Can We Say that Longevity Has Led to an Epidemic of Age-Related Disease?

I noticed an easy read of an open access position paper today that asks whether the common wisdom regarding the prevalence of age-related disease today is an open and shut case. Can we definitively say that, in comparison to our ancestors, we are not just living longer and are generally far wealthier, but are also suffering higher rates of cancer, cardiovascular disease, diabetes, and other chronic diseases suffered at the end of life? The general consensus as presented by the media and onlookers is that yes, it's an epidemic - really a terrible misuse of the word, since these age-related conditions are not infectious in nature - and there you have it. But here's a counterpoint:

Over the last 110 years, average global life expectancy has more than doubled from 31 years of age to 65 years of age. This trend is expected to continue, and many of the children born after the year 2000 can expect to live to celebrate their hundredth birthday. In the last 20 years alone, average life expectancy has increased globally by 6 years.

During the same period, doctors have announced a global epidemic of the most common killers: cardiovascular disease, diabetes, chronic kidney, and chronic obstructive pulmonary disease. One of the most important reasons for the more frequent recognition of these diseases is the fact that their diagnostic criteria have changed and become much more acute during the past few years.

These changes in diagnostic criteria have made it difficult, or even impossible, to compare the present statistical data regarding these diseases to historical data for the same illnesses. Due to this difficulty, there is no evidence-based comparison of the prevalence of any disease at present and in the past. Before announcing a global epidemic, a fair epidemiological comparison should be made, based upon the same definitions and using identical diagnostic tools.

In essence this is an argument based on the challenge of distinguishing between the consequences of longevity upon risk and levels of age-related disease and the effects of increasing wealth and improved medical technologies upon diagnosis rates. If you have more money and better medicine, you are more likely to be diagnosed, treated, and entered into the records than otherwise. Following this argument to its conclusion suggests that the effects of increasing wealth and longevity on disease rates are in fact lower than the raw data would imply, and that this effect will always be present in an age of improving technology and increasing wealth.

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

A Popular Science Article on Autophagy and Longevity

From Science News: "the cells of organisms from yeast to humans regularly engage in self-cannibalism. Cells chew on bits of their cytoplasm - the jellylike substance that fills their bellies - and dine on their own internal organs ... It may sound macabre, but gorging on one's own innards, a process called autophagy, is a means of self-preservation, cleansing and stress management. ... A munch here gets rid of garbage that might otherwise clog the system. A nibble there rids cells of malfunctioning parts. One chomp disposes of invading microbes. In lean times, all that stands between a cell and starvation may be the ability to bite off and recycle bits of itself. And in the last decade or so it has become clear that self-eating can also make the difference between health and disease. ... Starvation inhibits an important biological signaling system, known as the mTOR pathway - named for a key protein involved in regulating cell growth and survival, cell movement and protein production. The inhibition of mTOR sets off a cascade of reactions inside the cell that end in autophagy and may be crucial to prolonging cell life and ultimately fending off cancer. A drug that inhibits mTOR, called rapamycin, has been shown to extend life span in mice. It and calorie restriction are [amongst a handful of] methods proven to prolong longevity, suggesting both may work through autophagy to make cells live longer."

Link: http://www.sciencenews.org/view/feature/id/70887/title/Dining_In

Working Towards Replacement Neurons for Parkinson's Disease

Parkinson's researchers were among the first to earnestly attempt to create a specific cell type for transplant, and have continued to work at this. The obvious symptoms of Parkinson's are caused by the progressive loss of a thin population of dopamine-producing neurons, and therefore a way of replacing those specialist cells wholesale would be a way to temporarily reverse the course of the disease - perhaps for years or even decades in the best case. Thus these researchers now make up one of the more experienced scientific communities involved in cell therapy research, and can be counted on to rapidly pick up promising new developments in the control and reprogramming of cells. In past years, the focus has been on producing cells for transplant:

Once researchers have demonstrated control over cellular reprogramming, the ability to turn one cell type into another by providing suitable signals, the focus starts to shift away from transplants and on to reprogramming cells in situ: instructing the body - or the brain in this case - to directly produce more of the needed cell type. Here's an example for Parkinson's disease (PD):

In the first step towards a direct cell replacement therapy for Parkinson's, the team reprogrammed astrocytes to dopaminergic neurons using three transcription factors - ASCL1, LMX1B, and NURR1 - delivered with a lentiviral vector. The process is efficient, with about 18 percent of cells expressing markers of dopaminergic neurons after two weeks. The next closest conversion efficiency is approximately 9 percent, which was reported in another study. The dopamine-producing neurons derived from astrocytes showed gene expression patterns and electrophysiolgical properties of midbrain dopaminergic neurons, and released dopamine when their cell membranes were depolarized.

The Penn team is now working to see if the same reprogramming process that converts astrocytes to dopamine-producing neurons in a dish can also work within a living brain - experiments will soon be underway using gene therapy vectors to deliver the reprogramming factors directly to astrocytes in a monkey model of PD.

I'll go out on a limb and suggest that transplants are probably not the be-all and end end-all future of tissue engineering. By the time the 2020s roll around, I'd guess that most of the new therapies moving into US trials and clinical use overseas will be based on delivering increasingly precise and targeted reprogramming instructions into the body rather than introducing new cells or taking the patient's cells and working with them outside the body to produce tissue for transplantation.

