A general interest article on supercentenarians from the Sacramento Bee: "Avice Nelson Clarke paused in her recollections of her long-ago childhood in England to make a remarkable understatement. 'I've seen lots of life already,' she said. At 111, with memories spanning the horse-and-buggy age, the Space Age and the digital age, she is on the outside edge of the nation's trend toward increasing longevity. The oldest old - supercentenarians, as aging experts refer to them - remain rare: Clarke is one of four Sacramento-region residents who reported their ages as 110 or older in the 2010 U.S. census. ... The census recorded a total of 46 Californians in the supercentenarian category. Another 27 people in the Sacramento region reported their ages as 105 to 109, census figures show. While the number of centenarians has boomed in recent decades 96,000 across the country in 2010, according to the Social Security Administration, up from 37,000 only 20 years ago the nation's population of people 110 and older has remained fairly stable. ... The world's verified oldest person ever, Jeanne Calment, died in France in 1997, age 122 years and 164 days. ... Despite the world's aging population, no one's come close to that since then. That speaks to the limits of the human life span. ... Through blood tests and gene sequencing of the oldest old, scientists want to discover the secret of their extraordinary longevity ... How have they managed to live so long? We think their longevity is inherited. They have virtually nothing else in common. Some are smokers, and some never smoked. Some are drinkers, and some never drank. They don't have the same diets. But they have long-lived parents and siblings. It must be in the DNA. ... The key age is the early 80s for men and 90 for women. If you can get to that age without dementia or major heart disease or stroke, it's the idea of getting over the hump into healthy aging. ... Even so, 40 percent of the oldest old [survive] illnesses that prove fatal to others. ... Maybe they have some kind of functional reserve. The people who live the longest seem better able to deal with illness. They have a propensity to remain independent much longer than the rest of us."

Link: http://www.sacbee.com/2011/09/20/3923381/supercentenarians-the-oldest-old.html

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

Sirtuins are most likely a dead end, or more charitably a stepping stone for researchers seeking after the mechanisms that link natural variations in metabolism to natural variations in life span, especially those induced by the practice of calorie restriction. It was one of the earliest identified pieces of the puzzle, but possibly not a useful piece in the final analysis. This has become increasingly likely as an outcome over the years as meaningful results failed to emerge from drug development based on the manipulation of sirtuins. But this happens all the time: it's larger than usual news in the scientific community only, I think, because very large sums of money have moved into this line of research over the past years, and it's one of the earliest threads that might have led to drugs that modestly slowed aging.

Though I should note, as usual, that it is a massive strategic error for the research community to focus on undertaking expensive research programs that can - at best reasonable expectation - only produce a very modest slowing of aging after the usual couple of decades of work from early results to broadly available clinical application. That strategic error is, unfortunately, well entrenched and well underway. The real and important battle of the next decade is to convince the research community, on the merits of the proposal, to ditch work on metabolic manipulation in favor of SENS-like biological repair approaches that offer the possibility of actual, working, meaningful rejuvenation of the old at the end of an expensive, large-scale twenty year research program.

But back to sirtuins, which are today's news. Here are a couple of items for you from around the web:

Longevity Gene Debate Opens Trans-Atlantic Rift

the idea that sirtuins promote longevity appeals to scientists because of experiments that were started in yeast and repeated in two other standard laboratory organisms, the roundworm and the fruit fly. It is these foundation experiments that have now come under attack by David Gems and Linda Partridge, researchers on aging at University College London. In an article published Wednesday in the journal Nature, they and colleagues have re-examined experiments in which roundworms and flies, genetically manipulated to produce more sirtuin than normal, were reported to live longer. Both experiments were flawed, they say, because the worms and flies used as a control were not genetically identical to the test organisms. The London researchers report that they have repeated the experiments with proper controls and found that extra sirtuin does not, after all, make the worms or flies live longer.

Is The 'Longevity' Gene Sirtuin One Big Research Error?

And in the last decade, sirtuin has probably been one of the industry's biggest bets, ever since high levels of this protein were linked to longer, healthier lives in a variety of animals and it was suggested that they could be behind the increased longevity seen with calorie restriction (drastic restriction of calories, without malnutrition is known to increase longevity and retard age-related diseases). So how did we get here, 10 years on, concluding that it is all a mistake?

So it all goes. The bottom line for us is, however, that even if sirtuins were the key to replicating calorie restriction, they wouldn't be the basis of the future medicines of rejuvenation. Rejuvenation biotechnology can only be based on means of repairing the damage of aging, not changing metabolism a little to gently slow down aging. Other than the SENS Foundation, I don't see any research-focused organization seriously pushing this viewpoint at the present time. That's a big problem: it means that most of the money going into aging and longevity science will have little to no effect on the future of your life span: it will be going towards a continuation of the present trend that adds a small fraction of a year to the life expectancy of adults with each passing year. The newborns get a bigger fraction of a year for their measure of life expectancy at birth, but none of us reading this now are lucky enough to be that fresh to the picture. Bigger gains than this modest trend, a trend that will see us dead with only a couple of additional years to show for it if it continues as-is, will require a radical shift in the research community's strategic vision, and a focus on repair-based biotechnologies. Not surtuins, in other words, and nothing that looks much like sirtuin research either.

