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2016 Reminder Healthy Living Can Add Up To 14 Years to Your Life

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The Ethics of the Future: Human Genetic Engineering and Human Immortality Medicine is Coming in 19 years!!

Posted: January 1, 2015 at 12:46 pm

The Ethics of the Future: Genetic Engineering and Immortality Medicine

2015 is Going to Be a Fascinating Year for Longevity Science

By Professor Mark

How do you feel about the potential for great advances in Human Longevity Science that have been occurring in recent years? Do you feel excited about the prospect of living a much longer life, or are you indifferent? Are you nervous about the prospects of what this sort of tinkering with genetics and human nature might bring?

Is the potential for a vastly expanded lifespan going to be something that everyone can enjoy, or will it be an advantage simply for those that can afford it? If you could live 100 years longer, would you want to? Would you care if the opportunity were afforded to you as an individual? Would such a huge opportunity lead to a new and beautiful life on earth, or would earth somehow take these momentous advantages and turn the world on its head?

My Beliefs Regarding Advanced Genetic Engineering

Many years ago, when I was an undergraduate at Penn State, our professor posited similar questions in our Genetics Class, which played a major role in affecting my beliefs toward the subject of hyper-longevity and Genetic Engineering. The class was large, with more than 100 students, and my professor asked the class what their opinions were regarding the use of genetic manipulation and engineering to alter human life.

Surprisingly, the class was completely silent. In response to this silence, the professor called up two students to debate the subject. One of my classmates volunteered to voice his opposition to genetic engineering, and I chose to volunteer, providing an argument in favor of it.

My opponent voiced his opinion to the class that genetic engineering for this purpose would be ethically wrong because it is not in man’s best interest to play God. Most of our classmates seemed to agree, nodding subtly in agreement.

Personal Aesthetic: Choosing to Be Different

I felt as though I was standing upon a grand crossroads of history. As I looked around the class, it felt as though all of my classmates, for all of their cliquish differences, were being incredibly closed-minded, like they just accepted what they had been told all their lives and were afraid to think for themselves.

After the professor gauged the response of the students, I had my opportunity to argue in favor of this advanced human genetic engineering. I glanced around the class, and felt my argument come together cleanly in my mind. I saw white girls with bleached hair stretching down their backs, more than a few of which had fake breasts. I saw black girls with expensive weaves and complex and expensive hairstyles.

There were white students mimicking their hip hop and rap idols, and I even saw a young Asian student that had very obviously dyed her hair red. In my class I saw a great commingling of different styles. People both attempting to exemplify American standards of beauty and those taking on the aspects of other cultures, adopting them as their own.

As I looked around at all of this, recognizing the great diversity in my class, I had a strong feeling that there was not one person in the class that didn’t have at least one thing they wanted to alter about the characteristics they were born with. I continued thinking to myself, that these students probably wanted to be different in a variety of different ways: some wanted to be smarter, some taller. Some girls wish they had larger breasts, and some guys wanted larger penises. Others probably wish that they didn’t have to go through the trouble to put in contacts and hair dyes to look like the person they wish they were. For myself, I would have given anything just to be a few inches taller.

A Call for Genetic Freedom

After standing quietly for a moment, with all of these thoughts running through my at head a rapid place, I spoke from my position, in the back of the class, and suddenly stated loudly: Genetic Freedom!

I felt that just those two words spoke for themselves, but my professor threw a dejected glance in my direction, and I could detect her shaking her head almost imperceptibly. Her silence was a sign that she needed more. After the brief silence, I continued. I argued to the class that the individual should have full control to alter his DNA as he sees fit, so long as it doesn’t negatively impact society or the rights of anyone else.

She seemed thoroughly unhappy with the argument, and the class began to chatter loudly, nearly in unison. After the short spate of controlled chaos, the class continued with liveliness and energy, but I felt that others in the class largely shunned me as a result of the fervent beliefs I expressed in regard to what legitimately amounted to the potential future of the human race.

Will People Be Able to Resist Genetic Alteration?

I still laugh to myself to this day about how my belief met such incredulity in the face of so many. In the future, once science makes it possible to make such powerful changes to humanity at the genetic level, I am confident that these same students, if given the actual opportunity to improve themselves through futuristic genetic methods, would absolutely jump at the chance with no second thought.

It wouldn’t be Playing God. It wouldn’t be unethical. It would simply be the new reality. In fact, once the time comes to pass when Genetic Alteration becomes a reality, the exact same people today that seek out plastic surgery and cosmetic surgery will clamor for these procedures as soon as they become available. In the end, I believe I made a B in the course, which is regretful, because I’ve always remained highly interested in genetics.

The Future of Humanity: The Organic and the Engineered

Another of my professors at Penn State, himself with a doctorate in genetics, explained an interesting aspect of human evolution, one which I had never thought of before. He explained that the many races that make up humanity as a whole developed their differences as a result of dispersing far from one another, and slowly adapting to their new environments over time.

After they migrated, geography, distance, and other factors kept them from interacting heavily with one another, which caused their minor adaptations to become more pronounced. In the same way that they developed their own habits and cultures, their aesthetic and physical makeup also changed. Some grew taller, others grew paler, and each individual culture became maximally resistant to the diseases which were prominent in their area.

Even though these physical and genetic changes were significant, any healthy woman on earth could still mate with any other healthy man, no matter how different he looked or acted. What he said that truly sparked my mind was that if the different races of human beings stayed geographically isolated from one another for longer period of time, eventually the different races could have changed enough to where they could no longer produce children with one another.

Could Genetically Engineered Humans Evolve Beyond Humanity?

This can also apply to the future of genetic engineering. The modern world is so interconnected that geography has no impact on the ability of humans to breed with one another, but genetic enhancement may lead to a point at which a human born today would not be able to mate with an individual that was the result of generations of genetically altered parents.

As Genetic Engineering becomes more advanced, humans may change enough at the genetic level to prevent interbreeding between lineages which have undergone these advancements and those that chose not to. This change would of course be gradual, first reducing the ability to conceive before denying that ability altogether. At this point, it would take genetic engineering just to create a viable child for two disparate humans. Interestingly enough, it may even come to pass that different species of humans evolve from such endeavors, as distinct from one another as they are from humans themselves.

The beginning of this story could begin sometime in the next hundred years, as scientists and medical specialists develop the ability to safely and effectively alter DNA to meet the specifications of the individual.

The Future is Coming: the Great Human Divergence and the Neo-Sapient

The people that choose to reject Genetic Modification and Advanced Longevity Treatments in the near future will create an interesting binary world. This could be the beginning of a grand human experiment. This could be the focal point of a genetic divergence so strong that it literally fragments the human race, creating a new class of post-humans that have advanced to a point where they qualify as their own unique species.