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

Targeting via Nanoparticles versus Macular Degeneration

The use of nanoparticles to precisely deliver compounds to cells and specific locations within cells has a far broader application than just cancer therapies. Any existing drug that can be targeted this way can be made far more effective: provided in much smaller doses and with greatly reduced side-effects. For example: "Hitching a ride into the retina on nanoparticles called dendrimers offers a new way to treat age-related macular degeneration and retinitis pigmentosa. A study [shows] that steroids attached to the dendrimers target the damage-causing cells associated with neuroinflammation, leaving the rest of the eye unaffected and preserving vision. ... There is no cure for these diseases. An effective treatment could offer hope to hundreds of millions of patients worldwide. ... [Researchers] tested the dendrimer delivery system in rats that develop neuroinflammation. The target was microglial cells, inflammatory cells in charge of cleaning up dead and dying material in the eye ... When activated as 'trash collectors,' the cells cause damage via neuroinflammation - a hallmark of each disease. The microglial cells gobble up the dendrimers, and the drug then shuts down the cells' activity. ... Surprisingly, the activated microglia in the degenerating retina appeared to eat the dendrimer selectively, and retain them for at least a month. The drug is released from the dendrimer in a sustained fashion inside these cells, offering targeted neuroprotection to the retina. ... The treatment reduced neuroinflammation in the rat model and protected vision by preventing injury to photoreceptors in the retina. Though the steroid offers only temporary protection, the treatment as a whole provides sustained relief from neuroinflammation."

Link: http://www.eurekalert.org/pub_releases/2011-12/mc-nhm121311.php

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

Micromachines Steered Through the Blood

Nanotechnology can be used to build assemblies of designed molecules that seek out specific cells - such as cancer cells - but an alternative approach to targeted therapies is to build machinery large enough to be controlled from outside the body, such as the microcarriers demonstrated here: "Soon, drug delivery that precisely targets cancerous cells without exposing the healthy surrounding tissue to the medication's toxic effects will no longer be an oncologist's dream but a medical reality ... sing a magnetic resonance imaging (MRI) system, [researchers] successfully guided microcarriers loaded with a dose of anti-cancer drug through the bloodstream of a living rabbit, right up to a targeted area in the liver, where the drug was successfully administered. This is a medical first that will help improve chemoembolization, a current treatment for liver cancer. ... The therapeutic magnetic microcarriers (TMMCs) [are made] from biodegradable polymer, [measure] 50 micrometers in diameter - just under the breadth of a hair - [and] encapsulate a dose of a therapeutic agent (in this case, doxorubicin) as well as magnetic nanoparticles. Essentially tiny magnets, the nanoparticles are what allow the upgraded MRI system to guide the microcarriers through the blood vessels to the targeted organ. During the experiments, the TMMCs injected into the bloodstream were guided through the hepatic artery to the targeted part of the liver where the drug was progressively released."

Link: http://www.eurekalert.org/pub_releases/2011-03/pm-wf-031511.php

The Global Forum for Longevity

The Global Forum for Longevity is an industry-sponsored forum taking place later this month; fairly mainstream, no talk of radical life extension or other forms of futurism that might lead to intellectual discomfort for some. I mention it because it is a symptom of the growing interest in biogerontology on the part of the vast insurance industries of the world - which should not be a surprising phenomenon. To find people likely to pay close attention to the future of longevity science, you want to look amongst the folk who stand to gain or lose a great deal of money due to changes in human life spans. Life insurance, pensions, and other forms of making money through managing statistical risks on life expectancy data are, taken together, a very big business indeed.

So here an insurance conglomerate is, as many of them are, sponsoring an event to help spread knowledge through the system: from scientists to actuaries to risk managers and other decision makers in the food chain. Building bridges and forming communities is in and of itself a form of risk management in the long term: it is a way to lower the likelihood of unpleasant surprises by trying to better understand what the scientific community believes are likely outcomes for longevity science over the decades ahead.

Some quotes from the conference site:

We are living in an era of radical change. Longevity offers us all an opportunity to make more ambitious life choices and look to the future with renewed hope. This is why it is vitally important that we move quickly to meet the challenges which it poses for our society.

Drawing on its expertise as an insurer, AXA is playing its part by creating a space to convene an exchange between decision-makers and experts working to ensure this phenomenon is better defined and fully grasped: the Global Forum for Longevity.

...

Our conviction as an insurer and observer of demographic and societal changes worldwide, is that longevity is not a fate to be endured but instead an opportunity. We need to respond quickly in order to meet the challenges which it poses to our society.

"Challenges." One thing to bear in mind here is that the big insurance groups are inextricably tied in to the unsustainable pension promises made by politicians past and present in many countries around the world - unsustainable even with modest increases in longevity, never mind what is likely to result from the biotechnology revolution. So there is a certain amount of long term public relations work being undertaken by various parties so as to avoid becoming the sacrificial goat in the end when the system of entitlements collapses. You can make your own decision as to how much of the motivation behind this conference falls into that bucket versus the knowledge transfer aims discussed above.

Empires end when an entrenched elite can spend from the public purse and take on debt without immediate consequence or forethought, destroying the value of their currency in the process. Assuming (perhaps optimistically) that present economic empires survive the next couple of decades, a combination of foolish promises and increasing human longevity will be the rock that sinks them.

