In a self-repairing system, a little damage is actually a good thing - it wakes up the repair mechanisms and sets them to work, producing an overall net benefit. Thus a given form of damage may be good or bad for system longevity, depending on its degree, where it happens, and whether it is noticed by the repair mechanisms. This is why you'll see superficially contradictory research papers on reactive oxygen species, the damaging oxidant molecules emitted by mitochondria, and their impact on aging. See this, for example: "researchers have identified a pathway by which reactive oxygen species (ROS) molecules, which are usually implicated in the aging process due to their damage to DNA, can also act as cellular signaling molecules that extend lifespan. ... Increased ROS, and their effects at the cellular level, can lead to oxidative stress, which is involved in many diseases and aging. But ROS are also necessary for the proper functioning of the immune system and other biological functions. ... Inhibiting a signaling pathway called Target of Rapamycin (TOR), which is involved in sensing nutrients and cell growth, increases lifespan in yeast, as it does in mice. ... a key way this occurs is by altering the function of cellular powerhouses called mitochondria so that they produce more signaling ROS. ... The concept that ROS are important cellular signaling molecules, and not just agents of damage and stress, has grown to be widely accepted. Remarkably, in this study, we show that their purposeful production by mitochondria can even provide an adaptive signal that can delay aging. ... Trials targeting the TOR pathway as an anti-cancer strategy in humans are already underway. Our study suggests that carefully augmenting mitochondria and ROS production in humans may also be beneficial in combating aging and associated diseases." Note that "carefully augmenting mitochondria and ROS production" is a fair description of the results of exercise, and is one of the ways in which exercise works to improve long-term health. You may recall that researchers demonstrated that antioxidants applied generally tend to block this effect by mopping up the ROS that act as signals to the body's repair systems.

Link: http://opac.yale.edu/news/article.aspx?id=8625

You might recall that late last year I pointed out a large Japanese longitudinal study on incidental moderate exercise and lifetime medical costs:

The authors followed up 27,738 participants aged 40-79?years and prospectively collected data on their medical expenditure and survival covering a 13-year-period. ... The present results indicate that the multiadjusted lifetime medical expenditure from the age of 40?years for those who walked ?1?h per day was significantly lower by 7.6% in men and non-significantly lower by 2.7% in women than for those who walked <1?h per day. This decrease in lifetime medical expenditure was observed in spite of a longer life expectancy (1.38?years for men and 1.16?years for women) among those who walked ?1?h per day.

In another, more open access recent paper, the same authors have crunched the numbers for variations in weight among study participants. The story is much the same, as one would expect:

Although four previous studies have examined the association between obesity and lifetime medical expenditure, the results were inconsistent. ... We therefore conducted a 13-year prospective observation of 41,965 Japanese adults aged 40-79?years living in the community, which accrued 392,860 person-years. We examined the association between BMI and lifetime medical expenditure, based on individual medical expenditure and life table analysis. We collected data for survival and all medical care utilisation and costs, excluding home care services provided home health aides, nursing home care and preventive health services in participants of this cohort study.

...

In spite of their short life expectancy, obese men and women had approximately 14.7% and 21.6% higher lifetime medical expenditure in comparison with normal weight participants, respectively.

Don't get fat, don't stay fat, and don't be a couch potato. Thus speaks the weight of evidence - but then we all knew that, right? Being unhealthy has definitive material costs in the long term: years of life shaved off, the rot of your body and mind, and the monetary cost of medical services you would otherwise not have needed. There are plenty of people in this world, far too many, who don't presently have the luxury of choice when it comes to being healthy: the genetically impaired, the immune-damaged, the infected, the wounded. Why fritter away your choice for the sake of eating and laziness? It is almost a gesture of contempt.

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

It is known that centenarians - and their immediate families - tend to have better immune systems, a capability that is increasingly important in old age as people become more vulnerable to infections. Here is more research to illustrate this fact: "Aging is characterized by a progressive alteration of homeostatic mechanisms modulated by environmental and genetic factors. It is associated with a pro-inflammatory status. In centenarians, an increase of pro-inflammatory cytokine production balanced by anti-inflammatory immune response that would promote longevity is observed. Cytokine dysregulation is believed to play a key role in the proposed remodeling of the immune-inflammatory responses accompanying old age. IL-22 is a pro-inflammatory cytokine belonging to the IL-10 family and represents an important effector molecule of activated [T cells]. We recruited 17 healthy centenarians (4 males, 13 females, range 100-105 years). All ultralongeval subjects were living at home or in a nursing home. Sixteen healthy, sex-matched individuals (4 males, 12 females, range 60-95 years) were also recruited as controls. Centenarians displayed significantly higher circulating IL-22 levels compared to control population. It's well known that IL-22 is a pro-inflammatory cytokine produced by activated T lymphocytes and NK cells. IL-22 stimulates the production of acute phase reactants and promotes the antimicrobial defense. The results of the present study show, for the first time, that there is an increase of IL-22 in healthy centenarians. This pro-inflammatory condition probably is protective against infection, promoting the longevity of these subjects."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21640395