I think back to the genetics course I mentioned earlier. I remember the absolute ocean of diversity that was contained within the 100-student course, and I was able to visualize a future in which Genetic Modification leads to even greater diversity, and a uniqueness that has never existed in the history of the human race. It made me think of the diversity of the universe, and the unlimited options for diversity that it represents. As someone with an affinity for astronomy, I find it utterly inconceivable that planet earth is home to the only lifeforms in the universe.

Of course, along with my great optimism, I do recognize that there are risks and unknowns related to the future of Genetic Modification. There is even the potential that the science behind Genetic Modification could be used for Genetic Warfare. There is certainly the potential that the same science that creates a new humanity could be used to destroy large swathes of it. I can imagine an apocalypse that is not nuclear and grandiose, but genetic and nanoscopic.

Post-Humanism and the Search For Other Worlds

In the end, will humans be able to develop interplanetary travel and colonization in order to insure itself against such potential apocalyptic scenarios? It’s a subject that I am particularly concerned with, and is the core reason why I support NASA and the United States Space Program. As the world moves faster and the dangers become greater, it is imperative that we are able to save humanity even in the case of a state of mutually assured destruction.

If there truly is a Genetic Revolution on the horizon, it is vitally important that we use all of the resources we have available in order to make our dreams of space colonization a reality. Imagine a future so spectacular: A future where a multitude of post-human species advance outward from earth in order to colonize space like a rainbow across the galaxy.

This journey will be arduous and epic, as earthlings spread across the cosmos in order to find new viable homes and potentially interact with other life forms.

What Would Aliens Be Like?

Can you imagine how literally otherworldly that would be? If we found advanced aliens, would they have unlocked the key to eternity? Would we have done the same? There is no doubt that the first time that we make contact with an extraterrestrial species, they will come from worlds and cultures which are absolutely unimaginable in the face of everything that we have experienced.

I may have delved a bit into the realm of science fiction, but the future of humanity in the face of Genetic Modification has the potential to be every bit as exciting and otherworldly as the potential future that I just described. It instills a tremendous sense of fear, awe, and most importantly, unlimited potential.

Do You Think That You Could Handle Immortality?

If you ask the average person out on the street about the potential future afforded by Genetic Engineering, Advanced Longevity, and Immortality medicine, you’ll likely get a number of different responses, some positive, some negative, others simply incredulous. If you surveyed 100 people, I believe that you would find that the majority would ultimately reject the idea of immortality.

Some people think that eternity would take the excitement out of life. Others fear that they would eventually just become a broken shell of their former selves as their bodies physically decline in spite of science’s ability to prevent death. For many, the concept of eternity is just as fearsome as the concept of death itself. It’s not all that different from the way that people feel about retirement these days. They are frustrated because they have to work so hard all through the healthiest part of their lives only to be too frail and broken down by the time they retire to enjoy it.

Longevity Medicine and the Future

That’s why Longevity Medicine is so important. We want our retirement years to last as long as possible, and we want to be able to enjoy them. Maybe one day, we will be retired as long in our lives as we are at work, or longer! That’s what the approach to immortality will be like!

There are a growing number of people that are optimistic about a lengthy future. They understand that even with regard to a concept like immortality, life is the sum of individual experience. Some will take advantage of a life bordering on immortality, while others would simply choose to be boring. People that live lives full of happiness and vitality shouldn’t be deprived the opportunity to extend that joy, simply because there are others who wouldn’t appreciate it!

The arguments stemming from the subject of Human Immortality continue to become both more interesting and more complex, both for those that long for such a fate, and those that oppose the concept. No matter how you feel about the idea of Advanced Longevity, there is no doubt that such opportunities to live lives we now consider unimaginable will eventually come to pass.

As long as human beings are able to engage in scientific advancement without destroying ourselves or sending ourselves back to the stone age, such opportunities will present themselves to the human race in the near future.

Gene Therapy and Stem Cell Therapy: The First Steps to Hyperlongevity

The seeds of these future endeavors are being planted today, in the fields of gene therapy, genetic medicine, and stem cell therapy. This is also the core concept behind medical treatments which seek to optimize hormone production in the body in order to alleviate the medical conditions associated with hormone imbalance and aging.

Hormone Replacement Therapy: Streamline Your Body for the Future!

Treatments such as Testosterone Replacement Therapy, Sermorelin Acetate Therapy, and Bio-Identical Human Growth Hormone Replacement Therapy seek to correct common hormonal imbalances that occur as a result of the aging process. There is even a strong argument that these hormone imbalances are actually the root cause of many symptoms of aging, including frailty, osteoporosis, and cognitive decline.

There are many Health, Wellness, and Longevity Physicians that believe that these forms of Hormone Replacement Therapy are some of the must effective means to prolong a healthy and active life when used in combination with a healthy and conscientious lifestyle. These medical treatments are the best way to decrease your mortality risk so that you are more likely to experience the next great advancement in Anti-Aging Medicine.

If you feel that your quality of life has been on the decline as a result of changes in your body and mind resulting from the aging process, I strongly encourage you to get your hormone levels checked, because there is a significant chance that you may be suffering from a reversible form of hormone deficiency.

The Future of Human Genetic Engineering

This is truly an exciting time to be alive. We are quickly approaching the point at which scientific breakthroughs in health science will continue to occur at an ever-increasing pace, with groundbreaking new health advances occurring on a regular basis. The following years will be incredibly interesting, because there are a multitude of clinical trials regarding the promise and potential effectiveness of both gene therapy and stem cell therapy.

By 2012, these studies, and other similar studies, were already displaying high levels of potential to both treat and protect both animals and humans from disease. Beyond Hormone Optimization and Genetic Therapy, the next stage of advancement will most likely be in the field of nanomedicine. Beyond nanomedicine is femtomedicine.

At this stage of scientific inquiry, this is as far as even the most forward-thinking physician or philosopher could imagine, but there is no doubt as we create new medical treatments and expend our knowledge of medical science, new opportunities for advancement will be conceptualized that could be even more life-altering and fantastic than those that we just mentioned.

When you consider the future of medicine and longevity, you realize that human beings as they are now aren’t simply the end result of millions of years of evolution, but also a gateway to the next state of terrestrial life, a transitional state between what was and what will be, an opportunity to experience even greater consciousness and enlightenment by conquering time, itself.

What is the Idea Behind Human Immortality?

When we discuss the idea of human immortality, it doesn’t just mean allowing a human being to live forever, human immortality represents the idea that it will be possible, with future biomedical and genetic enhancements, for human beings to experience a practical immortality in which one is able to live as they were in the prime of their life, for all of their life.

It seems just as you master your body and your mind in the late twenties and early thirties, your body and mind start to enter a slow and unstoppable decline. What if you could preserve that period of physical and psychological perfection forever? It is during this period that the average person reaches his or her functional peak as an individual, with regard to strength, cognitive ability, immunity, and overall health.

How Much Better Would Life Be if You Lived to 200?

