One of the ways in which general health practices - such as exercise and fitness - steer cognitive health is through the state of the blood vessels in your brain: if they are deteriorating more rapidly, then more microinfarcts will occur, destroying more of the function of the brain, one tiny piece at a time. This is a mechanism quite distinct from the root causes of dementias like Alzheimer's disease, as this study illustrates: "This study was untaken to investigate the association of micro brain infarcts (MBIs) with antemortem global cognitive function (CF). ... Subjects were 436 well-characterized male decedents from the Honolulu Asia Aging Autopsy Study. Brain pathology was ascertained with standardized methods, CF was measured by the Cognitive Abilities Screening Instrument, and data were analyzed using formal mediation analyses, adjusted for age at death, time between last CF measure and death, education, and head size. Based on antemortem diagnoses, demented and nondemented subjects were examined together and separately. ... In those with no dementia, MBIs were strongly associated with the last antemortem CF score ... This suggests that microinfarct pathology is a significant and independent factor contributing to brain atrophy and cognitive impairment, particularly before dementia is clinically evident. The role of vascular damage as initiator, stimulator, or additive contributor to neurodegeneration may differ depending on when in the trajectory toward dementia the lesions develop."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22162060

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

Reactive oxygen species (ROS) are damaging molecules that can rip up important cellular machinery; all machinery in a cell is an arrangement of atoms, and promiscuously reactive molecules can gum up the works, pull out important parts of the machinery, and otherwise cause all sorts of issues. In discussions of our biology, the term free radical is often used interchangeably to refer to these reactive molecules. They are produced within our cells as a byproduct of some of the most important mechanisms of metabolism, a fact shared by the vast majority of species, dating back far into evolutionary time. As for all aspects of cellular chemistry with such deep origins, evolution has has a very long time indeed in which to build feedback loops and interlaced machinery that depend upon the existence of ROS, co-opting these molecules for diverse purposes in signaling and regulating the operation of cells and tissues.

Thus ROS generation and damage is not just a harmful side-effect of being alive and having cells that are churning away, but it is also fundamental to the complex processes by which our metabolism maintains cellular homeostasis in the face of day to day challenges. Here are a couple of open access papers that summarize what is known about the more important roles of ROS in the body - in the first paper, section 6 is where you'll find the focus on aging, while the second paper looks at the intersection of muscle, ROS, and exercise.

Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging

ROS are a normal side product of the respiration process, and they react with lipids, protein, and DNA, generating oxidative damage. Indeed, mitochondria are the major site of ROS production, but also the major targets of their detrimental effects, representing the trigger for several mitochondrial dysfunctions. In this review, we will focus on this deadly liaison, with particular attention on ROS production, mitochondrial ROS targets, and their role in apoptosis, autophagy, and aging. ... At physiological levels, ROS function as 'redox messengers' in intracellular signalling and regulation, whereas excess ROS induce cell death by promoting the intrinsic apoptotic pathway. Recent work has pointed to a further role of ROS in activation of autophagy and their importance in the regulation of aging. This review will focus on mitochondria as producers and targets of ROS and will summarize different proteins that modulate the redox state of the cell. Moreover, the involvement of ROS and mitochondria in different molecular pathways controlling lifespan will be reported, pointing out the role of ROS as a 'balance of power,' directing the cell towards life or death.

...

The decline associated with aging is caused by the accumulation of ROS, as supported by cellular and biological data from different model systems and organisms. Indeed defects in antioxidant defense mechanisms fail to protect against oxidative damage, reducing lifespan and causing cardiomyopathy, neurodegeneration, and cancer. ... The relationship between mitochondria dysfunctions observed during aging and ROS production is still debated. However, it is clear that the decline of the integrity of mitochondria as a function of age is implicated in aging and age-related diseases.
Given this wide scientific evidence, many studies were aimed to identify the molecular mechanisms responsible for ROS deleterious effects on the aging process.

Reactive Oxygen Species in Skeletal Muscle Signaling

Up to the 1990s of the past century, ROS have been solely considered as toxic species resulting in oxidative stress, pathogenesis and aging. However, there is now clear evidence that ROS are not merely toxic species but also - within certain concentrations - useful signaling molecules regulating physiological processes. During intense skeletal muscle contractile activity myotubes' mitochondria generate high ROS flows: this renders skeletal muscle a tissue where ROS hold a particular relevance. According to their hormetic nature, in muscles ROS may trigger different signaling pathways leading to diverging responses, from adaptation to cell death.

...

As an example, many studies have concluded that inactivity-induced ROS production in skeletal muscle contributes to disuse muscle atrophy. On the contrary, growing evidence also suggests that intracellular ROS production is a required signal for the normal remodelling that occurs in skeletal muscle in response to repeated bouts of endurance exercise. How can the same trigger promote such opposite effects? Based upon current knowledge, it appears that the mode and the situation characterizing skeletal muscle cells exposure to ROS may account, at least in part, for this apparent paradox. Transiently increased, moderate levels of oxidative stress might represent a potentially health-promoting process, whereas its uncontrolled persistence and/or propagation might result in overwhelming cell damage thus turning into a pathological event: for instance, the role of ROS in inflammation fits well with this model.