The problem with ethics as a profession is exactly that it has become a profession: the salaried ethicist knows that his continued employment depends upon finding problems with research and development. Money, even modest amounts of the stuff, is a powerful incentive. So where there are no problems, there are still groups of people who are effectively being paid to invent problems - and you wonder why medical science isn't moving as fast as it might be.

This form of institutional corrosion is well entrenched throughout the Western world now, of course, and so you'll see plenty of things like this open access whine-slash-justification-for-a-paycheck:

Optimistic predictions of the feasibility and effectiveness of life extension should be critically reviewed in the light of their ethical and social implications. Some anti-aging scientists claim that arguments against anti-aging medicine will simply be dismissed by research outcomes. We would claim that the problem is not with the availability of results, but with defining the nature of what we consider "results".

The idea that life extension research will necessarily translate into what some judges interpret as a result (i.e. the cure of aging) is problematic, because the translational process from potential life extension interventions into reality is not only a matter of science. Suppose we have laboratory advances that are promising for the future translation of laboratory work to the clinic. This result would matter scientifically, but would not solve the ethical and social questions of life-extending interventions. Even if we should succeed in the laboratory, the problems of equitable access to such interventions, the impacts of the future implementation of life extension on health care systems, the risk of pressure to make use of life extension techniques - all these issues will still be with us. Here, more than ever, it must be stressed that the "nature" of what we consider "results" matters not only scientifically, but also ethically and socially. Ethical and social debate on these issues is therefore much needed, along with scientific research and discussion.

Roughly translated: "I don't actually know enough about contemporary longevity science to write about it comprehensively or well, but I do know how to write successful grants. Please pay me and my colleagues more money rather than putting those resources to work on actual research." The middle section of the paper is particularly offensive on that count, an incomplete overview that plays up the bad and the unknown while failing to mention important topics such as SENS, systems biology, tissue engineering, and so on and so forth. There are admittedly far worse things going on in the world these days than the efforts of a legion of minor parasites who've manage to redirect research funding to build an industry that actively opposes research, but the noisy parasitism of the ethics profession manages to be more aggravating than its cost should make it.

Strange things happen to cultures when they lose sight of what matters, begin to value abstractions such as "society" over real individuals, and empty talk over tangible progress. I'd say it's a form of collective cabin fever brought on by the shrinking world and the absence of a frontier: with no hard-to-reach destination for the best, brightest, and most motivated to head for when matters become less than tolerable, there is no escape valve to prevent a network of diverse cultures from nonetheless degenerating in lockstep. The only form of protest that really matters in the long term - when it comes to applying pressure for change - is emigration to a remote region in order to build better lives. The sooner that the next new frontier is opened by technological progress in orbital flight the better in my view.

What I'll here call hyperactivism is a poisonous sort of dysfunction that you'll find in activist and advocate communities associated with struggling industries or long-standing initiatives that have failed to fulfill early visions of growth. It comes about because the early supporters in any new field tend to be passionate, driven, ornery, and focused: if they didn't have these characteristics, they wouldn't be up for the job of fighting over and again to persuade people to see things their way. If you are trying to build a new venture, then you need these people: they are worth their weight in gold, and they will help you succeed.

When an initiative does succeed attracting broad support and a large community, the energy and quirks of the early activists are tempered by a sea of more sedate, everyday folk. Sometimes the pioneers are quietly airbrushed out of the official histories - once an initiative becomes large enough for its leaders to want it to look like a shiny, official, professional machine, then the original barnstormers and larger than life personalities start to be seen as a liability. Justifiably or not, they are shuffled to one side of the growing crowd. In this way, the ultimate accolade of success is to be made irrelevant in the movement you helped found: accepting that likelihood up front is the way to peace of mind for activists and advocates.

But when things don't go according to plan, and what was intended to be great fails to achieve its original promise, or moves too slowly, then the problems start. Some of the early activists, untempered by large numbers of new volunteers and supporters, become poisonous. Their hyperactivism manifests itself in perfectionism, attacks on members of the community, and other displays of frustration or bitterness: to their eyes, failure was avoidable, and the problem must be the other people involved.