Having Friends Is Good For The Health, Says US Study

Not having any social bonds or friends can cause severe health problems in the long term.

According to researchers from the Brigham Young University, having and keeping friends over a long period of time actually contributes to a longer, healthier life.  Julianne Holt-Lunstad, one of the key researchers of the study, states that having no friends translated to the stress and potential damage created by smoking nearly a pack of cigarettes per day.

The study

Holt-Lunstad and other researchers analyzed existing data from over 140 studies and attempted to create a causal pathway between health and social bonds.  The data involved in the study were from more than 300,000 individual test subjects.  The study was published in the scientific journal PLoS Medicine.

Based on their analysis, having no strong social bonds with other people produced the following harmful effects on a person:

1. Having no friends to talk to and bond with meant a person was almost like an alcoholic.

2. Having no social bonds was also measured as being more harmful than not exercising regularly.

3. According to the study, obesity’s effects on the human body paled in comparison to having no friends at all.

What is a real friend?

To make friends and keep the good ones, you have to know what a real friend does.

1. A real friend trusts you for who you are and respects you for your  identity and practices.

2. Growing and changing doesn’t mean that you will lose a real friend.  Real friends understand that people are always in a state of change – but they do not lose sight of the reason why they became friends with you in the first place.

3. Real friends do not stifle you or make you feel that you have to be somebody you are not.  Real friends give people the necessary to grow and establish their own identity, separate from friends and peer groups.

4. Privacy and confidentiality is important in a real friendship – and real friends know how to keep to themselves the things they hear from a confiding friend.

5. Real friends are able to absorb or accept how people express what they think and what they feel.

6. Real friends are a joy to be with when you are facing personal challenges, because they can provide a certain measure of support so you can beat these obstacles in life.

7. A real friend does not drive away people who want to help.

8. Being with a real friend produces happiness – there is no pressure to be with the person, but a genuine desire drives you to bond with each other.

9. A real friend never takes advantage of another person, no matter what the circumstances are.

10. A real friend creates and nurtures an emotional bond that allows both of you to grow and reach your full potentials as a human being.

How do you make friends?

If you haven’t been socializing lately, you may feel that your social skills are quite rusty.  You may feel that no one would be interested in talking to you and being friends with you.

This is not true.  While the world is a hard place to live in, people are often very open and happy to accept newcomers and new friends.  You just have to leave your shell of elusiveness and isolation to make new friends.

Do you want to make new friends? Try the following places and events:

1. Identify other issues in your life and try finding a support group that fits your needs.  Support groups exist in every city and state in the United States, and many of these support groups have online presence, which means they won’t be hard to find.

2. Watched any good theatrical productions lately?  The theater is a good place to find good people to chat with and make friends with.

3. Love rock n’ roll music or country tunes?  Then go to a concert – we’re pretty sure that concerts are packed with enough people for you to find at least one or two people to connect with.  You just have to start a good conversation.

4. Other places that you can visit include art shows, book launches, poetry reading shows, etc.  Visit events that interest you – so you can meet and talk to like-minded people.

Having trouble reaching out to new people? Try the following:

1. Make good conversation with the new acquaintance and focus on listening rather than going on and on about yourself.  People generally love good listeners and they will warm up to you faster if you show that you genuinely want to know more about them.

2. After warming up to the new acquaintance, you may want to invite the other person to lunch or another event that he or she may be interested in.

3. If you’ve learned enough about your new acquaintance, watch out for news or updates in his field of interest.  Then you can call or drop him an email about the news – this is a great way to create a two-way channel of communication between budding friends.

4. If the person is doing something (like building a model airplane), offer your assistance – but don’t be too pushy, as this will make the other person avoid you.

How do you keep good friends?

Once you have made a good friend (or good friends), you have to make sure that your friendship does not die out – like a candle left out too long outside.  Here are some steps to maintain a good friendship for the long term:

1. A good friend is interested and participates in the interests and passions of his own friend.  Make sure that you join your friend in activities that he likes, and vice versa.

2. Small things like playing video games or even sharing a tasty meal can mean a lot to friends.  Talking and listening is a also an excellent way to show that you care for another person.

3. Keep the lines of communication open with your new friends.  Do not isolate yourself for no reason or cut them off when you feel frustrated or depressed.  Instead, keep an open line and talk to them about your problems . You might be surprised how efficient friends are in cheering other people up.  You have to be there for them too, when they need someone to lean on or listen to them.

4. The effort to maintain the friendship should not be one sided.  The  effort and responsibility should be shared equally by both parties, so make sure that you do your part and you remind your friend that he should exert effort as well.

5. Show your home to your friend – this act alone will tell your friend that you are comfortable with him and you trust him as a friend.

Sources:
newsmaxhealth.com
download.ncadi.samhsa.gov

The International Aging Research Portfolio Launches

A little while back, I was invited to preview an independent project under development at the behest of Alex Zhavoronkov, one of the trustees of the UK-based Biogerontology Research Foundation, a group with strong ties to the Methuselah Foundation and SENS Foundation communities. That project is now launched and open to the world: it is the International Aging Research Portfolio - "tracking international progress in aging research".

The site grants users access to research and funding information for over a million [projects]. The IARP is a fully searchable, flexible and highly scalable knowledge-management system developed to enable organizations to collaborate, track, analyze, structure, make decisions and set directions for future research efforts in aging. ... Aging research spans many areas of natural and social and behavioural sciences and requires a high degree of interdisciplinary and international cooperation. The goal of IARP is to provide a centralized decision support system for scientists, research institutes, funding organizations and policy makers involved in aging research.