Think about how different and exciting that life would be if you could have the body and mind of a 29 year old for 120 years. There are a number of people that think that humans should not have this opportunity, but it sounds much better than spending the whole sum of those years in slow and steady decline.

How Much Better Would Life Be if You Could Live Indefinitely?

Immortalists subscribe to the belief that individuals that truly enjoy life and are creative or passionate enough to find interesting or fulfilling things to do would be able to easily take advantage of a significantly lengthened lifespan. I do understand how such a long life would feel to someone that lacks passion or imagination, however. I can imagine two hundred years of absolutely drudgery. If one does not have the propensity to invest or save to create wealth, I can imagine two hundred years of hard work with nothing to show for it.

With luck, a more automated world would allow us to enjoy our lives while actually working less. Imagine a world of eco-friendly machines could do the work of one hundred men. This could be a wonderful world of leisure for all, but it could also lead to a world where machines are used as a method of control and domination, like in Frank Herbert’s dystopian novel Dune.

The Temptation of Human Immortality

Whether the opportunity for Human Immortality comes in twenty years or two hundred years, there will be those that seek out the opportunity for such a life, and there will be those that choose to reject the opportunity for immortality.

The central question that Immortalists posit is a simple one: Why would anyone actually want to die or grow old? When you think of it that way, it sounds absolutely silly. Who would ever want to do such things? But in reality, it seems as though most human beings are resigned to such a fate.

Who Really Wants to Grow Old?

More than simply growing old, who wants to lose their lust for life or their libido? Who wants to experience their own body slowly deteriorate as they are beaten down by illness and disease? Human Immortalists are those that are willing to fight against what is perceived as inevitable by society at large. They believe that those that have resigned themselves to decay and death are simply not willing to imagine a post-human age where they could evolve beyond the inevitability of death.

It seems that many humans think of Human Immortalists as harbingers of doom which are going to bring about a new genocide. They believe that Immortalists are going against the will of God by altering the Human Genetic Code in an attempt to foster extreme lifespans, improved aesthetic, and vastly improved health outcomes.

The Great Schism of Humanity

There is a strong chance that a rift will develop between those that choose genetic alteration and those that choose to forgo such opportunities. In the end, it is likely that humanity will rift into two distinct groups. Over time, greater and greater numbers will opt for Genetic Modification, and those that opt out of such procedures may potentially lose footing in society as a result of their choice.

If modification indeed has the ability to create such disparity, genetically modified humans will spread their genes with one another, and their offspring may have greater potential for both prosperity and intellect, which will create a socioeconomic rift between GM Humans and Unmodified Humans.

Will Post-Humans be able to act ethically under these circumstances? Will Unmodified Humans be able to accept a place in the world where they are unequivocally inferior to their GM counterparts? This new world will be different and exciting, and it’s up to us to create a civil world where we can act in the best interest of all.

What Other Strange Opportunities May Become Available in the Future?

On top of our ability to vastly extend and improve our long-term health, the future will also provide us with enhanced opportunities with regard to personal aesthetic. We will not only be able to cure conditions such as psoriasis which plague millions in the world today, but many may choose to move beyond mere optimization and may choose to fully customize their appearance. Perhaps one may choose not to have olive or alabaster skin as many in society desire today, but go for a different color all together.

What if someone chose to color their skin orange, green, or blue? What if they wanted to be leopard print or covered in zebra stripes? This may appear otherworldly and unnatural to our minds, but when presented with an entire array of customization, what would be so strange about doing something like that to stand out? How different would it be to dying your hair blue or rainbow, if there were no dangers in undergoing such a change?

But, given enough time and scientific innovation, skin color and other basic augmentations like genetic breast and penis enlargement will be just another evolution in the concept of general aesthetic. The potential for more extreme changes would eventually become possible. What if humans wanted to take on the characteristics of animals? What if someone wanted the ears or tail of a cat, for example? There would even be the potential to do even more drastic things that we can barely imagine today.

Genetically Engineered Pets

These genetic advancements won’t occur in a human vacuum. They will also apply to animals as well. Today people are paying top dollar for basic genetically modified hypo-allergenic dogs, and glow-in-the-dark mammals have even been developed in laboratories.

In the future, it is likely that scientists will come up with scientific modifications which significantly enhance both the aesthetic and intelligence of animals. It’s even likely that animals will experience the benefits of genetic engineering more quickly than humans, as this future will largely be facilitated by means of animal testing.

The Post-Human Era Starts with Basic Genetic Engineering and Ends with Post-Humanism, Hyperlongevity, and Potential Immortality

You may not be able to tell, but we are already in the midst of the first phase of the Post-Human era. The beginning of this era was marked by the first time that egg and sperm from two different individuals was combined and implanted into an adoptive mother. It was such a grand event in retrospect, but the passing into this new era was not met with massive celebrations, but simply with concerns over the ethics of the new future.

Post-Humanity will have a litany of moral conundrums to unravel, some that we can imagine, and others that are unfathomable to us today. The state of the mortal mind is simply not equipped to handle the moral and ethical quandaries that the genetically modified mind will face. What if there are other lifeforms just like us in other parts of the galaxy, that have also learned to take control of their very existence on the cellular level? What if the number of unique alien civilizations in the universe is unlimited? What if we as earthlings are just one form of intelligent life among a countless litany of others?

The Current State of Genetic Modification and Gene Therapy

Today, scientists, researchers, and physicians are taking the first step into this future, with the quickly growing field of genetic therapy. We are on the cusp of doing some truly amazing things, like genetically altering viruses in order to protect humans from genetic disorders and conditions. At first, these initial treatments have been risky, reserved for those in most dire need, but as medical science becomes more well-versed in these therapeutic advancements, they will become safer and more widely available to the general public. Could you imagine reducing your risk of cancer by 80% just with a single injection? That may be the future for you.

The Current State of Organ Regeneration and Stem Cell Therapy

Another aspect of genetic therapy has to do with the advancing field of Stem Cell Therapy. There are new, state of the art treatments available which utilize stem cells in order to improve the health of the heart. Patients that have experienced heart attack or heart disease can be treated with stem cells which have the ability to develop into new and healthy muscle tissue.

Similar techniques have also been used in order to regenerate other parts of the body or parts of individual organs. In one famous case, scientists biomanufactured a windpipe for a patient with the patient’s own cells. They were able to do this by taking the stem cells and allowing them to grow in culture before pouring them over a scaffold in the shape of a windpipe. Just by providing the cells with the nutrients to grow, they were able to recreate a human windpipe in the laboratory just in a matter of days.

Because the windpipe was created from the patient’s own cells, the body did not reject the windpipe when it was surgically implanted into the body. This is one of the first successful cases where a patient’s life was changed through the scientific advancements of genetic organ replacement.

Stem Cell Therapy Will Be Available in the Near Future: Hormone Replacement Therapy is Here Today!