You see some of this going on in the cryonics community, an example of success on the small scale amidst a failure to achieve the grand goals originally envisaged for the movement. Which is to say that the few people who choose to be cryopreserved have a good chance of successfully achieving that goal, thanks to decades of largely volunteer efforts, but the vast majority of people in the world don't know, don't care, and go to the grave and oblivion just as they always have. So, understandably given human nature, you'll find a degree of hyperactivism amongst the long-standing members of the cryonics community. I noticed a perfectly passive-aggressive example of the type from Cryosphere the other day - which is disappointing, given the normally useful output there. It prompted a response in Alcor CEO Max More in his latest update, which I think is somewhat more useful.

Outside of pure mathematics and logic, perfection is not attainable in the real world. Even the flawless achievement of one goal means giving up another goal of inferior but substantial value (the economists' concept of "opportunity cost"). And achieving some aspects of a desired goal will mean giving up others. You may want a car that gets excellent gas mileage, but that will probably mean giving up the level of performance you hoped for. You may want to delay having children until you've accumulated more wealth and experience, but your fertility level may decline.

Tradeoffs clearly exist in cryonics, although you wouldn't know it by listening to most critics. We would all like cryonics to be perfect, but we know that gains come at a cost. We would like the costs of membership dues and cryopreservation charges to be lower. We would like the quality of cryopreservations to be higher. We would like everything to be run by medical professionals at low cost and with total commitment.

You can't have everything, no matter how much a hyperactivists might wish for it. Hyperactivism is something that we're all prone to, being human as we are, and it is also something to watch for when we support our favored organizations. It is important to keep the community honest, to criticize what should be criticized, and help other members of the community achieve success where possible - but if you have come to the point at which you feel that attacking other parts of the community is helpful, then somewhere you crossed the line.

I'm of the mindset that the right response - when you find yourself at that point of frustration with an existing initiative or organization - is to channel your passion into support for an existing alternative, or start such an alternative yourself. It is better to build than to tear down, and if your frustrations are in fact based on a meaningful or useful point then you have a shot at irrefutably demonstrating that point by building a better initiative, a better product, a better community. Many people in the cryonics community have worked on doing just that over the last decade - and progress springs from this impulse to achieve better results, not the impulse to attack those who are somehow not doing things your way.

By virtue of the fact that very large sums of venture capital, big pharma investment, and public funding have been sunk into the examination of sirtuins in connection with longevity in mammals, I think we'll see a strong sirtuin research contingent in the scientific community for some years to come - and this regardless of the ultimate merits of this work. While there are promising signs that sirtuins may do something useful in terms of enhancing cellular housekeeping, after some years of research we have yet to see any of the promise of slowed aging that looked possible at the outset. See, for example:

• A Possible Reason For Sirtuin Uncertainty
• Critiquing the Sirtuin Model of Calorie Restriction

Research and development always takes longer than expected, but at this point I look at research into sirtuins as an early step forward on a much longer road - a part of the foundations of some later work, and producing little of direct use in and of itself. The newer technologies and newer companies who work on the same strategy of slowing aging via identification of ways to manipulate metabolism will leap over the work of the last five years, producing a hundred-fold more genetic and biochemical data in the process. Biotechnology is advancing so rapidly that each generation of development is made obsolete before it even hits its stride. It will be interesting indeed to see what comes after the present generation of biotech startups like Genescient and Halcyon Molecular.

But back to sirtuins: here is an optimistic open access paper from researchers who do see a bright future for the development of sirtuin-based therapies.

How does aging occur? Can we delay the aging process? These are questions that have been asked for hundreds if not thousands of years.

...

Aging is one of the most fundamental biological processes. It results in a decline in physiological function and an increased risk for pernicious diseases such as cancer. Oxidative stress has been proposed as a major cause of aging, but experimental tests of this hypothesis have been discouraging. Calorie restriction (CR) prevents age-related decline, but there are still gaps in our knowledge of the exact mechanisms underlying this feat. Finally, a tenuous balance exists between aging and cancer, calling for a search for interventions that prevent both aging and cancer. Recent work on the mammalian sirtuin SIRT3 has shed light on these long-standing issues and suggested new approaches to ameliorate the ravages of aging.

You might look back into the Fight Aging! archives for a quick overview of the relevance of SIRT3 to oxidative stress and longevity:

This research group proposes that Sirt3 acts on longevity through increasing antioxidants - we should all be appropriately skeptical, given the very mixed evidence for links between cellular antioxidants and longevity. That said, Sirt3 is located in the mitochondria, and the demonstrations of extended life spans through increased antioxidants have involved targeting those antioxidants to the mitochondria.