If you are a statistics addict, this might keep you occupied for a while. The aggregated funding data and trends in research are particularly interesting, and could be more so if further sliced and diced. For example, funding by theory of aging:

Color me surprised that funding of work on telomeres in aging is so very far ahead - but there's the purpose of data mining, to learn. The hope here is that data mining tools that operate on this large data set will provide compelling benefits for the research community, such as by making it easier to match up research proposals to funding sources based on the sort of awards made in the past.

Public sources of funds are over-represented in this database by virtue of being public sources and thus producing records that are generally more accessible. One can imagine a slow extension of such a data aggregation operation into the private funding space based on the same provision of compelling benefits. If you make it worthwhile by streamlining the process of fundraising (on the research side) and the process of finding suitable projects to fund (on the funding source side), then people will use the system and in the process support its evolution and growth.

Manipulating Stem Cells to Treat Vascular Disease

An example of a class of stem cell medicine that involves manipulation of existing populations of cells in the body: "Circulating through the bloodstream of every human being is a rare and powerful type of cell, one that can actually create new blood vessels to bypass blockages that cause heart attacks and peripheral artery disease. Though everyone has these cells - called endothelial progenitor cells - they are often dysfunctional in people prone to vascular disease. Now researchers [have] discovered that a molecule - called Wnt1 - can improve the function of endothelial progenitor cells, increasing the blood flow to organs that previously had been cut off from the circulation. The finding could enhance clinical trials already testing these powerful cells in patients hospitalized with cardiac arrest. ... A number of studies in the past few years have suggested that genes that play an important role during early development and get 'turned off' during adulthood may also get 'turned on' or expressed again in response to injury, such as heart attack. [Researchers] found that one gene in particular, Wnt1, was expressed during development of blood vessels, shut off during adulthood and then re-expressed in angiosarcoma, a cancer of endothelial cells. ... treating these special cells with Wnt1 not only greatly increased their function but also their number. Next, [researchers] investigated what effect the protein would have on a mouse model of peripheral artery disease, an illness in humans caused by decreased blood flow to the extremities. They found that treating these animals with a single injection of the Wnt1 protein resulted in almost three fold increase in blood flow in the affected areas."

Link: http://news.unchealthcare.org/news/2011/march/wnt1

Stopping Metastasis

Cancer would be far less threatening a condition if metastasis could be reliably blocked: "Like microscopic inchworms, cancer cells slink away from tumors to travel and settle elsewhere in the body. Now, [researchers report] that new anti-cancer agents break down the looping gait these cells use to migrate, stopping them in their tracks. Mice implanted with cancer cells and treated with the small molecule macroketone lived a full life without any cancer spread, compared with control animals, which all died of metastasis. When macroketone was given a week after cancer cells were introduced, it still blocked greater than 80 percent of cancer metastasis in mice. ... macroketone targets an actin cytoskeletal protein known as fascin that is critical to cell movement. In order for a cancer cell to leave a primary tumor, fascin bundles actin filaments together like a thick finger. The front edge of this finger creeps forward and pulls along the rear of the cell. Cells crawl away in the same way that an inchworm moves. Macroketone latches on to individual fascin, preventing the actin fibers from adhering to each other and forming the pushing leading edge."

View the Article Under Discussion: http://www.bnl.gov/bnlweb/pubaf/pr/PR_display.asp?prID=1117

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

Amniotic Membrane Used to Repair Cartilage

A novel methodology in regenerative medicine: "The objective was to evaluate the utility of cryo-preserved human amniotic membrane (HAM) as a support for repairing human articular cartilage injuries, which have a very limited capacity for self-healing ... The results [show] that cryo-preserved HAM is useful as a scaffold for growing human chondrocytes in cell therapy and for repairing human cartilage injuries. ... It provides a more regular surface and fills in the cavities and fissures ... The authors cultivated the chondrocytes (cells that form part of the cartilaginous tissue), isolated from human articular cartilage, on the amniotic membrane over a period of three and four weeks. The amniotic membranes were used to develop 44 repair models of arthritic human articular cartilage in vitro, which was assessed between four and 16 weeks later. The HAM also bonds well with the native cartilage. ... In some models, we could not differentiate between where the native tissue stopped and the neo-synthesised tissue began. ... This tissue had a fibrous appearance and high cellular density (cellularity), which in some cases was greater than that of the actual native cartilage."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-06/f-sf-amu062310.php

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

A Conservative View of Longevity Science

This opinion piece is an example of the sort of viewpoint held by those who believe that metabolic manipulation to modestly slow aging is the only viable way forward in longevity science: "When I tell people that anti-aging drugs are no longer a distant prospect, they often assume I'm talking about the quest for immortality. That's not surprising, given the buzz generated in recent years by visionaries who speculate about re-engineering the human body to last thousands of years. But actually I don't find that far-out prospect very interesting - it bears the same relationship to serious aging science that warp-drive spaceships do to aeronautical engineering. What really grabs me are experimental advances that may impinge on the lives of people I know, maybe even mine. ... the only practical, near-term way to substantially increase healthy life span today is to simultaneously lower the risk of all diseases of aging. The way we now mainly buy time - administering therapies for one progressive, old-age disease at a time when it's too late to do much good - can't do that. Anti-aging drugs could, and at the same time they would go a long way toward ending the ruinously costly game of diminishing returns we're playing in geriatric medicine, as we eke out incremental gains with ever pricier palliatives. In effect, they would be preventive medicines of unprecedented scope and efficacy, drastically lowering the risk of everything from Alzheimer's to osteoporosis to wrinkles in the way that hypertension drugs now cut heart-attack risk."