...

Supplementation with exogenous antioxidants is being widely studied to attain and maintain an 'ideal titration' of ROS within skeletal muscle: unfortunately, at the present, no clear indication of the benefits arising from supplemental antioxidant intake emerges from literature.

The evolution of knowledge regarding ROS in human metabolism, and the parallel evolution of the market for dietary antioxidant supplements, should be taken as a cautionary tale. Metabolism is complicated, and trying to alter its operation through the use of such blunt tools is probably not the most efficient way to use science to extend human life.

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

A progressive build up of advanced glycation end products (AGEs) is implicated in the aging process; they contribute to skin aging, for example. There are some research programs aimed at producing drugs or other treatments to break down the important AGEs in humans, but far too few of them, and poorly funded. Here, researchers look at AGEs in a mole rat species: "Mole-rat of the genus Fukomys are mammals whose life span is strongly influenced by reproductive status with breeders far outliving nonbreeders. This raises the important question of whether increased longevity of the breeders is reflected in atypical expression of biochemical markers of aging. Here, we measured markers of glycation and advanced glycation end-products formed in insoluble skin collagen of Ansell's mole-rat Fukomys anselli as a function of age and breeding status. Glucosepane, pentosidine, and total advanced glycation end-product content significantly increased with age after correction for breeder status and sex. Unexpectedly, total advanced glycation end-products, glucosepane, and carboxymethyl-lysine (CML) were significantly higher in breeders versus nonbreeders suggesting that breeders have evolved powerful defenses against combined oxidant and carbonyl stress compared with nonbreeders. Most interestingly, when compared with other mammals, pentosidine formation rate was lower in mole-rat compared with other short-lived rodents confirming previous observations of an inverse relationship between longevity and pentosidine formation rates in skin collagen."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22156473

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

Below you'll see optimism on the topic of longevity and the future, personal and otherwise, from the establishment political press, which is an unusual enough event to be worthy of remark. These are well-written general interest articles that don't look far beyond a high level overview of economics and exercise, so your mileage may vary - they don't touch on any of the more earnest scientific work on aging and rejuvenation such as SENS, for example. But take a look and see what you think:

Longevity: a Manual

"Genes account for one-fourth to one-third of longevity," estimated Howard Friedman, a professor of psychology at the University of California (Riverside) and the coauthor of The Longevity Project, published this year. "That leaves well over half not accounted for."

Most of the rest, for better or worse, is up to you. "The importance of choices people make is in so many ways responsible for the quality of life in old age," said Charles Reynolds III, a professor of geriatric psychiatry, neurology, and neuroscience at the University of Pittsburgh medical school. "Many people think they should be entitled to a good-quality 25 years after age 60. Well, they're not necessarily entitled, but they can put the odds in their favor."

One way - "the least speculative and the most obvious" - is with exercise, according to Simon Melov, a Buck Institute biochemist. "More activity is better than no activity, and most people are not doing anything. They're just sitting there." Exercise, he said, reduces the risk of cardiovascular disease and perhaps even a decline in cognition. One needn't run a marathon. Gardening, walking, swimming, woodworking - all of these are more active than just sitting.

No, Malthus, No: Living Longer Is a Blessing, Not a Curse

Long life may well be a blessing for the individual. But is it also a blessing for society? The fashionable answer is an increasingly anxious no. Choose your apocalyptic metaphor. The aging of America represents a "financial time bomb," The New York Times has proclaimed - with the solvency of Social Security, Medicare, and Medicaid (the last in line for nursing-home payments for patients who have depleted their assets) all at risk. Foreign Policy magazine has warned that a "gray tsunami is sweeping the planet," the United States included.

And yet the forecast that Americans' increased longevity is a collective downer for the nation ain't necessarily so. The fiscal threat, while real, provides too narrow a prism for understanding a question so complex. History suggests that the size of the total economic pie tends to grow larger as life expectancy rises. From 1950 to 2010, Americans' life expectancy at birth grew by 15 percent and, at age 65, by more than 30 percent - even as household incomes and the gross domestic product increased sixfold.

So, as counterintuitive as this may sound, it is possible, even likely - listen up, worrywarts! - for Americans to live longer and grow richer.

In fact the weight of evidence points strongly towards longevity and wealth moving hand in hand, influencing one another. People with longer time horizons make better decisions for the stewardship of resources, while at the same time increasing wealth means better medicine - more research, improved medicine, greater ability to purchase medical services, and so forth. See these items from the Fight Aging! archives, for example:

• Wealth and Longevity
• Longevity Tends to Change Economic Behavior for the Better
• What is Wealth?
• A Visualization of Wealth and Heath Over Time

Arguing against this view on the basis of the evidence is actually a pretty steep cliff to climb (not that that seems to stop the naysayers). Empires fall and regions become poor for all sorts of reasons, and the US is on the way to a sad end itself, but increasing life expectancy and growth in wealth are not amongst the causes.