When considered in the broader context, a great many lines of research turn to point towards our mitochondria and the damage they suffer over time. All the more reason to direct greater efforts towards nascent mitochondrial repair technologies rather than yet more metabolic tinkering.

The early posts at Chronosphere are well done and worth reading. The theme is a detailed and picture-strewn look at the history of cryonics, mixed in with considerations of our presently imperfect society and where it might be going next: "Chronosphere is your gateway to a fundamentally new way of living - in pursuit of physical immortality in a world of our own making - free from the tyranny of time, and the burden of injustice. Chronosphere will explore and create interfaces with the scientific, technological, social and moral resources needed to achieve these ends. Because we are all at risk of dying, cryonics will be a central focus of Chronosphere for the foreseeable future, but will be by no means be the only technology explored here. Interventive gerontology, with a strong emphasis on immediate, or very near term interventions to slow cognitive aging, will also be explored in detail. Join us on our quest to transcend the limits of time!"

Link: http://chronopause.com/

Over at Chronosphere you'll find a weighty set of posts that aim to provide a foundation for critiquing cryonics at the organizational level of achieving consistently good cryopreservations, and the development of professional organizational cultures and processes - such as record-keeping - required to support that goal. All industries require ongoing initiatives that provide solid, constructive critiques of present practice, for otherwise how are the participants to progress and improve themselves?

You be the Judge: Understanding and Evaluating the Quality of Human Cryopreservations from Cryonics Organization Literature and Case Report Data, Part 1:

The goal of this series of articles is to equip the reader with the tools necessary to make an accurate assessment of the quality of care cryonics patients, both individually and as a group, are receiving from their respective cryonics organizations.

You be the Judge: Understanding and Evaluating the Quality of Human Cryopreservations from Cryonics Organization Literature and Case Report Data, Part 2:

In a very real sense, that care starts the moment the member/patient experiences his first contact with the cryonics organization that will ultimately cryopreserve him. The tenor of that first contact will likely determine the nature and course of the member's subsequent interaction both with cryonics and his cryonics organization. If cryonics is presented as a developed product that is costly but nevertheless fairly routine, say like buying a home or an automobile, that's very likely how it will be subsequently be treated. If, on the other hand, there is heavy emphasis on the lack of infrastructure to provide help in an emergency and the need to exercise both personal responsibility and personal preparedness, outcomes will likely differ - at least statistically, if not in each individual case.

You be the Judge: Understanding and Evaluating the Quality of Human Cryopreservations from Cryonics Organization Literature and Case Report Data, Part 3:

not only is it important that those caring for the patient know what is expected of them, the cryonics organization must also know what the family/caregiver's needs are, both logistically and psychologically. Cryonics is unfamiliar territory for family, and the procedures attending [the preparatory period immediately prior to cryopreservation] can perturb what in many cases will be a fragile emotional and psychological equilibrium in the patient's home life. Organizations that fail to establish rapport, and work to ascertain and meet the needs of the patient's family, risk non-cooperation, obstruction and even litigation. Seemingly small details, such as protecting flooring or furniture from water damage, or arranging for a few minutes of private "alone time" with the patient before he is removed from the home or care facility after acute stabilization, can mean the difference between heartfelt assistance, and bitter belligerence from the next of kin.

The quotes above hit some of the points I have had in mind in past years when discussing the need for cryonics organizations to (a) become more professional in character, and (b) form up a better product offering for customers, one that provides more in the way of service and guidance than is presently the case. That theme continues into the last of the four posts, linked below.

You be the Judge: Understanding and Evaluating the Quality of Human Cryopreservations from Cryonics Organization Literature and Case Report Data, Part 4:

Nevertheless, the real solutions to the problems discussed here are not easy, because they demand the acquisition of professionalism, knowledge, and skill in the context of cryonics as medicine. I personally believe that Jerry Leaf and I came very close to doing that in the decade between 1981 and 1991. But we failed. Why we failed will be discussed at a later time. Suffice it to say that the problem of maintaining professionalism is a nettlesome one in medicine, engineering and other demanding disciples that are vastly more developed than cryonics is today, and there will be no quick fixes.

"No quick fixes" is a conclusion I agree with. Nothing worthwhile is quick and painless to achieve, and even small industries change slowly when it comes to company cultures. The only reliable path to faster change involves money, as change follows rapid growth in the number of paying customers in any human endeavor. Unfortunately that growth remains elusive for cryonics providers, just as it has throughout that past decades. From where I stand, I'd say that the best near-term path to the goal of transformative growth in revenue lies in developing spin-off technologies in cryobiology and related fields - but that's an opinion offered without any great insight into the inner workings of the industry as it exists today. It is simply taken from the standard business texts: if you've consistently failed to achieve good growth with option A, then perhaps it's time to try options B, C, and D.