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

One possible form of future immune therapy involves growing vast numbers of tailored immune cells, far more than would ever naturally be present in the body, and then infusing them to sweep away the target problem - cancer being an early target for this sort of approach. Here is some groundwork for these future therapies: "Adult stem cells from mice converted to antigen-specific T cells - the immune cells that fight cancer tumor cells - show promise in cancer immunotherapy and may lead to a simpler, more efficient way to use the body's immune system to fight cancer ... Tumors grow because patients lack the kind of antigen-specific T cells needed to kill the cancer. An approach called adoptive T cell immunotherapy generates the T cells outside the body, which are then used inside the body to target cancer cells. ... It is complex and expensive to expand T cell lines in the lab, so researchers have been searching for ways to simplify the process. [They] found a way to use induced pluripotent stem (iPS) cells, which are adult cells that are genetically changed to be stem cells. ... Any cell can become a stem cell. It's a very good approach to generating the antigen-specific T cells and creates an unlimited source of cells for adoptive immunotherapy. ... By inserting DNA, researchers change the mouse iPS cells into immune cells and inject them into mice with tumors. After 50 days, 100 percent of the mice in the study were still alive, compared to 55 percent of control mice, which received tumor-reactive immune cells isolated from donors."

Link: http://www.sciencedaily.com/releases/2011/09/110920111812.htm

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

I'd mentioned the book "100 Plus" a couple of weeks ago, authored by Sonia Arrison:

To my eyes, the book is essentially a fast overview of the last ten years of science, debate, important subjects, and noteworthy people in the aging research and longevity advocacy communities. ... 100 Plus is, I think, a good book to give to the average fellow in the street who would be flattened and slain by the attempt to read Aubrey de Grey and Michael Rae's Ending Aging. That book is where the meat is - but 100 Plus is a Cliff's Notes for the current state and direction of longevity science and the advocacy community supporting it. That is a useful thing: a person reading 100 Plus will wind up in roughly the same place as a casual reader of the high points of Fight Aging!

I notice that Arrison is doing the book promotion rounds with vigor. The resulting materials include a number of audio and video interviews, such as these from Changesurfer Radio:

100 Plus: The Coming Age of Longevity pt1

100 Plus: The Coming Age of Longevity pt2

Dr. J. chats with Sonia Arrison, a futurist and policy analyst who has studied the impact of new technologies for the Pacific Research Institute (PRI). They discuss her new book 100+: How the Coming Age of Longevity Will Change Everything, from Careers and Relationships to Family and Faith.

There is also official video of her presentation at the recent SENS5 conference, which you will find is posted to the conference YouTube channel, with thanks to the SENS Foundation volunteers for the time they take to make that happen:

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

A possible road to rejuvenating some portions of the declining mechanisms of tissue regeneration in the old: "The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. ... We demonstrated that we were able to reverse the process of aging for human adult stem cells by intervening with the activity of non-protein coding RNAs originated from genomic regions once dismissed as non-functional 'genomic junk' ... adult stem cells undergo age-related damage. And when this happens, the body can't replace damaged tissue as well as it once could, leading to a host of diseases and conditions. ... The team began by hypothesizing that DNA damage in the genome of adult stem cells would look very different from age-related damage occurring in regular body cells. ... They compared freshly isolated human adult stem cells from young individuals, which can self-renew, to cells from the same individuals that were subjected to prolonged passaging in culture. This accelerated model of adult stem cell aging exhausts the regenerative capacity of the adult stem cells. Researchers looked at the changes in genomic sites that accumulate DNA damage in both groups. ... We found the majority of DNA damage and associated chromatin changes that occurred with adult stem cell aging were due to parts of the genome known as retrotransposons ... By suppressing the accumulation of toxic transcripts from retrotransposons, we were able to reverse the process of human adult stem cell aging in culture." The next step would be to look at this process in old animals, and see what happens when it is reversed.

Link: http://www.sciencedaily.com/releases/2011/09/110920163215.htm

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

Great inroads have been made in recent years into an understanding of the accelerated aging condition called Hutchinson-Gilford progeria syndrome, or progeria. Despite its extreme rarity - there are less than a hundred sufferers known worldwide - the condition is of great interest to aging researchers, and this is because of what progeria might teach us about a range of important cellular mechanisms and their impact on "normal" aging.

The breakthrough discovery linking progeria with malformed lamin A protein back in 2003 came about as a result of advances in biotechnology. Thanks to rapid technological progress, the means to make this discovery became cheap enough that one determined researcher could push through to succeed in a comparatively short time frame. Ten years previously, that would have been impossible for such a small research effort.

Today the tools of cellular biotechnology are at least as far advanced over the state of the art in 2003 as that year was over the early 1990s. As a result new avenues are opening up in the investigation of progeria's mechanisms - and their relevance to the rest of us. A recent research release from EurekAlert!, for example, shows how application of the comparatively recent technologies of induced pluripotency (used to produce induced pluripotent stem cells, or iPS cells) are leading to further discoveries in both aberrant and "normal" aging:

Hutchinson-Gilford Progeria Syndrome is caused by a single point mutation in the gene encoding lamin A, which forms a protein scaffold on the inner edge of the nucleus that helps maintain chromatin structure and organize nuclear processes such as RNA and DNA synthesis. The mutation creates an alternative splice site that leads to the production of a truncated version of the protein known as progerin. Unlike the full-length protein, progerin does not properly integrate into the nuclear lamina, which disrupts the nuclear scaffold and causes a host of problems.

