Are you looking for another reason to exercise? Exercise can improve your life by increasing creativity, focus and intelligence.

Many people look at exercise as a requirement.  They know they are supposed to exercise, but they don’t necessarily enjoy it.  As a result, many dieters find that they are forcing themselves to exercise.  On the other hand, often people who aren’t trying to lose weight skip exercising altogether.  As you know, everyone should exercise because there are countless health benefits to exercising, which include fighting diseases like stroke, osteoporosis, diabetes and high blood pressure.

However, it is important to realize that exercise can improve your life in ways that are not necessarily even fitness related.  Exercise can allow you to find solutions, boost creativity and improve your focus.

A recent study at the National Cheng Kung University in Taiwan showed that the brainpower of mice improves when they are allowed to exercise. When mice are forced to exercise more than they normally would, the mice’s thinking power improves yet further.  Scientists noted major developments in the brain when the mice were pushed beyond their natural exercise inclinations.

So does the brainpower improve because of increased blood flow to the brain?  Interestingly, a recent study out of Columbia University and the Salk Institute showed that exercise’s improvements in focus and thinking result from more than just blood flow.  Scott Small and Fred Gage conducted this experiment.  They found that during exercise, muscles contract and chemicals and proteins are released.  One protein called IGF-1 releases chemicals in the brain that stimulate neurons to branch out in new directions. The end result is new connections between our brain cells.  These new connections are responsible for making us smarter!

As you boost your focus and mental ability, you also boost your creativity when you exercise.  Keith Sawyer, PhD the author of the book Group Genius: The Creative Power of Collaboration stated “Physical activity gets your mind into the bodily experience, so that subconscious connections can pop up.”  Exercise also releases cortisol from your body.  If there is too much cortisol in your system caused by stress, your ability to be creative shuts down.

Make sure that you do not force too much exercise on yourself.  After all, overtraining can lead to injuries and can be counterproductive to improving your life.  Exercise for at least 30 minutes at a time.  If you are looking to find creative ideas, consider exercising alone as an exercise companion may distract you.  Bring a small notepad and jot down ideas.

Once you understand these benefits of exercising, you will be more likely to want to integrate exercise in your daily routine.  If you are having difficulty focusing or being creative, you will quickly find that exercise can be the solution to your problems.

Sources:
living.health.com
smallbusiness.yahoo.com

Discuss this post in Frank Mangano’s forum!

How is it possible for evolutionary selection to favor genetic variants beneficial in human old age, long after reproduction is impossible? An open access paper examines this question: "Evidence points towards the existence of a strong heritable component of human longevity. Around a quarter to a third of the variability of lifespan can be attributed to the action of genes. One of the best examples of a gene affecting survival in old age is the apolipoprotein E gene APOE. ... One of the major ideas in the evolutionary theory of ageing is the suggestion that, because the force of natural selection declines with age, alleles with deleterious effects seen only at older ages can reach higher frequencies than those that have their effects earlier in life. Therefore, if a gene exerts an effect only after the end of the reproductive phase of the lifespan it has been thought unlikely that it could have been subject to significant direct selection pressure ... It is often claimed that genes affecting health in old age, such as cardiovascular and Alzheimer diseases, are beyond the reach of natural selection. We show in a simulation study based on known genetic (apolipoprotein E) and non-genetic risk factors (gender, diet, smoking, alcohol, exercise) that, because there is a statistical distribution of ages at which these genes exert their influence on morbidity and mortality, the effects of selection are in fact non-negligible."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848859/

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

Via EurekAlert!, another example of testing stem cells and heart regeneration: "Some patients with heart muscles seriously affected by coronary heart disease may soon be able to benefit from an innovative treatment. Researchers [are] evaluating the safety, feasibility and efficacy of injecting stem cells into the hearts of patients while they are undergoing coronary bypass surgery. These stem cells could improve healing of the heart and its function. The IMPACT-CABG (implantation of autologous CD133+ stem cells in patients undergoing coronary artery bypass grafting) protocol evaluates this experimental procedure, which is destined for patients suffering from ischemic heart disease, in which the blood supply to the heart is decreased and associated with heart failure. These patients undergo open-heart coronary bypass surgery, performed by the medical team to improve perfusion of the heart muscle. A few weeks ago, the first patient received progenitor CD133+ stem cells isolated from his bone marrow and enriched, [and] has been doing very well ever since. Already, improvement has been noted in the contraction capacity of his heart, which has improved its ability to pump blood."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-04/chdl-hcy_1041110.php

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

Eating small doses of chocolate has been shown to lower your risk of a stroke or heart attack.

