating sensation with saccharin and shunned the sweet taste, their sweet tooth returned within a couple of hours after rats received a chemical that blocked the enzyme PKMzeta in the brain's outer mantle, or neocortex, where long-term memories are stored. In the new study, they paired genetic engineering with the same aversive learning model to both confirm the earlier studies and to demonstrate, by increasing PKMzeta, the opposite effect. They harnessed a virus to infect the neocortex with the PKMzeta gene, resulting in overexpression of the enzyme and memory enhancement. Conversely, introducing a mutant inactive form of the enzyme, that replaced the naturally occurring one, erased the memory - much as the chemical blocker did."

Link: http://www.sciencedaily.com/releases/2011/03/110304092111.htm

A look at current research on the definite health and potential longevity benefits of calorie restriction in humans: "Animals who consume fewer calories live longer and healthier lives. Now, a seminal study at the University of California, San Francisco (UCSF) is testing whether the same is true for extreme dieters. The calorie restriction study centers on two primary questions: What allows people to live in a manner many consider food deprived? And does it slow down aging? Called CRONA (Caloric Restriction with Optimal Nutrition and Aging Study), the investigation is probing the biological processes affected by extremely low caloric intake, including the impact on telomeres - tiny pieces of DNA that protect cell chromosomes. Short telomeres have been linked to a host of health problems including diabetes, heart disease and premature death. The UCSF study is the first to broadly examine the psychological profile of successful extreme dieters, gauging how their cognitive sharpness, impulse control, stress and personality differ from normal eaters and overeaters. ... Testing and data collection will continue through summer. The scientists are still recruiting control subjects who are either obese or 'free eaters' - not restricting food intake but not overweight. Interested parties can email cronastudy@gmail.com. ... We need information about what it takes to change your eating pattern for a long time. There are so many diets out there - people lose weight for six months, then regain it. We need to study what it is about the calorie restrictors that makes them able to do this for years and years." The new information on the biological response to calorie restriction is, I think, much more valuable than yet another study on willpower in humans.

Link: http://www.ucsf.edu/news/2011/04/9740/extreme-dieting-does-it-lead-longer-lives

Cellular differentiation is the process by which stem cells and other progenitor cells divide to form specialized cell populations - of which there are a great many different types in the body. Much of stem cell research to date has been focused on finding out how to first obtain stem cells and then differentiate them to form specific desired types of specialized cell. This has been a challenging process, but advances in biotechnology are making it easier and less costly as the years go by.

Cells are programmable machinery; it seems to be the case that any given type of cell holds the potential to produce any other type of cell, if researchers just understood the right chemical and genetic cues and instructions. Thus in addition to the work of reverting specialized cells into stem cells, and differentiating stem cells into desired specialized cells, there is also the possibility of achieving transdifferentiation - converting one type of cell directly into another without passing through a stem cell stage.

In recently reported research, researchers are making inroads in converting various types of cell in the pancreas - which offers the possibility of a fairly direct path towards providing new beta cells to diabetes patients:

While the current standard of treatment for diabetes - insulin therapy - helps patients maintain sugar levels, it isn't perfect, and many patients remain at high risk of developing a variety of medical complications. Replenishing lost beta cells could serve as a more permanent solution, both for those who have lost such cells due to an immune assault (Type 1 diabetes) and those who acquire diabetes later in life due to insulin resistance (Type 2).

"Our work shows that beta cells and related endocrine cells can easily be converted into each other," said study co-author Dr. Anil Bhushan, an associate professor of medicine in the endocrinology division at the David Geffen School of Medicine at UCLA and in the UCLA Department of Molecular, Cell and Developmental Biology.

It had long been assumed that the identity of cells was "locked" into place and that they could not be switched into other cell types. But recent studies have shown that some types of cells can be coaxed into changing into others - findings that have intensified interest in understanding the mechanisms that maintain beta cell identity.

This is as much the age of controlling cells as it is the age of biotechnology. Researchers are presently building the foundation for complete control over the component machinery of the human body. Along the way to that goal lies the production of ever more effective general repair kits for all forms of damage that originate in missing or damaged cell populations - including one portion of aging itself.