"There is also evidence that defective lamin A accumulates during the normal aging process via the sporadic use of the alternative splice [site]. Therefore we are very keen [to] identify new aging markers and explore other aspects of human premature and physiological aging."

...

Compared to normal skin fibroblasts, cells from Progeria patients have misshapen nuclei and a range of other nuclear defects, including a disorganized nuclear lamina, loss of super-condensed DNA, telomere shortening and genomic instability. Yet, despite their "old" appearance and characteristics, these cells could be readily converted into iPS cells.

"The reprogramming process erased all nuclear and epigenetic defects and the rejuvenated pluripotent cells looked and acted like perfectly normal healthy cells."

Which is a very interesting result. You might compare it with another demonstration made recently in which damaged cells lost their damaged status when altered to become induced pluripotent stem cells. Unlike that case, however, here the induced pluripotent cells still bear the seeds of the damage: when they differentiate into other types of cell, those cells once again produce the bad lamin A and suffer the characteristic effects of progeria.

The researchers conclude that a therapy might be built through genetic manipulation and cell transplant, as they were able to fix the differentiated cells via that approach:

Genetically modifying progeria-derived iPS cells to shut down the expression of progerin staved off the premature appearance of aging phenotypes after differentiation. "Transplantation of the progenitor cells derived from the 'corrected' progeria iPS cells might hold the promise to treat these progeria children in the future."

As I have noted in the past, a comprehensive fix for progeria may well be of some benefit to those of us suffering "normal" aging as well.

A short open access paper: "Hormesis (a neologism coined from the ancient Greek term hormáein, which literally means 'to set in motion, impel, urge on') describes a favorable biological response to harmless doses of toxins and other stressors. Hormesis-stimulating compounds initiate an adaptive stress response that renders cells/organisms resistant against high (and normally harmful) doses of the same agent. On the theoretical level, hormesis may constitute (one of) the mechanisms that allows stressed cells to avoid senescence and death, and hence might have some impact on the (patho)physiology of aging. Thus, measures that reportedly prolong the healthy lifespan of multiple species, such as caloric restriction and the administration of resveratrol, may do so by inducing a hormetic response ... [Hormesis] is best represented by ischemic preconditioning, the situation in which short ischemic episodes protect the brain and the heart against prolonged shortage of oxygen and nutrients. Many molecules that cause cell death also elicit autophagy, a cytoprotective mechanism relying on the digestion of potentially harmful intracellular structures, notably mitochondria. When high doses of these agents are employed, cells undergo mitochondrial outer membrane permeabilization and die. In contrast, low doses of such cytotoxic agents can activate hormesis in several paradigms, and this may explain the lifespan-prolonging potential of autophagy inducers including resveratrol and caloric restriction."

Link: http://impactaging.com/papers/v3/n9/full/100380.html

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

Time flies - it really doesn't seem like it's been two and a half years since the SENS Foundation was launched to steer the SENS research program independently of the Methuselah Foundation umbrella. Come to think of it, it really doesn't seem like eight years since the Methuselah Foundation was just a tiny thing, a couple of advocates and the first few $5,000 checks in the bank. If you look back in the Fight Aging! archives, some of the first blog posts relate to the early days of the Methuselah Foundation.

People come and go across any organization's life span - and here is news of the departure of one of the SENS Foundation co-founders for a new venture:

On 19 September, 2011, Sarah Marr will be stepping down as our Executive Vice President at SENS Foundation. She has been a committed co-founder, and she will of course continue to be a trusted advisor and closely involved with the organization. But we couldn't have her term of full-time service with us pass without noting the significant contribution she has made to the professionalism of the organization and to the quality of our overall message. She helped make us, in a very real way.

From Sarah Marr's blog:

I think it's important to understand that the Foundation is a lifetime commitment for me. I'm a co-founder, after all, and I can't imagine a world in which I'm not extolling the virtues of the organization, its mission, and the wider concept of rejuvenation biotechnology; whatever else I'm doing, or whatever environment surrounds me.

Why am I stepping down? Because I have a personal project which I wish to pursue. And given the criticality of rejuvation biotechnology, you should get a feeling for just how important I consider this next project, but also how hard it has been to reach this decision. Why can I step down now? Because the team which we've built at the Foundation over the past two-and-a-half years is so very, very talented and capable.

Non profits set up for the long term must be able to thrive independently of the turnover of their staff and leaders - to have a continuation of capabilities and culture that are too robust to much miss the loss of any one individual's time and skills. Indeed, this is one of the implicit goals for the early stages of any venture, and a very good way of measuring success in advance of more obvious results in research, fundraising, licensing, and so forth.

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

Drugs for treating osteoporosis may double a person’s risk of developing cancer in the esophagus; as such, the use of safer and natural remedies must be considered.

It is hard to imagine how osteoporosis was once deemed to be a very rare disease — but it really was, before the turn of the 20th century. Now, the cases of this debilitating disorder has  been progressively increasing. In the US alone, osteoporosis reportedly affects around 30% of women in their postmenopausal stage, and 5% of old men.