News of a study linking telomere length and cancer risk, but it's still the case that the relationship could be indirect, such as both sides of the correlation being based on levels of biochemical damage. For example, it might reflect the state of mitochondrial biochemistry in a person: "A new study suggests that shorter length of leukocyte telomeres - chromosome markers of biological aging - are associated with an increased risk of cancer and death from cancer. ... Telomeres are a structure at the end of a chromosome involved in the replication and stability of the chromosome. Genetic factors and environmental stressors can shorten the length of the telomere, and telomere length has been considered to be an emerging marker of biological age. Some research has suggested that short telomeres and chromosomal instability contribute to malignant cell transformation. ... [Researchers] conducted a study to assess the association between leukocyte telomere length and risk of both new-onset cancer and cancer death. Leukocyte telomere length was [measured] in 787 participants, free of cancer in 1995 ... Analysis indicated that short telomere length at the beginning of the study was associated with new cancer independently of standard cancer risk factors. Compared with participants in the longest telomere length group, participants in the middle length group had about twice the risk of cancer, and those in the shortest length group had approximately three times the risk. Cancer incidence rates were inversely related to telomere length, with participants in the group with the shortest telomere length having the highest rate of cancer."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-07/jaaj-lob063010.php

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

Hormesis is the process whereby suffering a little biochemical damage switches metabolism into a high-repair, damage-resistant mode, thereby extending life. Here, researchers examine changes in gene expression associated with hormesis: "Ionizing radiation generates oxidative stress, which is thought to be a major cause of aging. Although living organisms are constantly exposed to low levels of radiation, most studies examining the effect of radiation have focused on accelerated aging and diminished life span that result from high-dose radiation. On the other hand, several studies have suggested that low-dose radiation enhances the longevity of Drosophila melanogaster. Therefore, investigation of the biological effects of low-dose radiation could contribute to a more comprehensive understanding of the aging process. In this study, microarray and quantitative real time-PCR were used to measure genome-wide changes in transcript levels in low-dose irradiated fruit flies that showed enhanced longevity. In response to radiation, approximately 13% of the genome exhibited changes in gene expression, and a number of aging-related genes were significantly regulated. These data were compared with quantitative trait loci affecting life-span to identify candidate genes involved in enhanced longevity induced by low-dose radiation. This genome-wide survey revealed novel information about changes in transcript levels in low-dose irradiated flies and identified 39 new candidate genes for molecular markers of extended longevity induced by ionizing radiation. In addition, this study also suggests a mechanism by which low-dose radiation extends longevity."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20617381

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

A press release: "In a discovery that made headline news around the world, Dr. Zheng Cui, of the Wake Forest University School of Medicine, developed a colony of mice with super-charged granulocytes that successfully fight off many forms of virulent cancer. ... In a surprising turn of events Dr. Cui also found that a similar cancer-killing activity is present in the granulocytes of some healthy humans. ... When the Life Extension Foundation learned that this potential cancer cure was not being funded, it immediately made a $200,000 grant to fund the study at the South Florida Bone Marrow/Stem Cell Transplant Institute ... This new clinical trial will test this approach in humans with advanced cancer, including metastases, who have not been helped by conventional cancer therapies. The trial has received an IND (investigational new drug) status from the Food and Drug Administration (FDA) and Institutional Review Board approval. ... In January of this year, Dr. Maharaj notified the Life Extension Foundation that progress was being slowed because expected funding sources had dried up. Life Extension responded with another grant of $600,000 to further advance what could be a cure for cancer."

View the Article Under Discussion: http://www.prweb.com/releases/2010/07/prweb4239704.htm

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

A study found that the high intake of foods rich in trans fat can result to an increased risk of depression while eating foods rich in healthy fats like olive oil helps in reducing the risk.

Trans Fat

Trans fats can come from different sources and they naturally occur in meats and dairy products. They are commonly formed when vegetable oil is partially hydrogenated which converts it into semi-solids for a variety of uses and food applications. Food manufacturers have been using trans fat since it has a more stable flavor and longer shelf life. But different studies had found out that trans fat can increase the levels of bad cholesterol in the blood and result to health problems like hypertension, cardiovascular disease, chronic illnesses and obesity.

A few cities in the United States, including New York, had banned the use of trans fat in the preparation of food in restaurants and other food establishments. In addition to the known adverse effects of trans fat, a study from Spain includes a higher risk of depression to the list.