Stem Cell Therapy is exciting and will become increasingly common and popular over the next century in the United States. Today, there are a few places where Stem Cell Therapy is available internationally, especially in Asia, but they have yet to be medically certified, and there are still a number of pertinent risks involved. In the Western World, Stem Cell Treatments are currently going through clinical trials. Although the results are mixed, continual progress is being made.

There are many scientists that believe that Stem Cell Research will lead to a new future in medicine, but policies enacted during the presidency of George W. Bush have set the United States behind by at least a decade, and other nations in Europe and Asia are currently taking advantage of their head start, and may one day eclipse us in these new and futuristic medical therapies.

In just a few short years, genetic testing will become affordable enough that it will become a common and recommended part of prenatal care as well as regular checkups throughout the lifespan. Over time, more and more Genetic Disorders will be able to be effectively treated with Gene Therapy, and with every breakthrough, people will be that much more likely to live a longer and healthier life.

Once the clinical science is sound, it won’t even be a difficult ordeal for the patient. It would simply be like going to visit the pharmacist, or making a call to a specialist pharmacy. After receiving the medication, one will be able to administer the medication on his or her own and without the frequent oversight of a medical professional.

Not long after these Genetic Treatments are made available to the public, Stem Cell Therapies will quickly become more and more advanced as well. There are even companies that have expressed a desire to take your stem cells and develop them in a laboratory environment. The goal of this treatment would be to take your own stem cells and foster the healthiest cells to multiply. After these cultures are developed, they would be mailed back to you in order for you to inject them to alleviate health conditions and other symptoms related to the aging process.

Beyond Genetic Engineering and Stem Cell Therapies, will come new forms of medical treatment that we are just beginning to research today, but will surely flourish in the coming decades: nanomedicine and femtomedicine.

Nanoscience and the Healthcare of the Future

These are tiny, genetically engineered cellular machines that will be able to improve your health by altering the functions of your body in a positive manner. They will be able to repair and alter particular forms of cells so that they function optimally, even after a period of long life in which you would expect to see physiological breakdown. It is even believed that these treatments can also preserve and repair the brain itself! Isn’t that exciting?

There are countless people in the world that have a litany of big dreams, more than they could ever hope to accomplish in a single lifetime in some cases. They have these long checklists of things they want to do in their life, a whole wide world they want to explore. Some have an unquenchable thirst for knowledge, and want to read thousands of books or learn dozens of languages in their life.

There are countless more people that have spent their early lives living on the edge, and suffer from issues such as alcohol dependency or drug addiction which have harmed their bodies and their brains. With these forms of genetic and nanomedicine, it will be possible to repair the bodies and minds of these individuals, allowing them to make a fresh start. It is possible that addiction itself may become a historical curiosity as a result of these medical advances.

What Would Do If You Had 200 More Years to Live?

  • Would you learn to play multiple musical instruments?

  • Would you research for decades in order to write the perfect novel?

  • Would you visit every country on earth?

The number of dreams that humans have yearned for is nearly infinite, and most never live to achieve all of their dreams, if they achieve any of their dreams at all. If you are still alive in the near future, around 2032, you will be able to take full advantage of what Longevity Medicine and Anti-Aging Therapy have to offer!

Some time in the future, we will finally overcome the condition of aging. We will be able to prevent all illness and be able to live in perpetuity, as long as we don’t succumb to an accident or similar fate. This is the extreme vision of Immortality Medicine.

The First Immortals Could be Alive Today!

By the time we make it to the 22nd century, there will already be individuals that have taken the road to Hyperlongevity, and there will likely be millions of humans that have taken part in this great leap forward into Post-Humanism. They will not only be healthier, but smarter too, with further advances in Genetic Science that allow us to amplify the capacity of our brains.

As people continue to develop down this evolutionary road, will we even consider them humans anymore? They will represent a new version of humanity, and they will likely use a new term to define themselves, whether that be Neohuman or some other clever word or phrase.

I believe that this advance into Neohumanism will also lead to a new era in space travel and human colonization. With these extensive lifespans, many Neohumans will inevitably turn their eyes to the stars in a desire to find new worlds and discover new lands and extraterrestrial lifeforms. Brave Neohumans from all over the planet will take to interplanetary space vessels in order to colonize and experience new worlds and lands that are beyond the scope of human imagination.

Can I Live to Experience This New Era of Humanity?

All of the things we’ve discussed may seem incredibly exciting to you, but we understand that these innovations are going to come in the near future. If you want to take part in this grand human experiment, it’s important that you live long enough to seize these innovations as they come! There are steps you can take now to alleviate the negative symptoms of the aging process and increase your odds of experiencing the new, human revolution.

My suggestions will not ensure that you will live for the next twenty years or longer, but they will potentially drastically decrease your mortality risk so that you are able to seek out this new and exciting future that we have laid before you.

Today, the door to Neo-Humanism, Hyperlongevity, and even Human Immortality is slightly open, and there are many alive today that will experience these magnificent and life-altering advances.

Will You Take Advantage of the Advances of Hyper-Longevity and Anti-Aging Medicine? Are You Willing to Commit to a Longer and more Youthful Life?

It’s quite plain to see that we are at the crest of an event horizon, beyond which it will truly be possible to lengthen lifespans indefinitely. The most important thing is to breach that horizon. By taking steps to increase health and lifespan now, you allow yourself the opportunity to take care of further, greater medical enhancements down the road.

The most modern advances available today are in the form of Recombinant Hormone Replacement Therapies. By optimizing your hormone balance, you increase the odds that you will live long enough to experience the new, up-and-coming breakthroughs of the mid-21st century.

If you live just a few more years, new genetic medical treatments will become available which will significantly increase your lifespan. While you are enjoying the benefit of genetic medicine, researchers and medical scientists will advance and perfect Genetic Therapy and Stem Cell Therapy, allowing you to live even longer!

There are a number of Stem Cell and Gene Therapies going through clinical trials as you read this, which show great promise in preventing or treating serious illnesses which severely inhibit lifespan today. As the medical community becomes more adept at using these new tools for the purpose of treatment, they will begin to utilize these treatments as forms of Positive Medicine.

They will be able to treat patients before they even get sick in order to optimize their health and greatly improve lifespans as a result, because the incidence of illness will decline significantly. In addition, these same treatments will be able to streamline existing physiological processes, keeping the body physiologically stronger and more youthful. They will be able to tailor these treatments uniquely to the individual in order to give the best care to each individual patient.

Stay on the Cutting Edge of Longevity Medicine to Perpetually Extend the Human Lifespan

With each of these breakthroughs and treatments, we will come one step closer to Immortality. Eventually, scientists and researchers will crack the code of human life, and finally figure out how to allow us to truly live indefinitely. It may take 100 years or it may take 500 years to achieve true Immortality, but each life-extending advance will allow people to survive until the next great advance. Hyper-Longevity will eventually become a universal reality, barring accident, war, or any other form of life-ending catastrophe.