Osteoporosis is conventionally treated through drugs. However, a recent study shows how particular treatment drugs can possibly pose more harm than remedies. Worse, the possible side effects of osteoporosis medications include a highly-fatal disease.

Long-term Use of Osteoporosis Drugs May Cause Cancer

Oral biophosphonate drugs, such as Achnonel, Boniva, and Fosamax, may cause the development of a life-threatening disease. The recent study shows that long term and frequent users of these bone-building drugs are likely to develop and double their risk of having cancer in the esophagus. However, risks to individual users remain minimal, according to the same research.

Another separate and formerly conducted study, which also used the nationwide medical practice research registry about six million people located in UK, was further enhanced with the latest findings.  This is because the former study didn’t yield substantial proof regarding the doubled rate of substantial risks in developing esophageal cancer.

At present, a doubling of esophageal cancer risk were estimated to occur within five years or more of biophosphonate intake, though no stomach increase or colorectal cancer were reportedly discovered. According to Jane Green, Phd, of Oxford University, a further research is necessary to determine the extent of biophosphonates in relation to increasing risks of developing the fatal esophageal cancer.

Dr. Diane Wysoswki, PhD and FDA epidemiologist, noted that other doctors should think of the benefits and underlying risks before prescribing drugs to their patients, especially to those who are currently suffering from digestive problems. Wysoski was the first doctor who discovered 23 esophageal cancer incidences among users of the drug Fosamax in the country. She also advised  patients who are taking the said drug to strictly follow the directions found int he labels. These include taking the drug, with water, for around 30 minutes up to one full hour prior to breakfast consumption.

Alternative and safe solutions for osteoporosis

Given the possible fatal risks that can be associated with treatment drugs for osteoporosis, victims must know of other natural, alternative and effective solutions for osteoporosis without having to endanger their lives through the side effects of osteoporosis medications.

Avoiding exposure to environmental risk factors

Animal and human research shows that heavy metals substantially found in the environment, such as aluminum and tin, promote the development and worsening case of osteoporosis. Aluminum is a major concern, since it is widely-distributed and highly-accessible. Its sources include drinks that are contained in aluminum cans, processed foods, additives such as coloring agents and preservatives, cookware made out of aluminum, antacids, and even underarm deodorants. Exposure to tin is prevalent through foods that are contained and packaged inside tin cans. Some amounts of the said metal seep into the foods and drinks that the can contains prior to its opening; however, even higher amounts can seep into the drinks and foods if these remain inside the can for a time after opening it. As such, a key way of non-drug solutions for osteoporosis is to make very basic lifestyle adjustments, through avoiding exposure and contact with aluminum and tin sources.

Lifestyle Regulations: Diet and Exercise

Several dietary inclusions cause bone thinning, such as high intake of refined sugar, animal proteins, red meat and alcohol. These have been proven to decrease the body’s capacity of secreting digestive enzymes, which is an essential process that enables optimal calcium absorption. Consumption of such factors that promote bone thinning and loss must be moderated, or avoided as much as possible. Smoking, too, poses the same bone-thinning effects and risks; and for a plethora of other health-related reasons, the smoking habit must be abandoned. On the other hand, several studies have shown the positive relationship between enhanced bone health, and fruit and vegetable consumption. Foods rich in calcium include spinach, kale, broccoli, trurnip greens, and collard.

Another natural solution for osteoporosis is through a healthy weight management program. Women who suffer from being overweight and obesity reportedly pose a larger and heavier burden on their joints and bones. As such, healthy weight loss is able to treat and reduce the risk of developing osteoporosis. Studies have also shown that weight-bearing exercises, those that aim to build muscles, have a substantial capacity of strengthening one’s bones. At least 30 minutes of daily exercise, done 5 times within a week, even through non-weight-bearing exercise routines such as swimming, jogging, weight-lifitng, jumping, walking naturally aid osteoporosis treatment because bones and joints in key portions of the body are rendered phyisically active.

Key Supplementation

Nutritional supplementation are essential factors that treat and reduce the risk of developing otseoporosis.

Vitamin D, which is considered to be fat-soluble, takes on the significant role of enabling calcium absoprtion, and maintaining skeletal health. Certain foods are rich in the said vitamin, such as eggs, liver, and fish oil. However, the best source will have to be sunlight. 15-minute exposure to sunlight per day enables the skin to produce the necessary amount of vitamin D. Dietary supplementation, without sun exposure, must be increased to 15 mcg on a daily basis; however, lesser amounts are acceptable provided that the person has been amply exposed to sunlight. Older individuals, because of their restricted exposure to vitamin D from sunlight, should have even higher doses of vitamin D per day.

Intake and therapy through strontium, the trace mineral that serves as a major component of bones, can be attained through strontium concentrations found in parsley, Brazil nuts, molasses, and lettuces. Studies show that around 1-3 mg per day is all that is necessary for osteoporosis prevention. For those who already suffer from the disease, strontium supplementation also largely aids optimal osteoporosis treatment. Results of a particular research venture showed that strontium ranelate helped in increasing the density of bone minerals, while reducing fracture risks by over 40 %, in postmenopausal women who simultaneously suffer from osteoporosis.