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

Opposition to enhanced human longevity, which often advocates collectivism and the use of government force to prevent other people from extending their lives through biotechnology, is based on a range of factors: fear of change, the green-eyed monster of envy (who has set up shop in the environmentalist movement these days), and ignorance of basic economics. In the latter case, some folk naively believe all resources to be limited - jobs, wealth, and so forth - rather than growing with population and length of life. But all of these things are made by people, and the more people there are and the longer those people live in good health, the more creation will take place. But there are always naysayers who have convinced themselves that a hundred thousand deaths due to aging every day and the ongoing suffering of hundreds of millions is necessary because of their own vague and unrealized anxieties about the future. Here is one example: "Wolpe's own perspective is that our drive toward immortality is basically selfish. He sees few benefits to society, and a good deal of potential harm, in our living to 200 or beyond. ... There is a natural wisdom in replacing us. There's a natural wisdom in the idea that new people who arise in new circumstances have new perspectives on the world. ... Look at the generations living now from the World War II generation to the Baby Boomers, to Gen-X, all the way down. The young generation today, the people in their teens and 20's today were steeped in a different brine than I was as a Baby Boomer. They were brought up with technology at their fingertips. They move naturally and easily through that world. And the idea that if I got to live to, you know, 150 or 200, that that would be a good thing for anyone other than me, I think is a misguided notion. And there's a deep selfishness in the move towards immortality and these people like Aubrey de Grey and others who are really looking for that Fountain of Youth. ... If we don't change, for example, reproduction, if reproduction stayed between let's say, 20 and 40, that means that you would have another 80 years after reproducing that you'd be around. So there's even the question of how we're going to restructure the human lifespan. Is that a proper dynamic to have your children and then live another hundred years?" As usual, this is airy nonsense when held up against the reality of the vast and pervasive suffering caused by aging - suffering that we can work to address instead of just waffling about intangibles.

Link: http://bigthink.com/ideas/41527?page=all

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

Stem cell function, necessary to maintain tissue, declines with age. This most likely a part of the evolved balancing act between suppression of cancer and the need to keep tissues repaired and working - as you grow older, forms of molecular damage accumulate, increasing the risk of cancer resulting from the normal operations of cellular proliferation. That balance can already be shifted in mice in very beneficial ways, giving both less cancer and longer lives. While these are the early days yet, in our future lies a fusion of the fields of cancer research and stem cell science that will do the same for humans: "Adult stem cells exist in most mammalian organs and tissues and are indispensable for normal tissue homeostasis and repair. In most tissues, there is an age-related decline in stem cell functionality but not a depletion of stem cells. Such functional changes reflect deleterious effects of age on the genome, epigenome, and proteome, some of which arise cell autonomously and others of which are imposed by an age-related change in the local milieu or systemic environment. Notably, some of the changes, particularly epigenomic and proteomic, are potentially reversible, and both environmental and genetic interventions can result in the rejuvenation of aged stem cells. Such findings have profound implications for the stem cell-based therapy of age-related diseases."

Link: http://jcb.rupress.org/content/193/2/257.long

Correlations between character traits and longevity seem to be a growing area of study; interesting results, though of dubious importance, I think: "The relationship between personality and life span is not well understood, and no study to date has examined genetic influences underlying this relationship. The present study aimed to explore the phenotypic and genetic relationship between personality and life span, as well as genetic influences on all-cause mortality. ... Prospective community-based study including 3752 twin individuals older than 50 years. Neuroticism, psychoticism, extraversion, and social desirability and pessimism/optimism were measured at baseline using the Revised Eysenck Personality Questionnaire and the Revised Life Orientation Test, respectively. Information on age at death was obtained 16 years after the initial assessment of personality. ... Extraversion was inversely related to mortality with the risk of death decreasing 3% per unit increase of the extraversion score. Psychoticism and pessimism were positively related to mortality with a 36% and 39% increase in risk of death per unit increase in the respective personality score. Heritability of life span was 7%. ... Extraversion, psychoticism, and optimism/pessimism are significant predictors of longevity; extraversion is associated with a reduction, and pessimism and psychoticism are associated with an increase in mortality risk. Genetic influences on longevity in Australian twins are very low (7%). Our data also suggest a small, albeit nonsignificant, genetic influence on the relationship of pessimism and psychoticism with life span."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22155943

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

A brief summary of recent research into risk factors for disease and human longevity: "A set of currently known alleles increasing the risk for coronary artery disease, cancer, and type 2 diabetes as identified by genome-wide association studies was tested for compatibility with human longevity. Here, we show that nonagenarian siblings from long-lived families and singletons older than 85 [years] of age from the general population carry the same number of disease risk alleles as young controls. Longevity in this study population is not compromised by the cumulative effect of this set of risk alleles for common disease." The way in which you choose to lead your life is a more important determinant - for example, being sedentary and fat raises your risk of suffering the common diseases of aging far more than most known genetic variants. It is true that there are many gene variants associated with exceptional human longevity, but it still seems to be the case that environment and choice trumps small variations in your biology.