Trans Fat Can Increase the Risk of Depression

Researchers from the University of Navarra in Spain found that the consumption of foods and other source rich in trans fat can result to an increased risk of depression while eating foods rich in healthier fatty acids like olive oil can have the opposite effect. The study was based on the results of the SUN project which consisted of the more than 12,000 Spanish volunteers. The researchers found that study participants with the most amount of trans fat intake had a 48 percent greater risk of developing depression than participants who had less or no trans fat consumption. Their findings were published in the open online access journal PloS One. The study also found that monounsaturated fats and polyunsaturated fats like olive oil can lower the risk of depression.

The study was led by a professor of preventive medicine, Miguel Martinez. He noted that their study was based on a population with a very low trans fat intake. He added that, despite their limited trans fat consumption, they showed higher risk of suffering depression of about 50 percent. The trans fat consumption of the study participants only amounted to 0.4 percent of the total energy intake. Martinez explained that their findings are important especially to countries with high trans fat consumption like the United States which is at 2.5 percent.

The study participants consisted of more than 7000 women and 5000 men, whose ages averaged at 37. 5 years old. They were all part of the SUN project of the University of Navarra. The data gathered from the participants showed a strong link between trans fat intake and the risk of depression. The researchers said that the link was persistent and robust in each variation of the study. They were also able to observe the effects of healthier fats like monounsaturated and polyunsaturated fatty acids from olive oil to the risk of depression and found that these can help in lowering the risk. But despite the promising results, Martinez and his team said that their study will need further support from more studies and trials.

Depression

Depression is a serious health condition that causes drastic changes in mood, behavior and physical well-being. It has been found to significantly affect a person’s life as well as the lives of other people around him.  It is thought to be caused by different environmental, psychological and physical factors. In most cases, depression develops after physical and/or psychological trauma. But it can also happen for no apparent reason. Most people experience depression only once in their entire lifetime but others may suffer from a series of episodes with short intervals in between. For severe cases, medication may need to be taken permanently. Though depression can cripple a person’s ability to function properly, it is relatively more treatable than other psychological conditions.

The symptoms of depression includes unexplainable physical problems like headaches and back pain, sudden urge to cry for no clear reason, suicidal thoughts, difficulty in remembering, making decisions, concentrating and thinking, feelings of guilt and worthlessness, moments of self-pity and self-blame, tiredness, fatigue and lack of energy, edginess and increased indecisiveness, restlessness and agitation, excessive sleeping or insomnia, reduced sex drive, and feelings of frustration, unhappiness and sadness due to small things. The symptoms can vary depending on the person’s age and gender.

Medical professionals look at different possible causes of depression. The condition can be caused by changes in brain chemistry, dysfunction of neurotransmitters, hormonal imbalance, genetic make-up, early childhood trauma and sad life events like the loss of a loved one.

Health Benefits of Olive Oil

Olive oil is good for the heath. It is one of the richest sources of healthy fatty acids like monounsaturated and polyunsaturated fats. People living in the Mediterranean regions who have high olive oil consumption had been found to have better health and healthier hearts than people from other regions.

A study consisting of more than 5600 study participants found that following a Mediterranean diet can lower the risk of death from all natural causes. The researchers followed the participants for more than 6 years. They observed that people who are following a Mediterranean diet had 50 percent lower mortality rate than those who consumed foods rich in trans fat. They concluded that diet plans for the elderly needs to include more olive oil to promote longevity.

In 2004, the US Federal Drug Administration permitted the publication of claims saying that using olive oil can reduce the risk of coronary heart disease. Olive oil is not only rich in healthy fatty acids but it also contains health-promoting nutrients like phenolic compounds and antioxidants. The other compounds in olive oil like oleic acid and vitamin E prevents the oxidation of cholesterol and prevents it from creating plaques on the walls of the arteries. Olive oil also reduces the amount of free radicals in the body and the occurrence of inflammation. Health professionals recommend the regular use of olive for those with hypertensive conditions and people with high risk of developing cardiovascular disease. Olive oil has also been found to improve the cell’s response to insulin, making it a good recommendation for people with diabetes.

Sources
whfoods.com
foodnavigator.com
mayoclinic.org
mayoclinic.com

Discuss this post in Frank Mangano’s forum!