The role of vitamin K has recently been acknowledged to have a key effect in maintaining healthy bone metabolism. Those who regularly consume antibiotics, and victims who suffer from impaired liver function are at risk of suffering from deficiency of vitamin K. Reportedly, insufficient amounts of vitamin K in the body increases further loss of bone density, and also heightens bone fracture risks or incidences. Vitamin K1 can be largely found in vegetable oils and green vegetables, and vitamin K2 is reportedly  found in cheese and meat.

A comprehensive program that grounds and provides a natural solution for osteoporisis proves to be highly capable of reducing the risk of developing osteoporosis, decreasing bone loss incidences, and may even successfully reverse bone loss. It is important to note that a severe condition like osteoporosis can actually be alleciated in a safe, affordable, and natural way.

Sources
vitalitymagazine.com
osteoporosissolution.com
healthy.net
steadyhealth.com
webmd.com
articles.mercola.com

Discuss this post in Frank Mangano’s forum!

Cocoa is famous for its numerous health benefits, and one study gives us another reason to reach for that dark chocolate and give in.

A lot of people are in love with chocolates – and there is really nothing wrong with this, as long as the right kind of chocolate is consumed.  Dark chocolate is definitely way better than milk chocolate.  Aside from the health benefits provided by its rich cocoa content, it does not contain the same amount of sugar as the milk chocolate.  So the next time you feel the temptation to eat chocolate, give in – as long as it is of the dark kind. Remember this:  the darker the chocolate is, the higher is its cocoa content.

Recently, a group of researchers coming from Meiji Seika Kaisha’s Food and Health R&D Laboratories released the results of a study that they conducted regarding the effects of cocoa towards the promotion of a healthy heart.  The Japanese company’s researchers revealed that cocoa’s capability to potentially increase the levels of high density lipoprotein, or the good form of cholesterol, is linked to the presence of a protein that can enhance apolipoprotein A1 levels.  Also known as Apo-A1, apolipoprotein A1 is a compound that is needed for the body’s production of HDL cholesterol.

The researchers wrote in the Journal of Agricultural and Food Chemistry that polyphenols present in cacao may be responsible for acting on pathways that are responsible for the metabolism of cholesterol.  They looked at the human intestinal cell effects of polyphenols found in cacao such as procyanidin, catechin, and epicatechin.  Results have shown that these polyphenols raised the protein levels of Apo-A1 while simultaneously lowering alipoprotein B levels which carries LDL cholesterol to the cells.

The Health Benefits of Cocoa

Aside from its polyphenol contents, the health benefits of cocoa are also taken from its component called flavonoids, which serve as major antioxidants to prevent any possible damage to the cellular system.  Free radicals bring about oxidative damage inside the body which could be factors in the development of chronic diseases like heart failure and cancer. The powder of cocoa can also help in lowering blood pressure and improving the blood circulation of every individual. Compared to green tea, just one cup of cocoa has about three times the antioxidants that a cup of green tea has.

Numerous health experts believe that cocoa can only work to your advantage if you would take it in quantities that are just enough. Overconsumption, of course, has its drawbacks.  When choosing a cocoa formulation, go for something that contains the least amount of cocoa.  There are a lot of cocoa powders that are available in the market today which contains various additives such as hydrogenated oils and corn syrup that are high in fructose. Hence, choose to consume the unprocessed type of cocoa powder.

Researchers from Cornell University said that the most ideal way of taking full advantage of cocoa benefits is through drinking. Taking in a cup of hot cocoa every once in a while can work as a great antioxidant just like wine and tea. It can also help steer one away from the impairment of the immune system and other inflammatory processes.

Show Some Love to Your Heart

To live with a healthy heart requires a lot more than just having a healthy diet. It also includes regular exercise and an overall healthy lifestyle. Here a few tips on how to ensure that your heart remains healthy all the time:

• Limit your consumption of foods that have lots of trans-fat.  These are usually found in fried foods and margarine.
• If you have a sweet tooth, then you must also limit your sugar intake. High amounts of glucose in the blood could lead to the development of diabetes, and this interferes with blood viscosity.  A blood that is too viscous would cause problems in circulation and other organs of the body will not have their fare share of blood.  Because of this, the heart has to pump doubly hard to ensure that blood is supplied to all organs.  Overworking the heart could lead to its enlargement (cardiomegaly), or worse, heart failure.
• Only utilize extra virgin olive oil and add some garlic when you cook to help in lowering your cholesterol along with adding some Omega 3 fatty acids.
• Exercise for about 3 to 4 times a week and then stick to this routine.  Lifting weights is not required but doing cardiovascular, or aerobic, exercises can work wonders to your heart.  So set some time each day where you can perform exercises that you are capable of doing. What is important is that you have the desire to start incorporating changes in your lifestyle, one step at a time. Remember to stay hydrated too and warm up before each exercise session.
• To add up to your healthy diet and exercise, try your best to steer away from any kind of vices like smoking and drinking too much alcoholic beverages.
• Manage your stress levels and implement ways to cope.  Attend a yoga class, meditate each day or just simple do deep breathing exercises.  Take time to rest, get lots of sleep since this will help your body heal.
• Watch out for your weight too since obesity is one of the primary causes of heart disease.
• If your cholesterol level is high then you can naturally lower it by using several herbal extracts along with fish oil. It could help for you to know that 20% of your cholesterol level is sourced from the foods you consume while the rest of the 80% is produced by your liver. If your fat levels are high, then you must go easy on your carbohydrate and sugar consumption. To lower this, you can take in fish oil, some sufficient amount of vitamin C and even green tea.