View the Article Under Discussion: http://www.huffingtonpost.com/david-stipp/why-anti-aging-science-re_b_644308.html

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

Inflammation, Genetics, and Longevity

A review paper from Italian researchers who have been working on understanding inflammaging for a number of years: "Ageing is an inexorable intrinsic process that affects all cells, tissues, organs and individuals. Due to a diminished homeostasis and increased organism frailty, ageing causes a reduction of the response to environmental stimuli and, in general, is associated to an increased predisposition to illness and death. Actually, it is characterized by a state of reduced ability to maintain health and general homeodynamics of the organism. A large part of the ageing phenotype is explained by an imbalance between inflammatory and anti-inflammatory networks, which results in the low grade chronic pro-inflammatory status of ageing, 'inflamm-ageing'. It is strictly linked to immunosenescence, and on the whole they are the major contributory factors to the increased frequency of morbidity and mortality among elderly. Inflamm-ageing is compatible with longevity; even if centenarians have an increased level of inflammatory mediators in comparison to old subjects and they are very frail, they also have high level of anti-inflammatory cytokines together with protective genotypes. Actually, data on case control studies performed in Italian centenarians suggest that a pro-inflammatory genotype is unfavourable to reach extreme longevity in good health and likely favours the onset of age-related diseases such as cardiovascular diseases and Alzheimer's disease."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20549353

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

Nature’s Identity Crisis and Ours – SFGate

By Zach Bush MD, Paul J. Mills, PhD, Rudolph E. Tanzi, PhD, Michelle A. Williams, ScD

and Deepak Chopra MD

As our nation dives into sorrow and outrage over another merciless killing of a black man without cause, we must take the opportunity to transform a deep mindset. To achieve this, we will have to collectively shake off deep patterns of subconscious and conscious beliefs and experiences. The frequency of these instances of wrongful deaths and centuries of racially motivated abuses throughout the world creates hopelessness in our minds. For all of the rhetoric and grandstanding of our politicians and special interest groups, we do not see fundamental change happening. This hopelessness breeds violence, resignation, isolation, paranoia, and of course more fear.

Whatever the current crises happen to beright now it is COVID, racial injustice, police brutality, and street demonstrationsa familiar pattern has been nearly impossible to break. The crisis generates a public outcry, humanitarians face off against reactionaries, and once the worst of the crisis simmers down, things go back to normal. The great hope now, however, is that normal will finally be seen for its distorted abnormality.

In our view, this abnormality runs deeper than a pandemic or heart-rending injustice and inequality. A much-needed shift cannot take place until humankind passes through an identity crisis. How we see ourselves is presently through a distorted lens, and our illusions extend to the very basis of Nature herself. Human activity has despoiled Nature without conscience because humans, at our core, feel that this is our right as the planets superior life form. The contradiction here is that a truly superior life form would respect all of life, seeing the wonder and fragility of the miracle known as biodiversity.

Like many scientific terms, biodiversity sounds abstract and dry. To bring it home and give it vitality, one has to start with a simple fact: Each of us is as biodiverse as the entire planet. Our DNA was built from viral and bacterial DNA, and the constant communication between the genetic material of these micro-organisms keeps us dynamically alive, protected from disease and an intimate part of the chain of life everywhere.

Sadly, human activity has threatened biodiversity, and the stress we have placed on micro-organisms, even more perhaps than the extinction of species, is coming back to haunt us. The threat of COVID isnt isolated or unique. Natures most powerful urge is to keep life diverse and flourishing from the fundamental level of fungi, viruses, and bacteria, whose DNA outnumbers ours by a factor measured in millions and billions, if not more. Only in the past 30 years has research into the microbiome (the total mass of micro-organisms) brought to light how crucial Natures balancing act actually is. Without the bacteria, viruses and fungus that inhabit our bodies, human life would not be possible. As Earth is a symbiotic collection of diverse species cohabitating to give our planet life, so are we, and as with Earth, balance is the key.

The recent science discoveries in the microbiome have been a mind-bending experience as this once unseen world has come alive under our microscopes, through genome sequencing and through advances in computational biology. The notion that human DNA is somehow superior and separate from the DNA of bananas, mice, a cold virus, or mushrooms has toppled. It is humbling to realize that we arent at the center of life on earth. We mingle with planetary DNA with every breath, and the jet stream regularly populates the local air with viruses spinning around the globe in a matter of days. The ecosystems around us and within our own bodies team with millions of species of bacteria, fungi, protozoa, and parasites that vastly outnumber us and, humbling to realize, make us viable. We are at once a genetic speck in the vast thriving microcosmos of life, yet also in a position of critical responsibility to help maintain this extraordinary diversity.