You may feel that this is a science fiction world that I am describing, but it very well may be possible for you to experience this all for yourself. It is estimated that at some point between 2032 and 2052 we will have perfected medical practices which allow us to live significantly longer lives than we do today. Those that are optimistic feel that we are just twenty years away from this era, while those that are more cautious suggest that fifty years would be a more reasonable estimate.

Twenty to fifty years may not seem like that long in scientific study, but in terms of your own life, it is a significant period of time. Are you willing to make the sacrifices now in order to experience Hyperlongevity in the near future?

Eight Ways to Extend Your Lifespan

There are a lot of steps that you can take in your life today in order to significantly increase the odds that you survive to experience this new and amazing future. If you follow the suggestions below, conscientiously, you will maximize your potential to extend your life until further longevity advances develop in the coming decades.

These eight factors have been shown to be most important when determining the length of an individual’s lifespan:

  • Nutrition

  • Exercise

  • Environment

  • Social Circles

  • Vice

  • Climate

  • Calorie-Restricted Diet

  • Hormone Replacement Therapy

The Diet of the 21st Century: Caloric Restriction and Fasting for a Longer Life

A recent article in Newsmax Health explained that the future of longevity isn’t fad dieting or strenuous exercise, but a Calorie-Restricted diet which manages metabolism and ensures a long and healthy life.

Over the last century, there have been more than twenty thousand studies regarding caloric restriction in animal species from around the globe. All of these studies have unequivocally shown that restricting the calories in an animal’s diet has the ability to significantly increase the lifespan, and the same appears to apply to human beings..

This may sound like a starvation diet at first, but conscientiously and significantly restricting calories in the human diet is a powerful means to a longer life. Of course, most people consume at least 1500 calories per day and some consume several thousand! But, it appears that the sweet spot for human longevity is quite a bit lower than that 1500 calorie threshold.

For those that are struggling with Caloric Restriction, especially those that are currently overweight, HCG Injections can help relieve the feeling of hunger associated with the initial phase of the diet in order to acclimate to their new dietary lifestyle more effectively.

At first it may seem counter-intuitive, that too much of the Bread of Life can actually shorten the lifespan, but that absolutely seems to be the case. A diet that provides high levels of nutrients through the consumption of a small number of calories is the number one way to increase human longevity effectively. Intermittent Fasting and Caloric Restriction slow down aging and also reduce the incidence of a wide variety of illnesses that plague so many in America today.

The Modern Media and the Culture of Food in the West

In the United States, as well as other countries in the West including the United Kingdom, children were raised in a reality in which starvation was one of the greatest evils of the 19th and 20th century. The various forms of media available all showed the terrible fates of so many who were denied the food needed to live. Nowhere is this imagery more vivid in Western Civilization than in the footage captured after the end of World War II as the true horrors of the Holocaust were revealed to the world at large.

During the Cold War we also experienced further evidence of the horrors of famine as communist Russia and China struggled with providing their populations with proper nutrition, leading countless to die of starvation over many decades. Today, on modern television, there are advertisements for charities throughout Africa and Asia which show the plight of the starving in these third world nations.

I do not mean to discount the real and significant struggles that those that came before us experienced in the not so distant past, but it had a powerful impact on food culture in the West, particularly the idea that it is better to eat too much than too little. In our elementary education and beyond, we are confronted with story after story of mass famine, and it seems that part of the way that we culturally appreciate our current abundance is by partaking in it.

This appreciation for our abundance has led directly to a culture of overeating that borders on obsession. In the West, we simply love our food too much, and the expansion of cuisine in the West has allowed anyone to get whatever they want, when they want it, whether they go to the grocery store, the pizza parlor, or the Chinese buffet.

A Culture of Overeating Develops into a Culture of Force Feeding

Throughout the twentieth century, we have always been taught that we need to eat every last bite on our plates. Often times, we were also strongly encouraged, if not forced, to go back for a second portion. In addition to this, the proliferation of soda drinks has led directly to a significant increase in the empty calories that the average American consumes.

As the twentieth century barreled on, parents on average had less time to cook and prepare meals at home, which led to the greater proliferation of both fast food and microwavable dinners, loaded with sugars, salts, and carbohydrates which increased our caloric consumption even more!

During this age, restaurants like Burger King and McDonald’s became the captains of the fast food industry, generating billions of dollars in profit funneling cheap calories into the mouths of men, women, and children all across the country.

Because of all these pressures to overeat, the longevity gains that people in the West experienced as a result of modernization all began to slip away, the combination of unhealthy eating and an increasingly sedentary lifestyle is threatening today’s generation with the prospect of living shorter lives than their parents on average!

The United States would be stronger in every way, if it could foster greater consciousness about the importance of eating smarter to eat longer. If we all just made the proactive decision to engage in a lifestyle of at least mild caloric restriction, it would both decrease the price of health care and allow the citizens of this nation to live longer, happier, and healthier lives.

Do You Dream of a Healthier, Happier Life? Contact the Conscious Evolution Institute Today!

If you are a man or woman over the age of thirty and currently live in the United States, the Conscious Evolution Institute can help you improve your health and longevity. We provide Doctor-Monitored Bio-Identical Hormone Replacement Therapy to patients all across the United States.

With just a simple phone call, we can arrange for you to meet with one of our affiliate physicians in order to set you on the road to a new you. We offer a variety of Hormone Replacement options, including Testosterone Replacement Therapy, Human Growth Hormone Injections, Sermorelin Acetate Injections, and HCG Injection Therapy for Weight Loss.

We also provide nutrition and lifestyle counseling in order to help you maximize the results of your treatment by choosing foods, supplements, and exercises that will get your body running on all cylinders!

If you feel that you may be a candidate for Hormone Replacement Therapy, don’t hesitate, call us today, and one of our friendly specialists will walk you through the process and answer any and all questions that you may have.

For more information on Ten Ways To Live Ten Years Longer check out

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Infographics –

Posted: December 2, 2016 at 5:47 pm

Elon Musk has a new project in the offingand, no, it doesn’t involve Mars. This one is more prosaic, not to say more immediately realizable: it’s nothing less than to create a fully self-contained “energy ecosystem.” It’ll mean each man’s home is not just his castle, but is also his self-sufficient, sustainable power-generation plant.

In October of this year, the White House released a report titled “Preparing For the Future of Artificial Intelligence.” It’s a significant acknowledgement, from the highest organs of government, that AI is now a major part of our current and future lives. In this infographic, we’ve summarized the White House report’s key findings.

Computers that connect to the human brain could bring an end to Alzheimer’s. They could allow us to possess superhuman levels of memory and intelligence. They could change everythingand Bryan Johnson’s Kernel is making it happen.