Your heart’s health, and your general health as well, is in your hands – and the first step is to make the decision to start living healthy.  Each of your action and decision affects you, and the people around you, so nothing is really too small.  You see, even your choice of chocolate has the potential to affect your longevity.

Sources
nutraingredients.com
naturalhealthezine.com
healthy-heart-guide.com
womenfitness.net

Discuss this post in Frank Mangano’s forum!

From the Telegraph: "In as little as five years, researchers hope to be able to coax the heart into regenerating itself, repairing the damage caused by cardiac arrests and old age. ... It works in a similar way to stem cells but instead of the new cells being grown outside the body and then injected back in, the technique simply makes the cells [transform] at the point where they are needed. ... The main problem is that when beating muscles cells - known as cardiomyocytes - die during an attack there is no way to reactivate them and the surrounding connective tissue - known as fibroblasts - cannot take over their role.
Now [researchers] have discovered a way of reprogramming fibroblasts into cardiomyocytes. ... We first have to test if the same factors can convert human fibroblasts to beating heart muscle and then find ways to safely introduce these factors, or small molecules that mimic these factors, into the coronary circulation so they can reprogram the existing fibroblasts in the heart. I envision such factors being loaded into a stent that is placed in the coronary artery and can elute (allow to emerge) the reprogramming factors over 1-2 weeks. ... The team found that they needed a combination of just three substance - Gata4, Mef2c, and Tbx5 - to efficiently convert fibroblasts into cells that could beat like cardiomyocytes."

View the Article Under Discussion: http://www.telegraph.co.uk/health/healthnews/7928426/Damaged-heart-could-be-coaxed-into-mending-itself-claim-scientists.html

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

While the FDA tries to block commercial application of stem cell therapies in the US, veterinary practices continue to demonstrate that the technology is ready and potentially useful: "A Golden Retriever, plagued with arthritis, recently underwent a stem cell extraction and implant to help with mobility. ... From the sounds of things, you would never suspect McIntyre was a frail and feeble dog. And these days, he's moving around pretty well, thanks to anti-inflammatory medicines, physical therapy and a new experimental surgery involving stem cells. ... like family, she wanted McIntrye to feel better and have a better quality of life. Cells were taken from his belly fat and shipped to California. Stem cells were extracted and then implanted back into his joints by a vet in Alpharetta. ... He'll never be like a puppy as far as agility but it will just give him a quality of life where he doesn't hurt and suffer." Meanwhile, the actions of unaccountable, unelected bureaucrats at the FDA mean that US residents must travel overseas to find the same treatment offered to humans. More importantly, what might already be a wildly successful and growing field is slowed down to a comparative crawl. When you're forbidden to sell a product, few organization will invest in development.

View the Article Under Discussion: http://www.walb.com/Global/story.asp?S=12964756

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

The latest Methuselah Foundation newsletter is out: "2010: Where We Are Now: Methuselah Foundation took on a big challenge: extending healthy human life. From SENS to My Bridge 4 Life, we've supported and incentivized major initiatives and research to fulfill our mission. In 2010 we are focusing our attention on tissue and whole organ engineering. Read this newsletter and follow the links to our site to learn more about what we are doing now so you live longer and healthier. ... This year we are focusing our efforts on tissue engineering and organ replacement. We are looking ahead 10 years and projecting that, with our help, everyone who needs an organ will get an organ. ... Prizes have proven to be the most powerful tool for inspiring radical scientific breakthroughs. That's why we offer prizes, including the recently announced NewOrgan Prize. The end result will allow many people to live longer and - if history is an indicator - the many innovations that come as a result of this work are unimaginable today. To build a replacement organ, from a patients own cells, and have it fully function, scientists must first develop and preserve all the tissues that build that organ - including muscle, nerves, arteries and veins. ... Leaders in the science of organ engineering have joined the NewOrgan Advisory Board. ... The members of our Scientific Advisory Board are frontrunners in the research and development of new organ technology. "

View the Article Under Discussion: http://www.mfoundation.org/files/newsletters/july2010/newsletter.html

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

We life in an age of change and rapid scientific innovation in medicine. That in and of itself might be enough to explain why historical actuarial predictions of longevity have been low in comparison to the actual outcome: extrapolation of existing trends tends to do poorly in the face of consistently unpredictable innovation.

Nonetheless, a large industry is focused on getting these numbers right, or as close to right as is possible, as vast sums are promised to older folk, either as political entitlements or honestly obligated as a result of insurance contracts. Betting against increasing longevity seems like a fool's game, but nonetheless there is a lot of money to be made in that business - many large entities want to be protected from what is known as longevity risk, the risk that life spans will rise faster than expected and thus financial obligations will spiral out of control. Large entities are willing to pay for that insurance service, and taking on risk for a percentage is very much the core business of finance.