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20921414

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

Young mammals are capable of feats of regeneration: even in humans, it has been known for young children to regenerate lost fingertips. That capacity fades with age, however. Researchers are investigating the biochemistry of this behavior for much the same reasons as they look at regenerating species such as salamanders - if the capacity is there, perhaps it can be restored in adults. "Researchers, working with mice, found that a portion of the heart removed during the first week after birth grew back wholly and correctly - as if nothing had happened. ... This is an important step in our search for a cure for heart disease, the No. 1 killer in the developed world. We found that the heart of newborn mammals can fix itself; it just forgets how as it gets older. The challenge now is to find a way to remind the adult heart how to fix itself again. ... Previous research has demonstrated that the lower organisms, like some fish and amphibians, that can regrow fins and tails, can also regrow portions of their hearts after injury. ... In contrast, the hearts of adult mammals lack the ability to regrow lost or damaged tissue, and as a result, when the heart is injured, for example after a heart attack, it gets weaker, which eventually leads to heart failure. ... The researchers found that within three weeks of removing 15 percent of the newborn mouse heart, the heart was able to completely grow back the lost tissue, and as a result looked and functioned just like a normal heart. The researchers believe that uninjured beating heart cells, called cardiomyocytes, are a major source of the new cells. They stop beating long enough to divide and provide the heart with fresh cardiomyocytes."

Link: http://www.eurekalert.org/pub_releases/2011-02/usmc-nhm022311.php

It remains plausible that many cancers will suddenly become curable at some point in the next decade or so - even in their later stages - through the identification and targeted destruction of the cancer stem cells that power the cancer's growth:

The promise - the hoped for possibility - of cancer stem cells is that they represent a small, manageable, less complex range of biochemical targets to prevent and destroy cancer. The biotechnology of this year and next can flip genetic switches and safely destroy cells with specific markers - if we just know where to look, what to destroy, what to change.

Over the past few years, researchers have started the long process of cataloging cancers with identifiable stem cells at their root, and the unique signatures of those cancer stem cells. Those biochemical signatures in theory provide a template for targeted cell destruction therapies currently under development: engineered viruses, nanoparticle assemblies, immune therapies, and so forth. Given a distinct cell type, researchers can deplete its population without harming other cells or damaging tissues elsewhere in the body - a far cry from the present brute force approach of chemotherapy, and something that has been demonstrated numerous times in the laboratory.

On this topic I noticed a good open access paper today that provides an introduction to - and overview of - the near future of this branch of medical research.

Therapeutics formulated to target cancer stem cells: Is it in our future?:

When discussing potential targets for the treatment of cancer today, the conversation will generally lean towards targeted therapy of cancer stem cells (CSCs). With the identification of potential defining characteristics for CSCs, there have also been more questions raised as to which of these characteristics may make better targets. For many years, research seemed to focus on isolating CSCs by specific identifying markers but the research has seemed to shift towards identifying the way in which these stem cells behave that make them different from bulk tumor cells. Limited efficacy has been seen with the use of cell surface markers in clinical trials; however, there have been recent advances that target other aspects such as signaling pathways or genetic alterations seen particularly in CSCs. The following is a review of what information is out there and what seem to be the most promising paths on this journey to identifying therapeutic targets of self-renewing CSC sub-populations.

For the other side of the debate on cancer stem cells, you might look back into the archives. Not all researchers think that cancer stem cells are a viable target for therapies, or that they are in fact a sustaining force for cancer:

• The Skeptical View of Cancer Stem Cell Research
• Another Blow To Cancer Stem Cells

From my outsider's perspective, the competing evidence for and against the cancer stem cell hypothesis might be resolved if it turns out that only some cancers have clearly identifiable stem cells at their root. But we shall see how it all turns out: the research community is certainly going to spend a great deal of time and money over the next decade trying to destroy cancer by identifying and targeting its stem cells.

Just Five Minutes of Exercise Outdoors Boosts Mental Health, Researchers Say

In a bad mood? Improve it by going outside!

Here in New York and all around the country, summer is in the air.  It may say “May” on the calendar, but the weather sure doesn’t know that, as this week’s temperatures in New York City are headed for the 70s and 80s!

I hope it’s as nice where you are as it is here.  And if it is, instead of going to the gym after work to exercise today, head outside…even if it’s for just five minutes.  Because according to a new study on the mental health effects of exercising outside, the great outdoors can heighten your mood and your self-esteem.