From the New Scientist: "when young mice are learning, a molecular fragment known as an acetyl group binds to a particular point on the histone protein that DNA wraps itself around - with the result that the cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group. ... This acetyl "cap" was missing in the older mice that had been set the same tasks. From this, the team concludes that the cap acts as an "on" switch for the cluster of learning and memory genes: removing the cap switches off the genes. Next, by injecting an enzyme known to encourage caps to bind to any kind of histone molecule, [researchers] artificially flipped the switch to the on position in old mice. The acetyl group returned to the histone molecule and the mice's learning and memory performance became similar to that of 3-month-old mice. ... it is still not clear why the switch flips off as we get older. One possibility is that it might help us cope with other cellular assaults that come with ageing, such as oxidative stress, [which] would mean that switching it on might have damaging side effects."

View the Article Under Discussion: http://www.newscientist.com/article/dn18870-gene-switch-rejuvenates-failing-mouse-brains.html

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

Yet another study showing a correlation between chronic inflammation and abdominal fat: "Obesity-related increases in multiple inflammatory markers may contribute to the persistent subclinical inflammation common with advancing age. ... We used factor analysis to identify inflammatory factor(s) and examine their associations with adiposity in older adults at risk for disability. ... [Inflammatory markers] were measured in 179 participants from the Lifestyle Interventions and Independence for Elders Pilot (Mean ± SD age 77 ± 4 years, 76% white, 70% women). Body mass index, waist circumference, and total fat mass were assessed by anthropometry and dual-energy x-ray absorptiometry. ... Greater total and abdominal adiposity are associated with higher levels of an inflammatory factor related to CRP, IL-1ra, and IL-6 in older adults, which may provide a clinically useful measure of inflammation in this population. ... [The associations were determined] after adjusting for age, gender, race/ethnicity, site, smoking, anti-inflammatory medications, comorbidity index, health-related quality of life, and physical function. These associations remained significant after further adjustment for grip strength, but only waist circumference remained associated with inflammation after adjusting for total lean mass." Waist circumference is a better correlation with the amount of visceral fat packed around the organs in comparison to body mass index.

Link: http://www.ncbi.nlm.nih.gov/pubmed/22451470

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

Kingsley G. Morse Jr. is one of the regulars at the Gerontology Research Group mailing list. He maintains a spreadsheet of all the life span studies in various organisms that he has been able to find, and is generally willing to sell that data at white paper rates, should you happen to be interested. He recently posted a histogram assembled from the study results, which I'm sure you'll agree is interesting:

The history of working to extend life in laboratory animals - and of studying effects on longevity and mortality in humans - is largely a big null result. Other than calorie restriction, the effects of which were first formally cataloged by scientists in the 1930s, all of the excitement shows up in the past twenty years or so. The successes are a tiny fraction of the studies that showed nothing, or showed a result well within the margin of error, or produced results that could not be replicated. In mammals, mostly mice, the bulk of studies that do extend life significantly fall in to the 15% to 30% life extension bracket - on a par with moderate to severe calorie restriction. Only a few methods have been demonstrated to reach beyond that point.

To a large degree this is because near everything tried to date has been a form of metabolic manipulation - change the operation of metabolism to slow the effective rate at which damage accrues to the organism. I would be surprised to see any great improvement in the length of life lived by laboratory animals until the research community changes strategy to focus on actually repairing and reversing the cellular and molecular damage that causes aging. The difference between slowing aging and repairing aging will be as night and day when it comes to the practical results that can be achieved.

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

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Researchers are making the first inroads into implanted machinery that can adjust the workings of memory, potentially leading in the years ahead to ways to restore memory function in the old: "Scientists have developed a way to turn memories on and off - literally with the flip of a switch. Using an electronic system that duplicates the neural signals associated with memory, they managed to replicate the brain function in rats associated with long-term learned behavior, even when the rats had been drugged to forget. ... Using embedded electrical probes, [scientists] recorded changes in the rat's brain activity between the two major internal divisions of the hippocampus, known as subregions CA3 and CA1. During the learning process, [CA3 and CA1] interact to create long-term memory ... experimenters blocked the normal neural interactions between the two areas using pharmacological agents. The previously trained rats then no longer displayed the long-term learned behavior. ... the teams then went further and developed an artificial hippocampal system that could duplicate the pattern of interaction between CA3-CA1 interactions. Long-term memory capability returned to the pharmacologically blocked rats when the team activated the electronic device programmed to duplicate the memory-encoding function. In addition, the researchers went on to show that if a prosthetic device and its associated electrodes were implanted in animals with a normal, functioning hippocampus, the device could actually strengthen the memory being generated internally in the brain and enhance the memory capability of normal rats."