Some people do have better genes than others when it comes to a long life, though lifestyle choices do still seem to play a greater role. Here, researchers were looking to "determine whether offspring of parents with exceptional longevity (OPEL) have a lower rate of dementia than offspring of parents with usual survival (OPUS). ... [Participants were a] volunteer sample of 424 community-residing older adults without dementia aged 75 to 85 recruited from Bronx County starting in 1980 and followed for up to 23 years. ... Epidemiological, clinical, and neuropsychological assessments were completed every 12 to 18 months. OPEL were defined as having at least one parent who reached the age of at least 85. OPUS were those for whom neither parent reached the age of 85. ... The OPEL group had a lower incidence of Alzheimer's disease. After adjusting for sex, education, race, hypertension, myocardial infarction, diabetes mellitus, and stroke, results were essentially unchanged. OPEL also had a significantly lower rate of memory decline on the Selective Reminding Test (SRT) than OPUS. ... OPEL develop dementia and Alzheimer's disease at a significantly lower rate than OPUS. Demographic and medical confounders do not explain this result. Factors associated with longevity may protect against dementia and Alzheimer's disease."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20487085

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

A chemical compound called epigallocatechin gallate showed much promise by killing cancerous cells during a phase 2 clinical study.

According to a study performed by researchers from the Mayo Clinic, the extract of the world-popular green tea has been effective in regulating the growth and proliferation of cancer cells in patients with chronic lymphocytic leukemia (CLL).  The study was classified as a phase two human clinical trial, and the results were very promising indeed.

Epigallocatechin gallate vs. cancer cells

The compound epigallocatechin gallate was shown to have the ability to kill cancer cells in patients with CLL.  The compound prevented the cancer cells from surviving, thereby effectively reducing the total cancer cell count. The first phase of the human clinical trial of epigallocatechin gallate also showed similar, positive results.

What does this all mean?  According to one of the Mayo researchers, Dr. Tait Shanafelt, the two clinical trials show that epigallocatechin gallate showed some promise in stabilizing or normalizing the condition of patients with CLL.  While the compound is not classified as a definitive cure for the condition, it shows promise in slowing down the progress of the medical condition.

Instead of a cure, Mayo clinic researchers state that the compound should be viewed as a cancer preventive rather than cancer cure. And there was a catch: the patients that were subjected to the nutraceutical treatment were patients who had early signs of CLL (not advanced stage CLL).

The study involved thirty-six respondents and resulted in a fifty percent reduction of leukemia cell count at the end of the human clinical trial.  Including the patients from the first clinical trial, the total number of CLL patients involved in the study is forty-two.  A third clinical trial is needed before the Mayo Clinic researchers can make a definitive recommendation regarding the use of epigallocatechin gallate for CLL sufferers.

Other benefits of green tea

Tea is the second most drunk beverage in the world (right next to water). It contains natural antioxidants and caffeine (50% less than regular coffee).  And did I mention that it’s good for you for a lot of reasons?  It’s more than just a cancer preventive.  Here are some more health benefits of drinking green tea:

1. According to a study published by the American Medical Association, 40,000 respondents (from Japan; all of them drank up three cups of green tea per day) showed no evidence of cardiovascular anomalies and coronary heart problems since the study started back in the year 1994.  Not one individual from the 40,000 strong group developed any cancer, too!

2. Drinking green tea reduces the risk of dying from heart disease by twenty six percent (for males).  For women, drinking three to five cups of the precious elixir reduced the risk of dying from heart attacks and other cardiac problems by a staggering thirty-one percent.

3. Having chronic problems with sleep apnea (disturbances during sleep) and poor sleep quality, generally?   Reach for green tea.  US studies found out that chemical compounds in green tea can help prevent cognitive troubles resulting from poor sleep.

4. If you have trouble memorizing for school, don’t drink soda.  Instead, make yourself a nice, warm green tea brew.  There is no reason not to enjoy this beverage as it now comes in many natural flavors, like blueberry, cinnamon, etc.

All you have to do is choose your favorite flavor and use a French press to make an instant cup of tea.  Or you can just buy tea bags and allow the tea to infuse itself into the water for a few minutes.  I recommend this and that’s how I make my green tea.  The longer you keep the teabag in the hot water, the stronger the tea.

You can also add a bit of cinnamon to make the tea more interesting.  Since tea has caffeine, it can also help keep you more alert and awake when working or studying.   Green tea also has theanine, which has been shown to have beneficial effects in that region of the human brain that is responsible for alertness.

5. Suffering from poor immunity against common illnesses like the flu and the common cold?  Green tea is rich in chemical compounds called polyphenols, which can help boost your immune system.  Polyphenols can also help slow down aging by reducing the oxidative stress that the body experiences from free radicals.  Polyphenols are capable of disabling free radicals in the body.