A new study indicates that eating chocolate each day can be good for your heart.  According to this study from the German Institute of Human Nutrition in Nuthetal, Germany, eating small amounts of chocolate can reduce your risk of a stroke or heart attack by 40%.

To obtain their results, German scientists followed 20,000 people over eight years.  They sent them a daily questionnaire about their diet and exercise.  The people in this survey had no history of heart disease and had similar healthy habits.  Researchers found that those who ate about a square of chocolate a day obtained these positive results of a lower risk of stroke or heart attack.

Experts theorize that it is the flavonols in chocolate that are having this positive impact.  Flavonols can cause muscles in blood vessels to widen and thus lower blood pressure.

Brian Buijsse from German Institute of Human Nutrition stated, “It’s a bit too early to come up with recommendations that people should eat more chocolate, but if people replace sugar or high-fat snacks with a little piece of dark chocolate, that might help.”

Of course, don’t take these findings as an excuse to go out and gorge on chocolate!  Eating large amounts of chocolate can quickly pack on the pounds.  Also when you are choosing chocolate, be sure to opt for a choice with high cacao content.  Avoid milk chocolate bars from the grocery store as have a lower ratio of the beneficial elements.  They are also packed with sugar and often include artificial ingredients as well.

Aside from lowering your risk of stroke and heart attack, dark chocolate has other beneficial properties.  It boosts good cholesterol and lowers stress and anxiety.  The flavonoids in chocolate have also been shown to fight aging.

Sources:
news.yahoo.com
denverpost.com

Discuss this post in Frank Mangano’s forum!

A new European study releases their findings that teens can override the effect of the “fatso gene” through at least one hour per day of exercise.

A new European study whose results are published in the April edition of Archives of Pediatrics and Adolescent Medicine states that exercising just one hour per day can help teenagers to override the effects of the “fatso” gene.

There is no doubt that the obesity gene can make people gain weight.  One gene called the “FTO gene” has a particularly strong impact.  People with 2 copies of this gene weigh about 7 more pounds on average.

The EU and Spanish and Swedish governments funded this study which sought to find out if recommending one hour of exercise to teens was beneficial in fighting the effects of the fat gene.  Researchers had 752 teenagers wear a device, which monitored their physical activity.

As it turned out, those who had the obesity gene weighed the same as those without it… as long as they exercised.  However, if the teens had the gene and exercised less than one hour per day, they always had more fat and larger waistlines.

This new study supports the current advice given to children and teens in the U.S., which is to get one hour of physical exercise, preferably aerobic exercise, per day.

Dr. Alan Shuldiner of the University of Maryland, stated “The message is clear: genes are not destiny. Those with obesity susceptibility genes should be especially motivated to engage in a physically active lifestyle.”

This study is very good news.  As it turns out, even teens with the fat gene, are not destined to a life of obesity.  They can control their fate to some extent.

Of course, the fact of the matter is that everyone, not just teens, should be exercising every day.  The reasons are quite vast.  Exercise improves your mood and quality of life.  It can improve your sleep and boost your energy level.

Exercise has also been shown to prevent a variety of diseases, everything from certain types of cancer to heart disease to osteoporosis.

Sources:
news.yahoo.come
mayoclinic.com

Discuss this post in Frank Mangano’s forum!

Greater understanding of the immune system means a greater ability to reprogram its components - such as errant immune cells that cause autoimmune diseases. From EurekAlert!: a study "describes a unique therapeutic 'nanovaccine' that successfully reverses [type 1] diabetes (T1D) in a mouse model of the disease. In addition to providing new insight into diabetes, the research also reveals an aspect of the pathogenesis of the autoimmune response that may provide a therapeutic strategy for multiple autoimmune disorders. ... [Researchers] wanted to find a way to counteract the harmful autoimmune response without compromising general immunity. They discovered that our bodies have a built-in mechanism that tries to stop the progression of autoimmune diseases like T1D. Essentially, there is an internal tug-of-war between aggressive T-cells that want to cause the disease and weaker T cells that want to stop it from occurring ... The researchers also developed [a] nanotechnology-based 'vaccine' that selectively boosted the weak white blood T cells, enabling them to effectively counter the damage caused by their overactive T cell relatives. ... their nanovaccine blunted T1D progression in prediabetic mice and restored normal blood sugar in diabetic mice. ... If the paradigm on which this nanovaccine is based holds true in other chronic autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and others, [nanovaccines] might find general applicability in autoimmunity."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-04/cp-ra040510.php