Researchers from the University of Essex discovered this after reviewing the health habits of over 1,200 people from 12 separate studies.  Among the information collected from these men and women of all ages was their state of mental health (i.e. were they diagnosed with any kind of mental health disorder and cognitive dysfunction) and the kind of activities they did outside, such as walking, bicycling, gardening or horseback riding.

All of the individuals who exercised regularly showed improvements in their mental health, but those who saw the most significant improvement were those who performed what the researchers call “green exercises.”  Green exercises are any of the aforementioned exercises performed outside.  Other green exercises include farming, walking, gardening, fishing or boating.

“We believe that there would be a large potential benefit to individuals, society, and to the costs of the health service if all groups of people were to self-medicate more with green exercise,” said Jo Barton in a statement.  Barton co-authored the study with her colleague, Jules Pretty.

Their complete findings can be found in the journal Environmental Science & Technology.

Oh, and if you’re someone who loves the ocean, then you’re going to love this:  the biggest mental health effects were found among those who live near the water, like the ocean, a river or lake.

So, it seems, the closer you are to blue, the less likely you are to get “blue.”

As with many studies, this probably confirms the obvious.  But this research is illuminating nonetheless because up to now, no one really knew just how long it took to be outside to reap the mental health benefits.  And according to the researchers, it takes as little as five minutes.

So you know what that means?  No more excuses.  No more saying, “I can’t go outside for a walk because I don’t have any time on my lunch break.” Everybody has at least five minutes they can spend outdoors to walk.

Now, ideally, you’ll be exercising for longer than five minutes, but as I always say, some exercise is better than no exercise.  And that’s every bit as true for the mind as it is for the body.

Sources:
newsmaxhealth.com
news.bbc.co.uk

Discuss this post in Frank Mangano’s forum!

The FDA-approved drug Chantix may be causing more problems by producing adverse side effects like aggression, experts say.

Smoking cessation is a big problem for dependent smokers. Withdrawal symptoms and nicotine cravings are two of the top reasons why many cannot stop smoking.

A few years ago, the US FDA approved a drug, Chantix, that was touted as the prescription drug to help people kick the smoking habit.  According the drug’s medical literature, Chantix works by acting on the specific brain receptors associated with the chemical nicotine.

Nicotine is an active ingredient in tobacco products that produces a feeling of well-being and relief.  In the long term, the body loses its ability to produce similar chemicals that provide stress relief and the feeling of satisfaction.

This is the reason why smokers become dependent on tobacco products.  It is possible to normalize the brain chemical production again, but it takes time and the withdrawal symptoms are painful.

The story of Chantix

When a smoker is prescribed Chantix to help kick the smoking habit, he can continue smoking until the 8th day of active treatment.  After this point in time, the patient must stop smoking so the drug can perform in its full capacity.  A patient can be prescribed the drug from 12 to 24 full weeks.

According to researcher Thomas Moore from the Institute for Safe Medication Practices, Chantix is actually a dangerous drug because it causes patients to feel aggression, violence and even suicidal thoughts.

Moore states that there should be regulation in the prescription of the drug.  According to him, military personnel and other similar armed professionals should not be given the drug given the adverse reports of its side effects since its approval in 2006.

The first documented, adverse side effect of the drug was made in the year 2007 when a musician from Dallas was shot down for displaying violent behavior toward his girlfriend’s neighbor.

Moore and fellow researchers were able to gather a total of 78 adverse cases of side effects from various sources, including reports sent to the US FDA.  Among the 78 adverse side effects, the researchers noted that ten cases involved serious assault, nine cases involved thoughts of committing homicide and seven cases involved other types of violent thoughts.  The FDA advises anyone on the drug Chantix to stop treatment if such feelings of aggression manifest during treatment.  It is also advised that you visit your physician if ever such side effects do occur during treatment.

Natural smoking cessation strategies

You don’t have to be dependent on smoking cessating drugs like Chantix or nicotine patches to kick the smoking habit.  Below are natural strategies that can help you quit the habit.  But the most important tool in your arsenal will still be the genuine desire to quit smoking because you want your health back.

1. A common withdrawal symptom when a person stops smoking is hunger.  This hunger is in part psychological and part physiological.  The body is sending out a signal that it needs its next dose of nicotine.  The body doesn’t need nicotine because it can produce its own natural chemicals to reward the body after a hard day’s work.  If you feel hungry after quitting smoking for a few hours, try drinking some water or eating a small, healthy snack.  Avoid over-eating though, as this doesn’t help the overall effort of keeping yourself healthy throughout the quitting process.

2. Deal with the emotional stress associated with smoking properly.  The first step is to reach out to those who are closest to you, like friends and loved ones.  It’s okay to tell them that you feel angry or frustrated.  Listen to them and allow them to provide you comfort and emotional relief.  Also, learn how to de-stress properly. Remove yourself form isolation, start exercising and keep yourself busy with doing something you like.