They represent some of the most technologically sophisticated machines ever devised by humankind: reusable space planes. The U.S. Space Shuttle is undoubtedly the most famous example of this type of vehicle, but what else has been done in this direction? Here’s a look at space planes past and future.

As our technology has evolved, so has the way we interact with itand nothing exemplifies this more than the dream of a seamless brain-computer interface (BCI). Forget clunky keyboards and touchscreens: BCI is all about directly uniting humanity with the tools it creates. Here’s a look at the history and methods of BCI technology.

Machines are now able to learn and evolve without human intervention. So, how does it work exactly? And what does it mean for the future of humanity? Here’s a quick lesson on the basics of machine learning.

Thanks to New Horizons, we’ve completed the preliminary reconnaissance of the Solar System. Now it’s time to send man across our cosmic neighborhood. Here’s what that mission might look like in a few decades.

Vehicle autonomy is the wave of the futurenot just for cars anymore, we’re seeing automated technology in trains, buses, ships and even planes. The major transport, logistics and shipping companies are scrambling to develop operator-less technology just to stay relevant. Here’s a look at what else is going driverless.

Humans dreams bigand, better yet, we make those dreams a reality. It’s enabled us to tame nature, build new nations, defeat disease, defy gravity and even reach the Moon. And we’re not done yetnot by a long shot. From the quantum internet to terraforming Mars, here are some of mankind’s most ambitious future moonshots.

Visionary, polymath, scientist, artist, engineerLeonardo da Vinci was the quintessential “Renaissance Man.” Whether it was flying machines, diving suits, automatons or advanced weaponry, da Vinci envisioned the future and set about designing it. Here’s a look at Leonardo da Vinci’s most futuristic contraptions.

There’s a new aerospace technology on the horizonusing plasma, the superheated “fourth state of matter,” to enhance the aerodynamic performance of aircraft. Here, we break down the mechanics and the uses of this exciting new technology that has the aeronautics and aerospace industries all abuzz.

On September 27, Elon Musk unveiled his most ambitious project yetcalled the Interplanetary Transport System (ITS), it’s nothing less than his long-awaited plan for, not only putting humans on Mars, but colonizing the Red Planet as well. In this handy infographic, we’ve distilled the ITS architecture into seven easy steps.

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Infographics –

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Marine Chemist Service, Inc. | Protecting People and …

Posted: December 2, 2016 at 5:47 pm

WelcomeMarine Chemist Service welcomes you to their newly revised website. In addition to a different look, the site has been updated with their latest products and services. There is also an abundance of useful, technical information ranging from safety to environmental topics. [Read More]

Credentials Marine Chemist Service is a highly diversified Virginia corporation that has two separate facilities, 10 different products and services, and 48 years of experience. The corporation also has one of the longest, continuously operating asbestos analytical laboratories. Throughout its history, MCS has trained approximately 15,000 student/employees, analyzed nearly 450,000 samples, and performed countless inspections aboard ship and within the facilities of land-side operations. This remarkable achievement has been made possibly through the efforts of 30+ biologists, chemists, geologists, industrial hygienists, inspectors, safety professionals, trainers, and a group of very efficient support personnel. [Read More]

History Well over four decades ago, in 1966, Bob and Sally Walker had a vision to develop a company dedicated to serving the maritime industry. Mr. Walker trained to become a National Fire Protection Association (NFPA) Certified Marine Chemist (which, in turn, lead to the company’s name). Mrs. Walker worked behind the lines, eventually taking care of all the books, paperwork, phones and more. Together, they worked hard in pursuit of their goal and in November of that same year, the Walkers formed Marine Chemist Service in the historic state of Virginia. [Read More]

In the News Marine Chemist Service is passionate about Protecting People and their Environment. That passion is often demonstrated by sharing free information via consultation and the Information/Links page found on its website. Marine Chemist Service also subscribes to several news organizations, participates in numerous committees and boards, and conducts its own original research. The content of some of the aforementioned is available here, [In the News]

Training Marine Chemist Service has trained approximately 13,500 student-employees throughout its history. The company offers over 30 courses, has four full time and other guest instructors, and two locations in the Tidewater area of Virginia. The company has also provided offsite training within the CONUS, including the states of Florida, Mississippi, North Carolina and Wisconsin. They have even provided training as far away as Bahamas and Japan. When requested, Marine Chemist Service has customized its courses to focus application on unusual hazards and/or unique work practices to protect against those hazards. [Read More]

Please enable JavaScript to get the full experience.

Marine Chemist Service takes great pleasure in servicing its clients needs. In that effort, MCS offers a continuously updated newsletter, as well as additional information on the below products and services.

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Marine Chemist Service, Inc. | Protecting People and …

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History of biochemistry – Wikipedia

Posted: December 2, 2016 at 5:46 pm

The history of biochemistry can be said to have started with the ancient Greeks who were interested in the composition and processes of life, although biochemistry as a specific scientific discipline has its beginning around the early 19th century.[1] Some argued that the beginning of biochemistry may have been the discovery of the first enzyme, diastase (today called amylase), in 1833 by Anselme Payen,[2] while others considered Eduard Buchner’s first demonstration of a complex biochemical process alcoholic fermentation in cell-free extracts to be the birth of biochemistry.[3][4] Some might also point to the influential work of Justus von Liebig from 1842, Animal chemistry, or, Organic chemistry in its applications to physiology and pathology, which presented a chemical theory of metabolism,[1] or even earlier to the 18th century studies on fermentation and respiration by Antoine Lavoisier.[5][6]

The term biochemistry itself is derived from the combining form bio-, meaning “life”, and chemistry. The word is first recorded in English in 1848,[7] while in 1877, Felix Hoppe-Seyler used the term (Biochemie in German) in the foreword to the first issue of Zeitschrift fr Physiologische Chemie (Journal of Physiological Chemistry) as a synonym for physiological chemistry and argued for the setting up of institutes dedicate to its studies.[8][9] Nevertheless, several sources cite German chemist Carl Neuberg as having coined the term for the new discipline in 1903,[10][11] and some credit it to Franz Hofmeister.[12]

The subject of study in biochemistry is the chemical processes in living organisms, and its history involves the discovery and understanding of the complex components of life and the elucidation of pathways of biochemical processes. Much of biochemistry deals with the structures and functions of cellular components such as proteins, carbohydrates, lipids, nucleic acids and other biomolecules; their metabolic pathways and flow of chemical energy through metabolism; how biological molecules give rise to the processes that occur within living cells; it also focuses on the biochemical processes involved in the control of information flow through biochemical signalling, and how they relate to the functioning of whole organisms. Over the last 40 years the field has had success in explaining living processes such that now almost all areas of the life sciences from botany to medicine are engaged in biochemical research.