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

This seems like a logical next step for tissue printing technologies: "researchers have rigged up a device that can spray skin cells directly onto burn victims, quickly protecting and healing their wounds as an alternative to skin grafts. They have mounted the device, which has so far only been tested on mice, in a frame that can be wheeled over a patient in a hospital bed. ... A laser can take a reading of the wound's size and shape so that a layer of healing skin cells can be precisely applied. ... We literally print the cells directly onto the wound. We can put specific cells where they need to go. ... [Researchers] dissolved human skin cells from pieces of skin, separating and purifying the various cell types such as fibroblasts and keratinocytes. They put them in a nutritious solution to make them multiply and then used a system similar to a multicolor office inkjet printer to apply first a layer of fibroblasts and then a layer of keratinocytes, which form the protective outer layer of skin. ... The sprayed cells also incorporated themselves into surrounding skin, hair follicles and sebaceous glands, probably because immature cells called stem cells were mixed in with the sprayed cells."

View the Article Under Discussion: http://ca.news.yahoo.com/s/reuters/100408/science/science_us_wounds_printer

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

Empires end when an entrenched elite can spend from the public purse and take on debt without immediate consequence or forethought, destroying the value of their currency in the process. Assuming (perhaps optimistically) that present economic empires survive the next couple of decades, a combination of foolish promises and increasing human longevity will be the rock that sinks them. From Reuters: "Like the subprime crisis faced by banks in 2008, the risk of people living for up to 20 years after retirement seems to have crept up on an industry based on using historical data to calculate people's chances of an early death. Now, pension funds and insurers say the mounting burden of protracted pensions payments is increasingly concentrated on a small group of providers: them. ... Nowhere better can the process be seen than in Britain, which is facing a crisis resulting from a combination of pension reforms and increased life expectancy. ... The many arguments in favor of a sovereign bond linked to longevity rest on one fundamental expectation: if pension providers can't pay, or become insolvent, governments will have to. Longevity bonds could make the process neater, and more politically palatable, than the collapse of a pension provider." The problem is not that some groups made bad bets, or that many people relied upon those bets being good. The problem is that these groups and their supporters can conspire with governments to bail themselves out with public funds and debt heedless of consequences.

View the Article Under Discussion: http://www.reuters.com/article/newsOne/idUSTRE6360LP20100407

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

From the MIT Technology Review, a look at another form of first generation immune therapy aimed at cancer: "Last year marked a first for engineered antibodies - the European Commission approved a new cancer drug called Removab (catumaxomab), an antibody specially designed to grab both cancer cells and immune cells in such a way that the immune cell can kill the cancer cell. (The drug is undergoing testing for U.S. Food and Drug Administration approval.) Now a handful of similarly complex molecules, dubbed 'bispecific antibodies' for their ability to target two things at once, are in clinical trials. The two arms of these antibodies work together in different ways to treat cancer or other diseases, by bringing together two types of cells, as with Removab, by targeting two different types of receptors on the surface of a cell, or even using one arm to deliver drugs to specific cells targeted by the other. ... While the concept of bispecific antibodies has been around for decades, the approach has only recently shown clinical success. The field has been driven forward by new ways of designing and making the antibodies, which take advantage of advances in protein engineering, as well as the success of single-target antibodies, such as herceptin, that are already on the market." This is an example of the way in which targeting technologies and new strategies from the biotechnology labs are slowly filtering into the old school drug development pipeline.