The human gut microbiome, which is essential for digesting food, contains trillions of bacteria, outnumbering our human cells by more than 10 to 1, and this is not even considering the far more diverse kingdoms of fungi and protozoa within us. Beyond the confines of the gut, each internal organ, from the liver to the breast, kidneys, and even the brain, is now recognized to depend on unique ecosystems of microorganisms that keep our cells healthy. Over 90% of the work done by enzymes in the human body is done by the microbiome. The same non-human life force works with endocrine cells within the gut to produce over 90% of serotonin, a neurotransmitter necessary for our much-touted human brain to function.

Once you realize that you and the planets biodiversity are one, nothing less than a shift of identity follows. An adage from ancient India, As is the greatest, so is the smallest, has never been truer. Microbiome diversity is the foundation for health and longevity, while the destruction of this diversity is the beginning of chronic disease of every variety. The adage could be expanded to As is the outside, so is the inside. The global microbiome functions as a communication network that actually passes electrical information throughout the cellular matrix to coordinate everything life needs to thrive at the cellular level, not simply nutrition and reproduction but repair and adaptation to changing conditions.

Nature is managing its own identity crisis now. Natures fluent communication network cannot be produced by a single species, but it can be threatened by one. At the exact moment in history when our existence is being understood as one thread woven in the tapestry of life as a whole, we are tearing the fabric apart, and all life forms will suffer. To give one instance, every year over 4 billion pounds of glyphosate (the active ingredient in the most commonly used herbicides) is sprayed into our soil, water, air, and foods, sterilizing the microbiome and harming the creatures, including us, that the microbiome nourishes.

Life on earth is at risk for extinction because of our war against diversity. The scale of damage is too frightening to contemplate, much less measure. We must transform now. The victims of this war are standing right in front of us. The soil, wind, and water, the First Nations, African Americans, Hispanics, Asians, and the tide of refugees. The worlds dispossessed and disenfranchised depend on us to emerge from our false assumed identity of superiority over and separateness from the whole of life. Reconciliation can begin today. Train your mind and eye to seek out and cherish diversity in every element of your life.

Breathe and explore a new ecosystem this week. Create and listen to a more diverse community, both within your body and all around you. Plant a seed and a new relationship this week. Get curious and explore what is different from you, so that we can quickly discover what we all share. Life everywhere calls out to be saved. Life everywhere calls out to be loved.

DEEPAK CHOPRA MD, FACP, founder of The Chopra Foundation, a non-profit entity for research on well-being and humanitarianism, and Chopra Global, a modern-day health company at the intersection of science and spirituality, is a world-renowned pioneer in integrative medicine and personal transformation. Chopra is a Clinical Professor of Family Medicine and Public Health at the University of California, San Diego and serves as a senior scientist with Gallup Organization. He is the author of over 89 books translated into over forty-three languages, including numerous New York Times bestsellers. His 90th book, Metahuman: Unleashing Your Infinite Potential, unlocks the secrets to moving beyond our present limitations to access a field of infinite possibilities. TIME magazine has described Dr. Chopra as one of the top 100 heroes and icons of the century.

ZACH BUSH, MD is an internationally recognized educator and thought leader on the microbiome as it relates to ecology, human health, and consciousness. Board certified in Internal Medicine, Endocrinology and Metabolism, and Hospice Care, his published biomedical research ranges from chemotherapy development to the role of the microbiome and agricultural toxins in human health and disease. He is founder and CEO of Seraphic Group, Inc., an IP development firm committed to developing root-cause solutions to bring balance to the biome of our planet. His non-profit, Farmers Footprint, is raising awareness of the synonymous nature of human and soil health, and working to create a roadmap to end chemical food production and ecologic destruction through the universal adoption of regenerative agriculture.

Paul J. Mills, Ph.D. is Professor and Chief in the Department of Family Medicine and Public Health and Director of the Center of Excellence for Research and Training in Integrative Health at the University of California, San Diego. He has expertise in Integrative Medicine and psychoneuroimmune processes in wellness and disease, with approximately 380 scientific manuscripts and book chapters on these topics.

Rudolph E. Tanzi, Ph.D. is the Vice-Chair of Neurology, Director of the Genetics and Aging Research Unit, Co-Director of the Henry and Allison McCance Center for Brain Health, and Co-Director of the MassGeneral Institute for Neurodegenerative Disease at Massachusetts General Hospital. He also serves as the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School. Dr. Tanzi discovered several Alzheimers disease genes, including all three early-onset familial Alzheimers genes, and serves as director of the Alzheimers Genome Project. He is also developing therapies for treating and preventing AD using human mini-brain organoid models of the disease, pioneered in his laboratory. Dr. Tanzi has published 600 papers, received numerous awards and was on the 2015 TIME100 Most Influential People in the World list. Dr. Tanzi is a New York Times bestselling author, who has co-authored Decoding Darkness and three bestsellers with Deepak Chopra: Super Brain, Super Genes, and The Healing Self.

Michelle A. Williams, SM 88, ScD 91, is Dean of the Faculty, Harvard T.H. Chan School of Public Health, and Angelopoulos Professor in Public Health and International Development, a joint faculty appointment at the Harvard Chan School and Harvard Kennedy School. She is an internationally renowned epidemiologist and public health scientist, an award-winning educator, and a widely recognized academic leader. Prior to becoming Dean, she was Professor and Chair of the Department of Epidemiology at the Harvard Chan School and Program Leader of the Population Health and Health Disparities Research Programs at Harvards Clinical and Translational Sciences Center. Dean Williams previously had a distinguished career at the University of Washington School of Public Health. Her scientific work places special emphasis in the areas of reproductive, perinatal, pediatric, and molecular epidemiology. Dean Williams has published over 450 scientific articles. She was elected to the National Academy of Medicine in 2016. The Dean has a masters in civil engineering from Tufts University and masters and doctoral degrees in epidemiology from the Harvard Chan School.