6. Substituting polyphenol-rich beverages like green tea for soda and the like can also reverse the spike in body weight.  Because green tea doesn’t have much sugar, it does not contribute much to your weight (apart from its water content).  If you are having trouble with ‘water weight’, then all you have to do is to sip on the green tea during the day instead of downing a whole cup in one go.  But don’t forget: being well-hydrated is more important.  Also, water helps the body lose weight by helping in better digestion and also by helping the body burn calories more efficiently.

7. According to researchers from the Chinese University of Hong Kong, the antioxidants present in green tea can also penetrate the tissues in the eyes and do a world of good there.  Increased antioxidant activity in any body tissue has always been linked to decreased inflammation and healthier tissues and cells.

8. All kinds of tea come from the same camella plant – and tea always has more than ten times the amount of antioxidant chemicals than regular vegetables and fruits.  So drink up!  Green tea can also help prevent dangerous blood clots from forming in veins and arteries (which can lead to heart attack and stroke).  You also reduce the risk for atherosclerosis when you drink plenty of tea, say Dr. John Weisburger, the US’s pro-tea champion and veteran researcher (who is also, incidentally, already eighty two years old!)

Cancer prevention

In the spirit of global cancer prevention, here are some easy steps that you can prevent different types of cancer.

Prostate Cancer

• In a European study, it was discovered that regular intake of legumes and other vegetables lowered the risk of prostate cancer over the long term.
• Nutrients like vitamin D, isoflavanoids and selenium can help reduce prostate cancer by stopping the chemical processes that can lead to the formation of cancer cells.

Skin Cancer

• Increase your intake of antioxidants prior to sun exposure or take an umbrella with you when going out into the direct heat of the sun for a long period of time!
• Beta-carotene has been linked to reduced risk of developing cancerous skin cells.

Lung Cancer

• Long term tobacco smoke has been linked to lung cancer – so stop the habit before it leads to something much, much worse than just stained teeth.
• Regular exercise produces a protective effect on the body – including the respiratory system. Get enough exercise to strengthen your breathing apparatus.

Sources:
sciencedaily.com
blogs.webmd.com
blogs.webmd.com
webmd.com
webmd.com
webmd.com
webmd.com
webmd.com

Discuss this article in Frank Mangano’s forum!

Via EurekAlert!: "A team of researchers has developed a method to produce cells that kill tumour cells in the lab and prevent tumours forming in mouse models of cancer. ... In this research, T cells were transformed into cells similar to another type, Natural Killer (NK) cells, which commonly act against viruses and cancer cells. ... We had shown that a gene called Bcl11b was essential for normal development of immune system cells - and of particular interest in the development of T cells. Here we can see the fruits of that work: we show, for the first time, that we can modify the developmental fate of immune system cells to produce a novel type that - if we can see the same effect in humans - could be of enormous value in cancer treatment. ... the Bcl11b gene was active only in T cells in the immune system and that its activity was needed at the earliest stages of production of T cells. When the team knocked out the Bcl11b gene, the mice produced no T cells. ... Remarkably, the mice lacking the Bcl11b gene produced a new type of immune system cell - the Induced T to Natural Killer cells. This is the first time we have seen these cells ... Even more important, we can see that these reprogrammed killer cells can attack cancer cells, whether in test tubes or in mouse models. ... The ITNK cells killed melanoma and lymphoma cells in experiment in test tubes and were much more efficient than unmodified Natural Killer cells in the mouse and in human."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-06/wtsi-mck061010.php

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

Welcome to Acupuncture.Com

By Mao Shing Ni, PhD, D.O.M., Dipl. ABAAHP

If you are a health nut, then you may want to consider stocking up on seeds this fall! Despite their tiny size, seeds are saturated with heart-healthy fats, vitamins, minerals and protein. Read on to discover which seeds are sprouting with loads of nutrients and flavor so you can munch your way to longevity.

A daily handful of seeds can help improve your muscle tone and circulation. They are abundant in the amino acid arginine, which helps fight heart disease, infertility, high blood pressure and impotence. More...

By J. Matthew Brand, MATCM, L.Ac.

Tai Chi Quan can be translated from the Chinese as the highest form of martial arts. As with all Chinese martial arts, it developed from Shaolin boxing several hundred years ago and has the distinction of being one of the three soft-style Taoist martial art forms, alongside Baguazhang and Xingyiquan. On a purely physical level, these forms strive toward harmony of movement, utilizing the entire body in unison while helping establish good structure in the body. On a spiritual and emotional level, one strives to transition through the forms while quieting the mind in a moving meditation. More...