In theory the people taking on that risk for a percentage know what they are doing, and they are the ones funding efforts to understand the risk - which in this case means models for future increases in human longevity due to advances in medicine and biotechnology. In practice? The risk gets sliced and diced and parceled out among the players in finance, that much is true. But I'm sure we all see the present results of that undertaking in other large industries, such as housing: when there is enough money involved the business becomes one of lies and politics, the fine art of pocketing profits, taking on unknown risks for short term gain, steering government policies, and raiding the public treasury to cover losses when it all goes south. When buying politicians and policy is a reasonable cost judged against the cost of contracts, buying politicians and policy becomes a part of doing business - and very lucrative, since it allows risk-bearers to try for the upside with the expectation that they will be bailed out if it fails.

Thus a web of perverse incentives grows, benefiting the connected few at the expense of the many. In the course of all of this, there is an increasing pressure (and ability) to obscure or water down unfavorable data, especially when the interests of profiteers and government appointees coincide. Again, we've all seen this come to pass numerous times in recent years and prior decades. It is the way of the world, and just as much so when it comes to the future of human longevity:

In 1981, the United Kingdom (UK) Office for National Statistics estimated that male life expectancy at birth would rise to 74 by 2031. It hit that age in 1994. In 2002, the 2031 estimate was 81, but we are now expected to pass that in 2019. This systematic underestimation of official life expectancy increases occurs around the world. It is not an accident. It is deliberate. Politicians put pressure on official agencies to do this, so that the full cost of longevity increases does not fall on them or the current generation of voters. The reason is clear: If more accurate and hence higher projection of life expectancy were produced today, then social security contributions would have to rise now rather than later - and this would be politically very unpopular.

The powers that be and their predecessors have accomplished what powers that be always manage in the end: to set up a system of wealth transfers and entitlements that is both unsustainable and stands in opposition to true progress. Thus the modern spectacle of people trying to argue that increases in human longevity are a bad thing! The collapse will come, the promises that cannot be kept will be broken, that much is certain - although it is true that modern innovations in fiat currencies have allowed the game to go on for a good deal longer and become a good deal more destructive than was usually the case in the past. But eventually they will run out of other people's money to loot. Along the way to that end those who are trying to prop up the house of cards will undoubtedly build a great deal more in the ways of lies, waste, and other unpleasantness.

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Another of the many benefits of calorie restriction is outlined in this paper: "The author focused on the functional decline of synapses in the brain with aging to understand the underlying mechanisms and to ameliorate the deficits. The first attempt was to unravel the neuronal functions of gangliosides so that gangliosides could be used for enhancing synaptic activity. The second attempt was to elicit the neuronal plasticity in aged animals through enriched environmental stimulation and nutritional intervention. Environmental stimuli were revealed neurochemically and morphologically to develop synapses leading to enhanced cognitive function. Dietary restriction as a nutritional intervention restored the altered metabolism of neuronal membranes with aging, providing a possible explanation for the longevity effect of dietary restriction. These results obtained with aging and dementia models of animals would benefit aged people."

Link: https://www.jstage.jst.go.jp/article/pjab/88/6/88_PJA8806B-04/_article

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

A mere 40% extension of life span in nematode worms via a novel method is a part of the general background noise of aging research nowadays: "The planar cell polarity (PCP) pathway is highly conserved from Drosophila to humans and a PCP-like pathway has recently been described in the nematode Caenorhabditis elegans. The developmental function of this pathway is to coordinate the orientation of cells or structures within the plane of an epithelium or to organize cell-cell intercalation required for correct morphogenesis. Here, we describe a novel role of VANG-1, the only C. elegans ortholog of the conserved PCP component Strabismus/Van Gogh. We show that two alleles of vang-1 and depletion of the protein by RNAi cause an increase of mean life span up to 40%. Consistent with the longevity phenotype vang-1 animals also show enhanced resistance to thermal- and oxidative stress and decreased lipofuscin accumulation. In addition, vang-1 mutants show defects like reduced brood size, decreased ovulation rate and prolonged reproductive span, which are also related to [longevity-enhancing genes]. The germline, but not the intestine or neurons, seems to be the primary site of vang-1 function. Life span extension in vang-1 mutants depends on the insulin/IGF-1-like receptor DAF-2 and DAF-16/FoxO transcription factor."

Link: http://dx.doi.org/10.1371/journal.pone.0032183

Source:
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Exercise already! Regular readers are no doubt sick and tired of hearing about it, but until such time as sensibly directed funding and hard work in the life sciences produce medical technologies that can do better for humans, regular exercise remains one of the two best tools we have to slow our inexorable slide into frailty and disease. It allows us to somewhat shift our life expectancy, and greatly reduce the risk of suffering all of the common chronic conditions of aging.

For those in the middle of life, looking at an ever-uncertain future of technological development, a few years added or subtracted might make all the difference in the world. When it comes down to the wire, will you make far enough to benefit from the first commercial rejuvenation biotechnologies, or will you fall short and be forced to take the second worst end of life option, with an unknown chance of eventual restoration? These are weighty questions, and burying your head in the sand is essentially the same as picking the poorest answer for yourself.

An article on this general theme from the popular press, which goes on to point out a range of data on exercise and specific age-related conditions:

"There's compelling data that older individuals participating in exercise programs show dramatic improvement in function and abilities," says Cedric Bryant, chief science officer for the American Council on Exercise in San Diego. In fact, experts suggest that many ills once attributed to normal aging are now being viewed as a result of chronic inactivity.