3. Reach out to other people like you who are also attempting to kick the habit for good.  Online forums on smoking cessation are free of charge and are full of folks who are in various stages of quitting.  Simply joining the forums can provide immense benefits because you can heart their stories and you will not feel as if you are loneliest person in the world.

4. Do you feel fatigued or physically tired because you’ve quit smoking?  Instead of getting a cigarette, try resting. If you need to adjust your bedtime to sleep earlier, then that’s a good idea. Sleep is much better than bringing yourself back to square 1 of your efforts.

5. Gradually reduce your number of cigarette sticks per day. Start with small steps and gradually reduce your tobacco consumption by half.   Then halve your current number of sticks again, until you’re down to two or one stick a day.  By doing this, you are giving your body time to readjust its chemical balance.  Going cold turkey rarely works, especially for first-time ‘quitters’.

Sources:
webmd.com
quitsmoking.about.com
quitsmoking.about.com

It is known that calorie restriction increases stem cell capacity in aging, thereby helping to maintain tissues for longer. From Extreme Longevity, a recent commentary on the mechanisms involved: "Like it or not food lovers, the single most effective known means of extending animal lifespan is through reducing daily caloric intake. Though not definitively proven in humans, the success of this intervention has been demonstrated in myriad species in more than 50 years of research. ... A protein called mTOR is responsible for this effect. mTOR combines with two other proteins to mediate several important cellular processes. These include translation of mRNA into protein, mitochondrial activity, and autophagy. Caloric restriction inhibits mTOR activity which leads to longer lifespan. The new studies [convincingly] demonstrate that reduction of mTOR activity causes preservation of stem cell health. They increase in abundance and proliferative potential. One study shows this occurs in intestinal cells, and the other in muscle cells. In the instestinal cell study, the authors showed that it was actually supporter cells called Paneth cells that aided the health of stem cells when they were taken from calorie restricted animals. They further showed this effect was mediated by mTOR inhibition and that it was achieved by increasing the activity of another protein called Bst1, important in cell proliferation. In the muscle study, calorie restricted animals had greater muscle stem cell proliferative capacity too. And this effect was also seen when the stem cells were transplanted into non calorically restricted animals, suggesting the microenvironment or niche around the stem cells was key. ... taken together, the two studies indicate that preserving and enhancing stem-cell function in multiple tissues is one of the ways in which calorie restriction slows the ravages of aging."

Link: http://extremelongevity.net/2012/06/29/caloric-restriction-extends-lifespan-by-increasing-stem-cell-function/

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

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LinkedIn Corporation 2016

Excerpt from:
Longevity Medicine | LinkedIn

Research into Laron dwarfism in a population in Ecuador has been taking place for a few years now: "People living in remote villages in Ecuador have a mutation that some biologists say may throw light on human longevity and ways to increase it. The villagers are very small, generally less than three and a half feet tall, and have a rare condition known as Laron syndrome or Laron-type dwarfism. ... though cancer was frequent among people who did not have the Laron mutation, those who did have it almost never got cancer. And they never developed diabetes, even though many were obese, which often brings on the condition. ... [this is] an opportunity to explore in people the genetic mutations that researchers [found] could make laboratory animals live much longer than usual. ... The Laron patients' mutation means that their growth hormone receptor lacks the last eight units of its exterior region, so it cannot react to growth hormone. In normal children, growth hormone makes the cells of the liver churn out another hormone, called insulinlike growth factor, or IGF-1, and this hormone makes the children grow. If the Laron patients are given doses of IGF-1 before puberty, they can grow to fairly normal height. This is where the physiology of the Laron patients links up with the longevity studies that researchers have been pursuing with laboratory animals. IGF-1 is part of an ancient signaling pathway that exists in the laboratory roundworm as well as in people. The gene that makes the receptor for IGF-1 in the roundworm is called DAF-2. And worms in which this gene is knocked out live twice as long as normal."