Q: I feel very stressed lately. Can you recommend a breathing method to help me stay calm throughout the day?

A: For overcoming stress, try this deep, slow breathing exercise:

1.Sit in a comfortable chair in a quiet place.

2. Sit on the tip of the chair with your back erect. Place your arms gently on your legs, which are bent at 90 degrees.

Visit link:
Acupuncture.Com - Home of Traditional Chinese Medicine

From the SENS Foundation: "To develop an unbreachable defense against cancer, SENS Foundation is pursuing the WILT (Wholebody Interdiction of Lengthening of Telomeres) strategy (OncoSENS) of systematically deleting genes essential to the cellular telomere-maintenance mechanisms (TMM) from all somatic cells, while ensuring ongoing tissue repair and maintenance through periodic re-seeding of somatic stem-cell pools with autologous TMM-deficient cells whose telomeres have been lengthened ex vivo. In addition to the deletion of one or more genes coding for essential element(s) of the telomerase holoenzyme, success will also require the deletion of some essential element of the machinery for the Alternative Lengthening of Telomeres (ALT) phenomenon, observed in a minority of cancer cells. Heretofore, the identity of that machinery has been elusive. Yeast cells have the ability to lengthen telomeres through a telomerase-independent mechanism involving telomere recombination, and there has been evidence for some time suggesting that ALT cancers lengthen telomeres through a similar process." The article goes on to look in detail at one plausible candidate mechanism for ALT, and how this new knowledge might be incorporated into WILT.

View the Article Under Discussion: http://www.sens.org/node/739

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

You're all, I hope, familiar with the Fable of the Dragon-Tyrant - easily the best modern fable about the scientific quest to build rejuvenation biotechnology and thereby defeat age-related frailty, suffering and death. If you have not yet read it, shame on you. Go and read it:

Once upon a time, the planet was tyrannized by a giant dragon. The dragon stood taller than the largest cathedral, and it was covered with thick black scales. Its red eyes glowed with hate, and from its terrible jaws flowed an incessant stream of evil-smelling yellowish-green slime. It demanded from humankind a blood-curdling tribute: to satisfy its enormous appetite, ten thousand men and women had to be delivered every evening at the onset of dark to the foot of the mountain where the dragon-tyrant lived. Sometimes the dragon would devour these unfortunate souls upon arrival; sometimes again it would lock them up in the mountain where they would wither away for months or years before eventually being consumed...

I see that some folk across the way a little in the longevity science community have the great idea that a web animation of the fable should be produced - something that could be dropped into many, many websites and seen by a large audience.

My friend Kent Kemmish, at Halcyon Molecular, has offered to put up $50 for someone who does the best animated flash version of Nick Bostrom's classic essay "The Fable of the Dragon-Tyrant" ... Let's say that the challenge stands for one month, until August 7th. My other friend Kevin Fischer is also putting in $50 for a total of $100. Would anyone else be interested in adding to that purse?

I think that this is a good idea with a great deal of merit, but that these folk are not going about it in quite the right way. From my point of view, producing a fair animation - let's say something that looks like the silhouette stop-motion techniques used in some older Eastern European animations of folktales - is going to take a little organization, a few months in total elapsed time from start to finish, and at minimum a few thousand dollars. If you expect to pull in donations through word of mouth and in $50 increments, then this is exactly the sort of project you'd want to run via a tool like Kickstarter. You need some form of way to track and communicate with donors, a way to accept donations, and a web page to showcase your idea and progress to date - why build all that yourself, when you could use Kickstarter?

So the folk who are pushing this should pick a leader, have him set up and manage a Kickstarter project, produce a few specification documents and showy sample pictures, and then reel in enough in the way of funds to get started with a developer who has a good portfolio, found via a contract marketplace like oDesk or 99designs. That's the way this is done. A wide range of indie developers in the writing world use Kickstarter to crowdsource funding for their work using ransom models and other fundraising methods. An alternate approach to the one above is if someone with deeper pockets were to simply commission the work on the simple animated version of the fable, they could then place it in escrow until the costs were recouped through donations, and finally release it online.

Step one would be to validate the cost - and that's as simple as finding someone who builds animations for websites (in Flash, Canvas, or whatever the cool kids are using nowadays) and then asking.