Link: http://www.eurekalert.org/pub_releases/2011-06/uosc-rmr061211.php

Not all tissue structures need to be tailored to the patient - indeed, most of the present tissue engineering industry is in fact directly serving the research and development community rather than clinics. Engineered tissue is used for a broad range of testing, for example, and many life science research programs can progress more effectively with access to tissue structures rather than cells in a petri dish. As costs fall, that becomes an ever more practical alternative, meaning that research becomes more efficient and faster. Behind these falling costs lies a world of automation and infrastructure, leading towards assembly lines that produce pieces of living tissue for use in research and medical development:

Artificial skin for use in transplants or to verify the safety of the active ingredients of drugs, cosmetics and chemicals is a rare commodity. It is currently produced manually on a laboratory scale, and cultivation takes six weeks. The production volume is therefore limited to 2,000 pieces of skin per month, each one only a square centimetre in size. At a lab in Germany's Fraunhofer Institute, automation technology supplier Festo has helped to marry process automation with skin cultivation. The company's automation specialists recently helped the lab change its systems to achieve faster skin cell production

...

The new BioPoLiS organic production laboratory at the Fraunhofer IPA is home to what it says is the only facility in the world for the fully automatic in vitro production of up to 5,000 human skin models a month. The plant reflects the importance of bio-production, a combination of biology and automation technology. ... A particularly noteworthy feature is the continuous process chain. A single production line is used to handle cell extraction, cell proliferation, the cultivation of a three-dimensional tissue structure and cryonic preservation of skin models. Each process step is conducted without interrupting any of the others.

...

The scientists involved in the project are not content merely to produce skin. They say they plan to develop the technology further in the next two years to the point where other types of tissue, such as cartilage, can also be produced automatically.

Tissue is machinery, and we humans have accumulated a great deal of experience in how to build large amounts of homogeneous, quality-controlled machinery in a short period of time. So there is every reason to think that mass production of tissue structures for research and regenerative medicine will result in industrial processes that have much in common with the automated assembly lines that produce appliances or cars. As demand increases, and especially if therapies that use standardized tissues rather than patient-specific tissues become widespread, then we will see a much more of this sort of thing. An industry of large, specialized tissue factories is not an unrealistic expectation for the 2020s, though I would imagine that such a factory will look a lot more like a hospital, clinic, or microchip fabrication plant on the inside than the name might suggest.

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

An interview from the Scientist: "Cartilage is a firm, yet elastic, connective tissue that cushions joints and minimizes friction between bones. It is made up mostly of a matrix of collagen and proteoglycans and lacks nerve cells or blood vessels. In fact, cartilage contains only one cell type, the chondrocyte. A joint injury is often followed by progressive degeneration of cartilage, but there is hope that stem cells injected into damaged cartilage can help repair it. University Hospital Basel tissue engineer Ivan Martin discusses a recent study that sheds light on the mysterious process of cartilage regeneration by tracking labeled, implanted cells using a conventional MRI scanner ... [For treating cartilage injury] there is a very promising, relatively new technique - the use of autologous cartilage cells, or chondrocytes, which are expanded ex vivo and injected into the defective area. Even more recently, people have considered using mesenchymal stem cells, which are the progenitors of chondrocytes. ... We cannot just continue injecting cells and looking two years down the road to see if there is a change or not in the clinical results. We need to have control over the treatment we apply in order to understand the mechanisms of action and to be able to predict with better reproducibility the clinical outcome. This [MRI-based] technique would possibly contribute or provide the technical means to address this important scientific question."

Link: http://the-scientist.com/2011/05/30/cellular-salve/

Researchers are very interested in establishing biomarkers of aging and longevity, as at present the only truly reliable way to distinguish between long-lived and not so long-lived individuals is to wait and see what happens - which isn't an efficient way to run studies of potential therapies for aging. Here's an example of one line of investigation: "Wound healing (WH) is a fundamental biological process. Is it associated with a longevity or aging phenotype? In an attempt to answer this question, we compared the established mouse models with genetically modified life span and also an altered rate of WH in the skin. Our analysis showed that the rate of skin WH in advanced ages (but not in the young animals) may be used as a marker for biological age, i.e., to be indicative of the longevity or aging phenotype. The ability to preserve the rate of skin WH up to an old age appears to be associated with a longevity phenotype, whereas a decline in WH with an aging phenotype. In the young, this relationship is more complex and might even be inversed. While the aging process is likely to cause wounds to heal slowly, an altered WH rate in younger animals could indicate a different cellular proliferation and/or migration capacity, which is likely to affect other major processes such as the onset and progression of cancer. As a point for future studies on WH and longevity, using only young animals might yield confusing or misleading results, and therefore including older animals in the analysis is encouraged."

Link: http://www.ncbi.nlm.nih.gov/pubmed/21667230