Among the vast number of different biomolecules, many are complex and large molecules (called polymers), which are composed of similar repeating subunits (called monomers). Each class of polymeric biomolecule has a different set of subunit types. For example, a protein is a polymer whose subunits are selected from a set of twenty or more amino acids, carbohydrates are formed from sugars known as monosaccharides, oligosaccharides, and polysaccharides, lipids are formed from fatty acids and glycerols, and nucleic acids are formed from nucleotides. Biochemistry studies the chemical properties of important biological molecules, like proteins, and in particular the chemistry of enzyme-catalyzed reactions. The biochemistry of cell metabolism and the endocrine system has been extensively described. Other areas of biochemistry include the genetic code (DNA, RNA), protein synthesis, cell membrane transport, and signal transduction.

In these regards, the study of biochemistry began when biology first began to interest societyas the ancient Chinese developed a system of medicine based on yin and yang, and also the five phases,[13] which both resulted from alchemical and biological interests. It began in the ancient Indian culture also with an interest in medicine, as they developed the concept of three humors that were similar to the Greek’s four humours (see humorism). They also delved into the interest of bodies being composed of tissues. As in the majority of early sciences, the Islamic world greatly contributed to early biological advancements as well as alchemical advancements; especially with the introduction of clinical trials and clinical pharmacology presented in Avicenna’s The Canon of Medicine.[14] On the side of chemistry, early advancements were heavily attributed to exploration of alchemical interests but also included: metallurgy, the scientific method, and early theories of atomism. In more recent times, the study of chemistry was marked by milestones such as the development of Mendeleev’s periodic table, Dalton’s atomic model, and the conservation of mass theory. This last mention has the most importance of the three due to the fact that this law intertwines chemistry with thermodynamics in an intercalated manner.

As early as the late 18th century and early 19th century, the digestion of meat by stomach secretions[15] and the conversion of starch to sugars by plant extracts and saliva were known. However, the mechanism by which this occurred had not been identified.[16]

In the 19th century, when studying the fermentation of sugar to alcohol by yeast, Louis Pasteur concluded that this fermentation was catalyzed by a vital force contained within the yeast cells called ferments, which he thought functioned only within living organisms. He wrote that “alcoholic fermentation is an act correlated with the life and organization of the yeast cells, not with the death or putrefaction of the cells.”[17]

Anselme Payen discovered in 1833 the first enzyme who called diastase[18] and in 1878 German physiologist Wilhelm Khne (18371900) coined the term enzyme, which comes from Greek “in leaven”, to describe this process. The word enzyme was used later to refer to nonliving substances such as pepsin, and the word ferment used to refer to chemical activity produced by living organisms.

In 1897 Eduard Buchner began to study the ability of yeast extracts to ferment sugar despite the absence of living yeast cells. In a series of experiments at the University of Berlin, he found that the sugar was fermented even when there were no living yeast cells in the mixture.[19] He named the enzyme that brought about the fermentation of sucrose “zymase”.[20] In 1907 he received the Nobel Prize in Chemistry “for his biochemical research and his discovery of cell-free fermentation”. Following Buchner’s example; enzymes are usually named according to the reaction they carry out. Typically the suffix -ase is added to the name of the substrate (e.g., lactase is the enzyme that cleaves lactose) or the type of reaction (e.g., DNA polymerase forms DNA polymers).

Having shown that enzymes could function outside a living cell, the next step was to determine their biochemical nature. Many early workers noted that enzymatic activity was associated with proteins, but several scientists (such as Nobel laureate Richard Willsttter) argued that proteins were merely carriers for the true enzymes and that proteins per se were incapable of catalysis. However, in 1926, James B. Sumner showed that the enzyme urease was a pure protein and crystallized it; Sumner did likewise for the enzyme catalase in 1937. The conclusion that pure proteins can be enzymes was definitively proved by Northrop and Stanley, who worked on the digestive enzymes pepsin (1930), trypsin and chymotrypsin. These three scientists were awarded the 1946 Nobel Prize in Chemistry.[21]

This discovery, that enzymes could be crystallized, meant that scientists eventually could solve their structures by x-ray crystallography. This was first done for lysozyme, an enzyme found in tears, saliva and egg whites that digests the coating of some bacteria; the structure was solved by a group led by David Chilton Phillips and published in 1965.[22] This high-resolution structure of lysozyme marked the beginning of the field of structural biology and the effort to understand how enzymes work at an atomic level of detail.

The term metabolism is derived from the Greek Metabolismos for “change”, or “overthrow”.[23] The history of the scientific study of metabolism spans 800 years. The earliest of all metabolic studies began during the early thirteenth century (1213-1288) by a Muslim scholar from Damascus named Ibn al-Nafis. al-Nafis stated in his most well-known work Theologus Autodidactus that “that body and all its parts are in a continuous state of dissolution and nourishment, so they are inevitably undergoing permanent change.”[24] Although al-Nafis was the first documented physician to have an interest in biochemical concepts, the first controlled experiments in human metabolism were published by Santorio Santorio in 1614 in his book Ars de statica medecina.[25] This book describes how he weighed himself before and after eating, sleeping, working, sex, fasting, drinking, and excreting. He found that most of the food he took in was lost through what he called “insensible perspiration”.

One of the most prolific of these modern biochemists was Hans Krebs who made huge contributions to the study of metabolism.[26] He discovered the urea cycle and later, working with Hans Kornberg, the citric acid cycle and the glyoxylate cycle.[27][28][29] These discoveries led to Krebs being awarded the Nobel Prize in physiology in 1953,[30] which was shared with the German biochemist Fritz Albert Lipmann who also codiscovered the essential cofactor coenzyme A.

In 1960, the biochemist Robert K. Crane revealed his discovery of the sodium-glucose cotransport as the mechanism for intestinal glucose absorption.[31] This was the very first proposal of a coupling between the fluxes of an ion and a substrate that has been seen as sparking a revolution in biology. This discovery, however, would not have been possible if it were not for the discovery of the molecule glucose’s structure and chemical makeup. These discoveries are largely attributed to the German chemist Emil Fischer who received the Nobel Prize in chemistry nearly 60 years earlier.[32]

Since metabolism focuses on the breaking down (catabolic processes) of molecules and the building of larger molecules from these particles (anabolic processes), the use of glucose and its involvement in the formation of adenosine triphosphate (ATP) is fundamental to this understanding. The most frequent type of glycolysis found in the body is the type that follows the Embden-Meyerhof-Parnas (EMP) Pathway, which was discovered by Gustav Embden, Otto Meyerhof, and Jakob Karol Parnas. These three men discovered that glycolysis is a strongly determinant process for the efficiency and production of the human body. The significance of the pathway shown in the adjacent image is that by identifying the individual steps in this process doctors and researchers are able to pinpoint sites of metabolic malfunctions such as pyruvate kinase deficiency that can lead to severe anemia. This is most important because cells, and therefore organisms, are not capable of surviving without proper functioning metabolic pathways.