Go here to read the rest:
Nature's Identity Crisis and Ours - SFGate

Longevity Science and the Social Justice Viewpoint

It is always a good idea to learn more about how the other half of the world thinks. Most people are closer to the values of social justice than the values of libertarianism, for all that that sort of "justice" (i.e. forced redistribution and mob envy) is just as destructive of wealth and progress as communism or fascism when put into earnest practice. It becomes a tyranny of egalitarianism, a leveling down, a tearing down of the high points of society, the groups that produce advances in technology. One of the values of reading In Search of Enlightenment is seeing the thinking that leads someone enmeshed in the culture of social justice - whose members characteristically belittle or reject scientific progress and the markets that drive it - come to advocate for longevity science and the defeat of aging: "Over the past decade I have worked at the intersection of issues in political philosophy/theory and the medical sciences. I have tried to help bridge what I take to be a troublesome divide between the field most concerned with ideals of justice and equality, and scientific advances (especially in the field of biogerontology) which could profoundly improve human health and prosperity. These two things are linked in important ways, but there is very little actually written by theorists on these kinds of topics. Bridging this gap is an up-hill struggle for a variety of reasons. The theoretical concepts and normative theories developed in political philosophy over the past 4 decades either ignored the realities of morbidity (e.g. like the fact that aging is a major risk factor for disease) or just assumed people went through their complete lives as 'healthy and productive members of society'. This meant the (almost exclusive) focus of theories of distributive justice was on the distribution of wealth and income. A fair society could be measured, so went the reasoning, to a large extent by the pattern of the distribution of a society's wealth. And the extent to which theories of justice have expanded, in the last 2 decades, to tackle topics like global justice and health, they are still constrained by the original assumptions and limited perspectives/concepts with which the dominant normative theories were originally devised. In other words, taking a theory of domestic justice designed to apply to a healthy and affluent society and then trying to make a few modifications once you take disease and debt seriously is not, imho, a recipe for success."

Link: http://colinfarrelly.blogspot.com/2012/06/how-to-put-aging-and-biogerontology-in.html

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

A Look at the Changes in Mortality in the Past Century

An article from the New England Journal of Medicine has been doing the rounds: it looks at some of the changing causes of mortality over the past century. These changes are signs of success in the progress of medicine and technology: both might be thought of as the search for ways to prevent suffering and death - one cause at a time. With each passing generation in a time of progress, some of those causes are largely eliminated, leading to a shift in focus and new targets. The degree to which infectious disease has been tamed is very clear from the graphics in the article, though there is always much more to be done on that front:

The article itself really isn't worth reading - the authors burble about policy without really saying anything, and certainly nothing meaningful is put forward. It's exactly the sort of thing you don't want to hear from people involved in research or medicine. If you can't clearly say "it's a priority to build new and better medicine, and we're working on a portion of that goal right now," then probably best to leave the conversation about medicine to other people. Here the peanut gallery has more to offer in the way of occasional meaningful comments:

The first thing to notice here is how much our mortality rate has dropped over the course of a century, largely due to big reductions in infectious diseases like tuberculosis and influenza.

On the large scale, medicine chases the priorities of the now - and in wealthier regions of the world that has become cancer and heart disease. The size of the cancer and heart disease research communities reflects the present degree to which the two groups of conditions contribute to human mortality. What it does not yet reflect is the new and more meaningful unified way of looking at the conditions that kill the most people: that they are all caused by aging, and stem at root from a limited range of mechanisms and changes that happen over the years as a byproduct of our normal metabolism. We rust, and that rust blossoms into a thousand different failure modes. Yet medical science is still largely focused on end states, and patching over catastrophic damage rather than preventing its origins.

To keep reducing the human mortality rate, the research community has to start in on prevention in the form of repair biotechnologies - ways to halt and reverse the earliest development of the age-related conditions that kill most people. It is as much a cultural change in the life sciences as it is a technical challenge, as the path ahead is fairly clear. This is why organizations like the SENS Foundation, mixing aggressive advocacy with targeted research work where few others are making progress, are so important. It is not so much that they will get the work done by themselves, but that they will spawn a sea change in the research community, such that many, many groups will tomorrow be performing similar work with similar end goals: to to be able to treat and reverse the course of aging.

You might think of a focus on aging and its causes as the germ theory of today's medical community: a unifying set of ideas and resulting research strategies that will bring the bulk of the medical community onto a better path forward, one that will lead to a more rapid improvement in the human condition, and longer, healthier lives for all.

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

Politics, Perceptions, and Money

Politics, perceptions, and money: these are the guiding trinity of research at the grand scale, the source of determinants for the work of thousands of researchers and the rate and direction of progress in broad fields of medical science - or so says the author of this article on the state of longevity science:

It has been clear for many years that the rate of aging is malleable in diverse species, and the discovery in 2009 that a drug called rapamycin can extend maximum life span in mice suggested that it's now technically feasible to develop anti-aging agents that really work as advertised. Unfortunately, I see no commercial interest in doing so.