View the Article Under Discussion: http://www.technologyreview.com/printer_friendly_article.aspx?id=24970

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

Manipulating the machinery of mitochondria - the respiratory chain that turns food into the chemical ATP that is used to power cellular biochemistry - can extend healthy life in a variety of species. Here, researchers dig deeper into the mechanisms by which this happens, finding that there are more than one: "In Caenorhabditis elegans longevity is increased by a partial loss-of-function mutation in the mitochondrial complex III subunit gene isp-1. Longevity is also increased by RNAi against the expression of a variety of mitochondrial respiratory chain genes, including isp-1, but it is unknown whether the isp-1(qm150) mutation and the RNAi treatments trigger the same underlying mechanisms of longevity. We have identified nuo-6(qm200), a mutation [that] reduces the function of complex I and, like isp-1(qm150), results in low oxygen consumption, slow growth, slow behavior, and increased lifespan. We [compared] nuo-6(qm200) [to] nuo-6(RNAi) and found them to be distinct in crucial ways, including patterns of growth and fertility, behavioral rates, oxygen consumption, ATP levels, autophagy, [as] well as expression of superoxide dismutases, mitochondrial heat shock proteins, and other gene expression markers. RNAi treatments appear to generate a stress and autophagy response, while the genomic mutation alters electron transport and reactive oxygen species metabolism. ... Most importantly, we found that [the] lifespan increase induced by nuo-6(RNAi) is fully additive to that induced by isp-1(qm150), and the increase induced by isp-1(RNAi) is fully additive to that induced by nuo-6(qm200). Our results demonstrate that distinct and separable aspects of mitochondrial biology affect lifespan independently."

View the Article Under Discussion: http://pmid.us/20346072

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

Via the Methuselah Foundation blog: "Today Methuselah Foundation launched the NewOrgan Prize, the Foundation's new longevity prize specifically focused on advancing the development of replacement tissues and organs for humans. Its goal is to accelerate advances in regenerative medicine, which will become the standard of care for replacing all tissue and organ systems in the body within 20 years, according to the U.S. Department of Health and Human Services. The first research team to construct a whole new complex organ (heart, kidney, liver, lung, pancreas) made from a person's own cells - one that is functionally equivalent and successfully transplanted - will be awarded the NewOrgan Prize. The goal of the Methuselah Foundation NewOrgan Prize is to achieve this medical breakthrough within the next 10 years. Today's launch is a call to action for competitors, candidates and contributors who want to participate in this crucial medical challenge aimed at extending healthy human life. ... Based on our success in spurring medical advances with incentives provided by the original Methuselah Mouse prize, we anticipate that over $10 million will be raised by the time the NewOrgan Prize criteria is met - and the prize presented - to the leading medical R&D team. At minimum, $1 million will be awarded to the research team that develops a whole new human organ that is functional and successfully transplanted."

View the Article Under Discussion: http://blog.methuselahfoundation.org/2010/04/methuselah_foundation_launches_neworgan_prize.html

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

One approach to stem cell therapy is to try to order existing stem cells to do more work, accomplished by introducing signaling molecules into the body - a drug, in other words. This methodology has reached the point of early clinical trials, as indicated in this press release: "Clinical-stage regenerative medicine company Juventas Therapeutics Inc. [has] started enrolling patients in a Phase 1 clinical trial to evaluate the safety and efficacy of its leading stem cell factor for treating heart failure. In preclinical studies of heart failure in pigs, JVS-100, as the factor is known, significantly increased cardiac function by promoting cell survival and increasing blood vessel formation in damaged hearts. JVS-100 works by encoding Stromal Cell-derived Factor-1 (SDF-1), a growth factor that in adults recruits stem cells from the bone marrow to create new blood vessels. The JVS-100-treated pigs showed significant improvements in cardiac function. ... We've led with heart failure because that's where our preliminary data was, and it's a great clinical opportunity. We also have strong data in the area of peripheral vascular disease and cosmetic wound healing. ... The factor can increase blood flow for patients who have peripheral vascular disease and accelerate wound closure and prevent scarring for patients who have had cosmetic surgery [so] we're looking to move both those toward clinic in the near future."