Just as physical exercise is beneficial, so too is exercising the mind. This open access paper examines structured mental exercise as a basis for therapy that might do at least some good for neurodegenerative disease patients: "Non-pharmacological intervention of memory difficulties in healthy older adults, as well as those with brain damage and neurodegenerative disorders, has gained much attention in recent years. The two main reasons that explain this growing interest in memory rehabilitation are the limited efficacy of current drug therapies and the plasticity of the human central nervous system and the discovery that during aging, the connections in the brain are not fixed but retain the capacity to change with learning. Moreover, several studies have reported enhanced cognitive performance in patients with neurological disease, following non-invasive brain stimulation [i.e., repetitive transcranial magnetic stimulation and transcranial direct current stimulation to specific cortical areas]. The present review provides an overview of memory rehabilitation in individuals with mild cognitive impairment and in patients with Alzheimer's disease with particular regard to cognitive rehabilitation interventions focused on memory and non-invasive brain stimulation. Reviewed data suggest that in patients with memory deficits, memory intervention therapy could lead to performance improvements in memory, nevertheless further studies need to be conducted in order to establish the real value of this approach."

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297818/

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

First time client. Felt like a long lost friend. Knowledgeable. Gentle. Answered all questions and took time to make sure I was comfortable throughout procedure. Will definitely return and will recommend to my friends. Thank You! Longevity Client

The staff & facility are outstanding. I made a decision to change from my previous skin care facility to Longevity & have absolutely been so pleased with the decision. Thank you!-Longevity Client

Longevity offers health, beauty and wellness services that are focused on helping you live your best life. Our medical spa is led by Darryl Robinson, M.D. and Kristen Forbes, R.N, who are committed to helping each and every client live a life of health, beauty and wellness. Our goal is to inspire you and help you live life to the fullest while enhancing your body inside and out. Whether your goal is weight loss, stress reduction, a more confident body image, or a healthier lifestyle, we are here to help you attain all of your health and beauty goals.

At Longevity, we provide a full suite of health, beauty and wellness services for our clients in Moore, OK, Norman, OK, South OKC, OK, and the surrounding areas. Our services include skin rejuvenation Ulthera skin tightening & Forever Young BBL PhotoFacials;Skin care acne treatments, microdermabrasion, chemical peels & microneedling; Medically supervised weight loss, detox services & nutrition.

Our medspa also offers unique beauty and wellness solutions such as Injectables Botox, Xeomin, Juvederm, Bellafill; Neograft hair restoration; Laser hair removal; Spider vein removal; Massage therapy & infrared sauna and medical grade skin care products.

Some of our newest additions to our South OKC spa include: Body waxing, bikini wax & Brazilian waxing services & South Sea spray tans! Tattoo removal & a more advanced laser hair removal system will be available on site, once a month! Check our monthly events for dates! With our state-of-the-art beauty and health solutions, you can look and feel your very best for the rest of your life!

Dr. Darryl Robinson offers experienced medical supervision ensuring that each patient receives the attention and care they need from a qualified professional. He will see to it that you get the best treatments for enhanced health and wellness. Together with your esthetician or licensed expert, you can enjoy an enhanced appearance and improved physical well-being with a customized wellness plan made specifically for you. When you look and feel great, you have the confidence to pursue goals in other areas of your life with more focus and vision. Let us help you take the steps toward improved health and a renewed lifestyle.

Contact us to schedule a consultation and start enjoying your rejuvenated and invigorated lifestyle. Longevity provides the support and solutions you need to create a healthy and improved body, mind and appearance. Give us a call at 1(405) 703-4990 for quality care from a licensed esthetician, certified expert, or qualified physician today.

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Via EurekAlert!: "injections of adult patients' own CD34+ stem cells reduced reports of angina episodes and improved exercise tolerance time in patients with chronic, severe refractory angina (severe chest discomfort that did not respond to other therapeutic options). The phase II prospective, double-blind, randomized, controlled clinical trial was conducted at 26 centers in the United States ... The objective of the trial was to determine whether delivery of autologous (meaning one's own) CD34+ stem cells directly into multiple targeted sites in the heart might reduce the frequency of angina episodes in patients suffering from chronic severe refractory angina, under the hypothesis that CD34+ stem cells may be involved in the creation of new blood vessels and increase tissue perfusion. ... While we need to validate these results in phase III studies before definitive conclusions can be drawn, we believe this is an important milestone in considering whether the body's own stem cells may one day be used to treat chronic cardiovascular conditions. ... At six months after treatment, patients in the low-dose treatment group reported significantly fewer episodes of angina than patients in the control group (6.8 vs. 10.9 episodes per week), and maintained lower episodes at one year after treatment (6.3 vs. 11 episodes per week). Additionally, the low-dose treatment group was able to exercise (on a treadmill) significantly longer at six months after treatment, as compared with those in the control group (139 seconds vs. 69 seconds, on average)." If you want access to this sort of treatment now, and are resident in the US, going abroad as a medical tourist is your only realistic option. Otherwise you may still be waiting five or ten years from now: the FDA moves to approve treatments very slowly, when it moves at all.