Link: http://www.nytimes.com/2011/02/17/science/17longevity.html

An introduction to what is known of telomeres can be found at the Scientist: "The ends of linear chromosomes have attracted serious scientific study - and Nobel Prizes - since the early 20th century. Called telomeres, these ends serve to protect the coding DNA of the genome. When a cell's telomeres shorten to critical lengths, the cell senesces. Thus, telomeres dictate a cell's life span - unless something goes wrong. Work over the past several decades has revealed an active, though limited, mechanism for the normal enzymatic repair of telomere loss in certain proliferative cells. ... Telomeres shorten as we age. By analogy to the cellular mitotic clock, telomeres have been postulated as a marker of 'genetic age,' and telomere length has been marketed as a simple predictor of longevity. Assays of telomere length have been bundled with recommendations for lifestyle modification and for drug therapy, neither based on appropriate clinical studies. Simple but appealing arguments relating telomeres and aging are currently controversial, likely simplistic, and potentially harmful. Telomere length does indeed reflect a cell's past proliferative history and future propensity for apoptosis, senescence, and transformation. Cellular aging, however, is not equivalent to organ or organismal aging. ... Studies in humans have attempted to relate telomere length to life span. In the provocative initial publication from the University of Utah in 2003, individuals around 60 years of age who had the longest telomeres lived longer than did subjects with the shortest telomeres, but the main cause of death in the latter group was, inexplicably, infectious disease; the persons with shorter telomeres did not have a higher rate of cancer deaths. Moreover, these findings have not been confirmed in other studies of older subjects. In another study evaluating a different population, telomere length failed to predict survival, but interestingly it correlated with years of healthy life. In a Danish study of people aged 73 to 101 years, telomeres correlated with life expectancy in a simple univariate analysis, but only before the researchers corrected for age, suggesting that the correlation was driven simply by the fact that younger subjects had longer telomeres. And a Dutch study of 78-year-old men found that while telomere lengths eroded with age, they failed to correlate with mortality."

Link: http://the-scientist.com/2012/05/01/telomeres-in-disease/

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

An open access commentary: "The mammalian heart must maintain its structural and functional integrity for decades, yet the response to damage in this vital organ is remarkably inadequate and often results in heart failure. Moreover, patients with chronic heart failure show profound metabolic changes, leading to peripheral abnormalities in addition to an initial cardiac impairment. Several evidences have suggested a relationship between the IGF-1 system and cardiovascular disease. Many cardiovascular risk factors, such as sedentary lifestyle, diabetes, smoking, oxidized low-density lipoprotein, obesity, psychological distress and reduced coronary flow reserve, have been associated with reduced IGF-1 levels. Conversely, human studies indicate that increased levels of IGF-1 are characterized by a decreased incidence of heart failure and mortality in elderly individuals. Nevertheless, the fact that IGF-1 can act either as a circulating hormone or as a local growth factor has confounded previous analyses of animal models in which transgenic IGF synthesized in extra-hepatic tissues was released into the circulation. Locally acting mIGF-1 isoform improves muscle regeneration and counters muscle wasting associated with diseases, including sarcopenia, muscular dystrophy and ALS. By contrast, circulating IGF-1 isoforms have been implicated in the restriction of lifespan and have contrasting effects on the heart when expressed as transgenes, variously promoting cell survival, or inducing prolonged hypertrophy with pathological consequences."

Link: http://www.impactaging.com/papers/v4/n6/full/100466.html

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

We live in a world of oral fixation, or whatever equivalent post-Freudian term you'd live to use. It's not too hard to drawn the lines that lead unbroken from the magic of early human societies, insofar as it touched on beliefs regarding the consumption of various things, and the magical thinking of modern societies illustrated by the popularity of useless potions and pills. On the one hand tricksters cloaked as shamans, and on the other hand tricksters cloaked as marketing professionals pretending to use the methods of science. For every hot field of medical science, there are frauds out there somewhere selling edible goods to the credulous, trying to claim some of the mantle.of legitimacy enjoyed by the scientific community while practicing what is in effect an anti-science of belief and deception.

But back inside the real scientific community, we see the oral fixation at work in the amount and range of work on ingested substances. On diet, on tiny portions of diet, on the ingestion of specific substances beyond count, looking for results of significance. Funding for this sort of thing is evergreen, and I think that much of it is a grand waste. The path to longevity is not a freeway passing through the human stomach, but from the weight of research devoted to what we eat you might be forgiven for thinking otherwise. Would that these researchers were spending their time on something more useful, but the fixation of broader society on the mouth and what we put into it steers the strategic direction of research and research funding.

Here are a couple of examples:

Mediterranean diet gives longer life

Scientists at the Sahlgrenska Academy have now studied the effects of a Mediterranean diet on older people in Sweden. They have used a unique study known as the "H70 study" to compare 70-year-olds who eat a Mediterranean diet with others who have eaten more meat and animal products. The H70 study has studied thousands of 70-year-olds in the Gothenburg region for more than 40 years. ... The results show that those who eat a Mediterranean diet have a 20% higher chance of living longer. "This means in practice that older people who eat a Mediterranean diet live an estimated 2 3 years longer than those who don't", says Gianluca Tognon, scientist at the Sahlgrenska Academy, University of Gothenburg.

Are there differences in mortality among wine consumers and other alcoholic beverages?

Wine consumers, especially in comparison with spirits drinkers, have been shown to have higher levels of education and income, to consume a healthier diet, be more physically active, and have other characteristics that are associated with better health outcomes. However, epidemiologic studies have been inconsistent in showing that, after adjustment for all associated lifestyle factors, consumers of wine have lower risk of cardiovascular disease and mortality than do consumers of other beverages. A study based on the long-term follow up of a group of older Americans concluded that the associated lifestyle habits and environmental factors of wine consumers largely explained their better health outcomes.