Despite this promising message, fewer than 5 percent of seniors follow the recommended guidelines for physical fitness (30 minutes of moderately intense exercise on most days). "Levels of activity in people 65 and older haven't budged in decades," says Miriam Nelson, director of the John Hancock Research Center on Physical Activity, Nutrition, and Obesity Prevention at Tufts University in Medford, Mass.

Even if they've never exercised, the middle-aged and older can still benefit by beginning now. Experts say sedentary people will actually fare better in percentage gains relative to active people, since they're starting from zero. "It doesn't matter how old you are," says Colin Milner, founder and CEO of the International Council on Active Aging in Vancouver, British Columbia. "It's never too late to start exercising."

As a specific example of the sort of low-level mechanisms by which exercise impacts long-term health, you might look at this paper:

A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats.

Exercise training, consisting of treadmill running at 60% of the initial VO2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass ... Exercise training also decreased the gap between young and old animals in other measured parameters ... We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.

Mitochondrial damage - and thus processes such as autophagy that attempt to reduce levels of mitochondrial damage - seems to be very important in aging. Given that many mechanisms associated with longevity are seen to influence autophagy, it should not be surprising to find exercise on that list.

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

Changes in the stem cell niche are a good part of the age-related decline in stem cell activity, which explains why old stem cells can perform like young stem cells if put into a young environment, and vice versa. Here researchers compensate for one of those niche changes: "Stem cells reside within a microenvironment of other cells - the niche - that is known to play a role in stem cell function. For example, after a tissue is injured, the niche signals to stem cells to form new tissue. It is believed that stem cells and their niche send signals to each other to help maintain their potency over a lifetime. But while the loss of tissue and organ function during aging has been attributed to decreases in stem cell function, it has been unclear how this decline occurs. [There are] a number of possible scenarios, such as whether the loss of tissue function is due to a decrease in the number of stem cells, to the inability of stem cells to respond to signals from their niche, or to reduced signaling from the niche. ... researchers discovered that as the stem cell niche [in flies] ages, the cells produce a microRNA (a molecule that plays a negative role in the production of proteins from RNA) known as let-7. This microRNA is known to exist in a number of species, including humans, and helps time events that occur during development. This increase in let-7 leads to a domino effect that flips a switch on aging by influencing a protein known as Imp, whose function is to protect another molecule, Upd, which is secreted from a key area of the niche. In short, Upd promotes the signaling that keeps stem cells active and in contact with the niche so that they can self-renew. And as aging advances, increasing expression of let-7 ultimately leads to lower Upd levels, decreasing the number of active stem cells in the niche. What leads to accumulation of let-7 in the niche of aged flies still remains an open question. The researchers also demonstrated they could reverse this age-related loss of stem cells by increasing expression of Imp."

Link: http://www.newswise.com/articles/researchers-find-a-way-to-delay-aging-of-stem-cells

Source:
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A piece by Aubrey de Grey at the Huffington Post: "as things stand, no amount of insight into age-related pathology can be sufficient to develop outright cures. Some diseases are the end results of aging, just as starvation is the end result of fasting. The nature of aging is such that many age-related infirmities are certain to afflict anyone who lives long enough. And this will remain the case, until a technology is developed which ameliorates the general decrepitude of old age which underlies these diseases. One can, therefore, identify the future direction of medicine by considering the nature of old age itself. What exactly is being taken from us, year after year, from cradle to grave? As time goes by, your hair goes grey, your face gets coarser, you put on weight, you become weaker, more susceptible to disease, and so on. But what do these things have to do with each other? Fortunately, the answer is not so complex as one might anticipate. Most people think of the science of aging as being very incomplete. It is true that aging as a process is not completely understood (biogerontology, the study of aging, involves many competing theories). But the state of disrepair that aging leaves people in can be observed directly, and in great detail. A comparison between two perfect snapshots of old and young tissue would provide us with a very multi-faceted damage report. The aged tissue is riddled with "junk" molecules (by-products of normal metabolic functions) in and between cells, which do not dissipate, not even as the body heals and replenishes itself day in and day out. It would also show an accumulation of unwanted cells, and a depletion of necessary cells. All this damage reduces our tissue function, then our organ function, and eventually it kills us. How this damage accumulates, and how it leads to our demise, are matters of some dispute. But the bare facts of how our tissues alter over time already provide us with enough of a compass with which to chart the future course of medicine."

Link: http://www.huffingtonpost.com/aubrey-de-grey-phd/age-related-diseases_b_985019.html

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

Here is a different way of looking at the material consequences of living a life that allows you to become obese: "The United States has the highest prevalence of obesity and one of the lowest life expectancies among high-income countries. We investigated the relationship between these 2 phenomena. ... We estimated the fraction of deaths attributable to obesity by country, age, and sex and reestimated life tables after removing these deaths. To allow for a possible secular decline in obesity risks, we employed alternative risks from a more recent period. ... In our baseline analysis, obesity reduced US life expectancy at age 50 years in 2006 by 1.54 years for women and by 1.85 years for men. Removing the effects of obesity reduced the US shortfall by 42% for women and 67% for men, relative to countries with higher life expectancies. Using more recently recorded risk data, we estimated that differences in obesity still accounted for a fifth to a third of the shortfall. ... The high prevalence of obesity in the United States contributes substantially to its poor international ranking in longevity."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21940912

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