Link: http://www.eurekalert.org/pub_releases/2011-07/nu-asc070711.php

Another example of calorie restriction slowing a specific aspect of the damage of aging: "restricting the caloric intake of adult female mice prevents a spectrum of abnormalities, such as extra or missing copies of chromosomes, which arise more frequently in egg cells of aging female mammals. ... We found that we could completely prevent, in a mouse model, essentially every aspect of the declining egg quality typical of older females. We also identified a gene that can be manipulated to reproduce the effects of dietary caloric restriction and improve egg quality in aging animals fed a normal diet, which gives us clues that we may be able to alter this highly regulated process with compounds now being developed to mimic the effects of caloric restriction. ... The long-term effects of a caloric restriction (CR) diet in humans are being investigated in ongoing studies, but some health improvements, including reductions in cholesterol levels and other cardiovascular risk factors, have already been reported. ... While the mechanisms by which caloric restriction produces its effects are still being investigated, several of the metabolic pathways involve a regulator of DNA transcription called PGC-1a, which is known to modulate genes involved in controlling mitochondrial number and function. [The researchers] also found that egg cells from female mice lacking a functional PGC-1a gene who were allowed to free feed through adulthood maintained the same egg-cell quality as seen in the CR mice. However, combining CR with PGC-1a inactivation did not increase the effects beyond those achieved separately, which suggests that the two approaches work in a common pathway."

Link: http://www.laboratoryequipment.com/news-Calorie-Reduction-May-Prevent-Infertility-070811.aspx

Some work here on IFG-1, not to be confused with IGF-1, which is also of interest in longevity: "When researchers at the Buck Institute dialed back activity of a specific mRNA translation factor in adult nematode worms they saw an unexpected genome-wide response that effectively increased activity in specific stress response genes that could help explain why the worms lived 40 percent longer under this condition. ... Scientists have identified a number of so-called 'longevity' genes active in many species. However, the mechanisms by which those genes impact lifespan remain poorly understood. ... the majority of research involving those genes has focused on transcription, the first level of cellular activity whereby DNA produces RNA. This research focuses on translation, whereby RNA specifies the production of proteins. ... [Researchers] inhibited expression of the mRNA translation factor, IFG-1, in adult worms. IFG-1 is important for growth and development ... "Turning down ifg-1 expression flips a switch that turned down growth and reproduction, but increased their healthspan as well as their lifespan. ... Our primary interest is to understand the biological basis of aging. This will help identify molecular targets that can be used to develop therapeutics that would slow age-related diseases and extend the healthy years of life."

Link: http://www.sciencedaily.com/releases/2011/07/110705123340.htm

The quality of the immune system in later years has a strong impact on mortality rates and frailty - and that quality varies with different genetic profiles. Thus it follows that among the genetic variants known to affect human longevity, some are involved with the immune system: "The ageing process is very complex. Human longevity is a multifactorial trait which is determined by genetic and environmental factors. Twin and family studies imply that up to 25% of human lifespan is heritable. The longevity gene candidates have generally fallen into the following categories: inflammatory and immune-related factors, stress response elements, mediators of glucose and lipid metabolism, components of DNA repair and cellular proliferation and mitochondrial DNA haplogroups. Because of the central role of HLA molecules in the development of protective immunity and the extraordinary degree of polymorphism of HLA genes, many studies have addressed the possible impact of these genes on human longevity. Most of the data available so far demonstrated a possible role of HLA class II specificities in human longevity but definitive evidence has remained elusive. Although the data are limited and controversial, it has been hypothesized that longevity could be associated with cytokine gene polymorphisms correlating with different levels of cytokine production, thereby modulating immune responses in health and disease. Because of the essential role of cytokines in immune responses, the regulation of cytokine gene expression and their polymorphic nature, the genetic variations of these loci with functional significance could be appropriate immunogenetic candidate markers implicated in the mechanism of successful ageing and longevity."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21726414