We live in a world in which ingestion of alcohol has a greater and more active research community associated with it than is the case for serious efforts to develop the means to reverse aging. There will be more and greater publicity and funding generated by debates over tiny changes in life span and risk of disease through alcohol in the diet than there will be for the most important advance in longevity research this year, or any of the other high points in longevity science from the past twelve months. Sad but true. Real longevity science and biotechnology doesn't have much to do with sticking things into your mouth - it's largely low-level manipulation of cells and biomolecules - and in this world of oral fixation that's something of a disadvantage when it comes to publicity and support.

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

News of "fracture putty," an evolution in the use of scaffold material for bone regeneration: recent studies "show promise to significantly shorten the healing time and revolutionize the course of fracture treatment. ... Healing of critical-size defects is a major challenge to the orthopedic research community. Large-bone defects must be stabilized and necessitate technologies that induce rapid bone formation in order to replace the missing tissue and allow the individual to return to rapid function. To date, no single material can suffice. ... In our experiences with large animal models, following the guidelines established by our animal care and use committee, we have been successful in formulating a product that contains mesenchymal stem cells and allows them to survive in the environment of the fracture long enough to elicit the rapid formation of new bone. ... To start the bone regeneration process, the [researchers] used adult stem cells that produce a protein involved in bone healing and generation. They then incorporated them into a gel, combining the healing properties [into] 'fracture putty.' [The] team used a stabilizing device and inserted putty into fractures in rats. Video of the healed animals at two weeks shows the rats running around and standing on their hind legs with no evidence of injury. [The] researchers are testing the material in pigs and sheep, too. ... Our approach is biological with the putty. Other groups are looking at polymers and engineering approaches like implants and replacements which may eventually be combined with our approach. We are looking at other applications, too, using this gel, or putty, to improve spinal fusion outcomes."

Link: http://medicalxpress.com/news/2012-02-uga-discovery-fracture-putty-broken.html

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

The April 2012 edition of Rejuvenation Research includes the proceedings of the SENS5 conference, so there's a lot of material you'll have already seen there. The sole open access paper is worth reading as an update on research into the use of Z-Phe-Ala-diazomethylketone (PADK) to boost lysosomal function. The lysosome, you will recall, is a form of roving recycling unit that exists within the cell. Its task is to break down waste and unwanted materials - and that function is vital, as demonstrated by the many ultimately fatal conditions caused by lysosomal dysfunction. Unfortunately for all of us, lysosomal functionality deteriorates with age. This is most likely due in large part to accumulating waste materials, such as lipofuscin, that lysosomes cannot break down. They instead bloat and malfunction.

One body of research aiming to fix this issue is organized and advocated by the SENS Foundation, and focuses on ways to safely break down the waste materials that cannot be handled by lysosomes. For example, through biomedical remediation and the use of tailored bacterial enzymes. Meanwhile, other research groups have worked on boosting lysosomal activity in various ways, which seems to have generated some benefits where successful. For example, reversing decline in liver function, and restoring mental capacity in mice engineered to generate the signs of Alzheimer's disease.

It is that second example that is the subject of this open access paper, showing that enhancing lysosomal activity can potentially help with aggregates of damaging material outside cells, as well as the state of the cell interior:

Positive Lysosomal Modulation As a Unique Strategy to Treat Age-Related Protein Accumulation Diseases

Knowing the link between lysosomal dysfunction and selective pathogenesis, one logical step toward therapeutic intervention is the enhancement of enzymatic activity in lysosomes. [Some age-related diseases] may be slowed or reversed by the positive modulation of the lysosomal system. Many studies suggest that lysosomal activation occurs with age and in diseased brains, but not to the necessary extent that would prevent the gradual loss of neuronal integrity and brain function.

Enhancement of lysosomal function has been proposed as a plausible strategy to reduce protein accumulation events in age-related disorders, including those events in Alzheimer disease, Parkinson disease, and Huntington disease. Several of the studies indicate that induction of protein degradation processes is an attempt to clear amyloid peptides and tau species, as well as ?-synuclein and mutant huntingtin. Another potential therapeutic strategy that may involve the endosomal-lysosomal system is the disaggregation of extracellular A? peptide, with the idea that the disaggregation would promote uptake of monomers and small oligomers into neurons and microglia where they are trafficked to lysosomes for degradation.

...

Of the list of lysosomal modulatory agents [provided in the paper] only PADK, diazoacetyl-dl-2-aminohexanoic acid methyl ester, glycyl-phenylalanyl-glycine-aldehyde semicarbazone, and bafilomycin A1 have been reported to elicit protection against protein accumulation pathology under appropriate low-dose conditions.

...

From the in vitro and in vivo findings, unique lysosomal modulators represent a minimally invasive, pharmacologically controlled strategy against protein accumulation disorders to enhance protein clearance, promote synaptic integrity, and slow the progression of dementia.

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