View the Article Under Discussion: http://www.medcitynews.com/2010/04/juventas-therapeutics-starts-phase-1-trial-for-heart-failure-therapy/

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

A good review paper: "Our understanding of autophagy has expanded greatly in recent years, largely due to the identification of the many genes involved in the process, and to the development of better methods to monitor the process, such as GFP-LC3 to visualize autophagosomes in vivo. A number of groups have demonstrated a tight connection between autophagy and mitochondrial turnover. Mitochondrial quality control is the process whereby mitochondria undergo successive rounds of fusion and fission with a dynamic exchange of components in order to segregate functional and damaged elements. Removal of the mitochondrion that contains damaged components is accomplished via autophagy (mitophagy). Mitophagy also serves to eliminate the subset of mitochondria producing the most reactive oxygen species, and episodic removal of mitochondria will reduce the oxidative burden, thus linking the mitochondrial free radical theory of aging with longevity achieved through caloric restriction. Mitophagy must be balanced by biogenesis to meet tissue energy needs, but the system is tunable and highly dynamic. This process is of greatest importance in long-lived cells such as cardiomyocytes, neurons, and memory T cells. Autophagy is known to decrease with age, and the failure to maintain mitochondrial quality control through mitophagy may explain why the heart, brain, and components of the immune system are most vulnerable to dysfunction as organisms age."

View the Article Under Discussion: http://pmid.us/20357180

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

Cytomegalovirus (CMV) is one of the reasons our immune systems decay with aging: too many immune cells become specialized to deal with CMV, leaving too few to deal with everything else. New research "explains how a virus that has already infected up to 80 percent of the American population can repeatedly re-infect individuals despite the presence of a strong and long-lasting immune response. The research involves cytomegalovirus (CMV), which infects 50 percent to 80 percent of the U.S. population before age 40. ... For most people, CMV infection goes undetected and they do not become seriously ill. ... When most viruses infect a host, the immune system remembers the disease and protects against re-infection. This is the case with smallpox, seasonal strains of flu and several other viruses. This immune system reaction is also the reason why vaccines made with weakened or dead viruses work against these pathogens. In the case of CMV, the body's immune system is continuously stimulated by ongoing, low-level persistent infection, but yet CMV is still able to re-infect. This research explains how CMV is able to overcome this immune response so that re-infection occurs. ... The results of this study primarily illustrate the significant barriers to creating a vaccine that will prevent CMV infection." But a vaccine won't do much for people already burdened by an CMV-focused immune system. What we want is a way to use targeted cell killing strategies to destroy CMV-related immune cells and free up space for more useful immune cells.

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-04/ohs-ore033010.php

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

Rapamycin recently showed promise as a potential treatment for Alzheimer's disease, and here more researchers are working on that: "A few weeks after a report that rapamycin, a drug that extends lifespan in mice and that is currently used in transplant patients, curbed the effects of Alzheimer's disease in mice, a second group is announcing similar results in an entirely different mouse model of early Alzheimer's. ... The second report [showed] that administration of rapamycin improved learning and memory in a strain of mice engineered to develop Alzheimer's. The improvements in learning and memory were detected in a water maze activity test that is designed to measure learning and spatial memory. The improvements in learning and memory correlated with lower damage in brain tissue. ... Strikingly, the Alzheimer's mice treated with rapamycin displayed improved performance on the maze, even reaching levels that were indistinguishable from their normal littermates. Levels of amyloid-beta-42 were also reduced in these mice after treatment, and we are seeing preserved numbers of synaptic elements in the brain areas of Alzheimer's disease mice that are ravaged by the disease process."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-04/uoth-adt040110.php

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

Rapamycin recently showed promise as a potential treatment for Alzheimer's disease, and here more researchers are working on that: "A few weeks after a report that rapamycin, a drug that extends lifespan in mice and that is currently used in transplant patients, curbed the effects of Alzheimer's disease in mice, a second group is announcing similar results in an entirely different mouse model of early Alzheimer's. ... The second report [showed] that administration of rapamycin improved learning and memory in a strain of mice engineered to develop Alzheimer's. The improvements in learning and memory were detected in a water maze activity test that is designed to measure learning and spatial memory. The improvements in learning and memory correlated with lower damage in brain tissue. ... Strikingly, the Alzheimer's mice treated with rapamycin displayed improved performance on the maze, even reaching levels that were indistinguishable from their normal littermates. Levels of amyloid-beta-42 were also reduced in these mice after treatment, and we are seeing preserved numbers of synaptic elements in the brain areas of Alzheimer's disease mice that are ravaged by the disease process."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-04/uoth-adt040110.php

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

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

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

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