The focus here is the mainstream of research, aimed at slowing aging by metabolic manipulation. This, as you all know by now, is the slow boat to nowhere in my view. The only practical way ahead that seems plausible to produce meaningful rejuvenation of the old in our lifetimes is some variant of SENS, the Strategies for Engineered Neligible Senescence: focus on repair and reversal of damage, not on slowing down the rate at which damage accrues. Repair is no harder, and arguably an easier path, and the end result will be far more effective in terms of years gained and suffering quashed. But SENS and other repair strategies yet to emerge into a coherent research program are the minority view in the field, still working to attain recognition and funding - bear that in mind when you read about the hurdles that groups with far more credit in the scientific community are struggling with. It's a long way from here to where we need to be, and there are two battles yet to win: firstly to persuade the research community to adopt the better strategic direction that SENS represents, and secondly to persuade some fraction of the world that reversing aging through biotechnology can and should be achieved within a matter of a few decades.

But back to the article:

Prominent advisors to the National Institute on Aging, as well as some of its officials, are enthusiastic about anti-aging drugs' huge potential to improve public health. In fact, a few years ago the NIA's founding director, the late Robert N. Butler, joined three visionary gerontologists to urge that the federal government mount a major program to accelerate development of such medicines, including funding for clinical trials and the preclinical research needed to make them feasible.

But the idea of investing taxpayer dollars in such a program has proved a very hard sell. As gerontologist Richard A. Miller once put it, "A president who announces a war on cancer wins political points, but a president who publicly committed the government's resources to research on extending people's life span would be deemed certifiable."

Which gets us to the root problem: Few people - including policymakers and medical experts who advise them - appear to realize that the ability to brake aging is now within our grasp, and that even modestly effective anti-aging drugs promise the biggest gains in public health since the advent of vaccines and antibiotics nearly a century ago. Indeed, I suspect most people still regard aging as an inalterable part of the human condition - a view reinforced by the fact that pharmaceutical companies just say no to anti-aging drug development.

An important line item that the author omits is that Big Pharma - and a hundred biotech startups, if there were any justice in the world - don't engage in longevity science because the FDA will not approve therapies for aging, and indeed could not possibly ever approve therapies for aging under its present regulatory regime. There is no way to sell to the clinics in the US marketplace, so there is no potential profit for US-based developers, so there is next to no venture funding for development of promising longevity science. Politics, perceptions, and money - and it's the political and regulatory establishment that is the biggest roadblock here.

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

Transdifferentiation to Simplify Generation of Cells to Order

Researchers are slimming down the process of generating specific types of cell to order, turning the multi-step induced pluripotency processes of the last couple of years into a single step: researchers "have succeeded in obtaining somatic stem cells from fully differentiated somatic cells. [Scientists] took skin cells from mice and, using a unique combination of growth factors while ensuring appropriate culturing conditions, have managed to induce the cells' differentiation into neuronal somatic stem cells. ... Our research shows that reprogramming somatic cells does not require passing through a pluripotent stage. Thanks to this new approach, tissue regeneration is becoming a more streamlined - and safer - process. ... One factor in particular, called Brn4, which had never been used before in this type of research, turned out to be a genuine 'captain' who very quickly and efficiently took command of his ship - the skin cell - guiding it in the right direction so that it could be converted into a neuronal somatic stem cell. ... This interconversion turns out to be even more effective if the cells, stimulated by growth factors and exposed to just the right environmental conditions, divide more frequently. ... Gradually, the cells lose their molecular memory that they were once skin cells. ... It seems that even after only a few cycles of cell division the newly produced neuronal somatic stem cells are practically indistinguishable from stem cells normally found in the tissue. ... So far, insights are based on experiments using murine skin cells; the next steps now are to perform the same experiments using actual human cells. In addition, it is imperative that the stem cells' long-term behaviour is thoroughly characterized to determine whether they retain their stability over long periods of time."

Link: http://www.mpg.de/5548755/stem_cells_skin_cells

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

More Evidence to Show that Excess Fat Causes Chronic Inflammation

Chronic inflammation is a bad thing - it greatly increases your risk of suffering age-related disease, and may be one of the more important mechanisms linking excess fat tissue to risk of disease and lowered life expectancy. Here is more evidence to show that being overweight exposes a person to greater inflammation: "Postmenopausal women who were overweight or obese and lost at least 5 percent of their body weight had a measurable reduction in markers of inflammation. ... Both obesity and inflammation have been shown to be related to several types of cancer, and this study shows that if you reduce weight, you can reduce inflammation as well. ... Women in the trial who were assigned to a weight loss intervention had a goal of 10 percent weight reduction during the course of one year achieved through a diet intervention with or without aerobic exercise. ... The researchers measured levels of C-reactive protein, serum amyloid A, interleukin-6, leukocyte and neutrophil in 439 women. At the end of one year, C-reactive protein reduced by 36.1 percent in the diet-alone group and by 41.7 percent in the diet and exercise group. Interleukin-6 decreased by 23.1 percent in the diet group and 24.3 percent in the diet and exercise group. ... there were greater reductions in these measures among women who lost at least 5 percent of their body weight. They also found that exercise alone, without a dietary weight loss component, had little effect on inflammation markers."

Link: http://www.eurekalert.org/pub_releases/2012-05/aafc-wll042412.php

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