Since then, biochemistry has advanced, especially since the mid-20th century, with the development of new techniques such as chromatography, X-ray diffraction, NMR spectroscopy, radioisotopic labelling, electron microscopy and molecular dynamics simulations. These techniques allowed for the discovery and detailed analysis of many molecules and metabolic pathways of the cell, such as glycolysis and the Krebs cycle (citric acid cycle). The example of an NMR instrument shows that some of these instruments, such as the HWB-NMR, can be very large in size and can cost anywhere from a few hundred dollars to millions of dollars ($16 million for the one shown here).

Polymerase chain reaction (PCR) is the primary gene amplification technique that has revolutionized modern biochemistry. Polymerase chain reaction was developed by Kary Mullis in 1983.[33] There are four steps to a proper polymerase chain reaction: 1) denaturation 2) extension 3) insertion (of gene to be expressed) and finally 4) amplification of the inserted gene. These steps with simple illustrative examples of this process can be seen in the image below and to the right of this section. This technique allows for the copy of a single gene to be amplified into hundreds or even millions of copies and has become a cornerstone in the protocol for any biochemist that wishes to work with bacteria and gene expression. PCR is not only used for gene expression research but is also capable of aiding laboratories in diagnosing certain diseases such a lymphomas, some types of leukemia, and other malignant diseases that can sometimes puzzle doctors. Without polymerase chain reaction development, there are many advancements in the field of bacterial study and protein expression study that would not have come to fruition.[34] The development of the theory and process of polymerase chain reaction is essential but the invention of the thermal cycler is equally as important because the process would not be possible without this instrument. This is yet another testament to the fact that the advancement of technology is just as crucial to sciences such as biochemistry as is the painstaking research that leads to the development of theoretical concepts.

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History of biochemistry – Wikipedia

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Longevity Secrets from the Grand Masters of TCM …

Posted: November 30, 2016 at 2:50 am

[Featured Article]

[Note from Editor: The Grand Master of Chinese Medicine is an honorary title granted by Chinese government, and selected by a panel of various experts. The first selection occurred in 2008-09 and 30 TCM experts were named the Master of Chinese Medicine in 2009. The selection will take place every 5 years. Here are some secrets of longevity from 10 of the 30 Grand Masters. For more information about them, go to:

Tietao Deng

Tietao Deng, 95 years old, tenured professor of Guangzhou University of Chinese Medicine. , 95)

1. Dont compete for fame, and let nature take its course; 2. Adjust diet and lead a regular life. 3. Do regular exercise, do Eight Pieces of Brocade every morning. He suggested, I have a secret bath prescription. Alternate hot and cold bath and they are relatively cold and hot alternation, which will make the blood vessels contraction and relaxation just like massaging the vessels.

Liangchun zhu

Liangchun Zhu, 94 years old, a famous TCM doctor in Jiangsu Province, he is an expert of TCM for cancer treatment ,94)

Since a long time ago Dr. Zhu eats a special kind of Yang Sheng congee, made by green been 50g, pearl barley 50g, lotus seed 50g, lentils 50g, dates 30g, lycium barbarum (goji berries) 10g, astragalus membranaceus 250g ( 30g for regular persons daily). Wash the first 5 and put them into a boiling casserole and add the water from astragalus membranaceus. Cook on high flame until it boils then change to low flame for 40 min. Then add goji berries into it and continue for 10 more min. Have 1/5 of the amount daily -dividing the dosage into taking half of it before breakfast and the other half after dinner.

Dexin Yan, 91 years old, the leader of Chinese Medicine in Shanghai, the master of balancing Qi and blood. , 91)

Dexin Yan

Longevity and aging are closely related to qi and blood balance. Smooth qi and Blood circulate the whole body and adjust the functions of internal organs to promote longevity. The main supplements I have are some Chinese herbals for Spleen, adding qi and increasing Blood circulation including red flowers, walnuts and so on. I suggest taking these herbals with water and empty stomach only once every morning not twice per day.

Guangxin Lu, 84 years old, Professor at Chinese Academy of Chinese Medicine, expert in TCM theory; , 84)Dr. Lu advises chewing and swallowing slowly, it may take a while for him to eat just an

Guangxin Lu

egg. Dr. Lu always says Eating should be with an enjoyable attitude. He eats 2 eggs every day and he believes that eggs contain a lot of lecithin which helps fight against aging. Getting up early every day, he rubs his ears and belly to make meridian vessels and blood circulates well. In addition, a foot bath before going to bed will let you sleep better.

Zhizheng Lu

Zhizheng Lu, 91 years old, a famous TCM doctor in Beijing; ,91)

Dr. Lu eats ginger after getting up in the morning. He believes eating ginger with dates and brown sugar promotes health and wellbeing. However, he advises only to eat ginger in the morning but not at night. Dr. Lu is in the habit of massaging and rubbing his face in the morning and having a foot bath before going to bed. The foot bath will pull the blood down and it is assists the brain in getting into sleep mode.

Zhongying Zhou

Zhongying Zhou, 84 years old, former president of Nanjing University of Chinese Medicine; ,84)

Dr. Zhou sees patients for 5 half-days every week. It is his greatest pleasure to see and help patients. His lifestyle and routine is very regular, and he never stays up late at night. Desire is the source of suffering; less desire leads to stronger mind. People should live with low-desire, and with a lot of calmness and tolerance.

Youzhi Tang, 85 years old, worked for Chairman Mao as a TCM doctor; ,85)

According to Dr. Tang, the secrets of longevity are: A nurturing life needs a nurturing mind; an open mind leads to happiness. Keep a hospitable and peaceful mind. He sees patients in clinic twice a week and is willing to accept new things. He enjoys thinking which keeps the brain working. In addition, he recommends making sure you have enough sleep, at least 7 hours a day, and take time for a lunch nap.

Zhenghua Li, 87 years old, the former president of Henan College of Chinese Medicine. ,87)

Zhenghua Li

Dr. Li practiced Chinese medicine for more than 60 years. He emphasizes nourishing the Stomach and Spleen, adjusting diet and never engaging in binge eating. He recommends paying attention to exercise and taking a walk after a meal. He walks in the living room for 15 min in the winter when he cant go outside. He writes in calligraphy (handwriting with special pen) to nurture life and taking care of the temperament.

Qi Zhang

Qi Zhang, 90 years old, chief expert of Chinese medicine on kidney diseases, , 90)

Dr. Zhang longevity secrets are keeping your spiritual aspect pleasurable and free from worry and anxiety. Ignore rumors and burdens that make you unhappy, instead just laugh at them. Eating and diets should follow the natural way, neither eating too much nor eating to light. He prefers a balanced diet and does not agree with avoiding foods with cholesterol. He says it is undesirable to eat only vegetables and be on diets to lose weight.

Peiran Qiu

Peiran Qiu (1913-201097 years olda tenured professor of Shanghai University of Chinese Medicine. He is a famous educator and doctor of TCM.

One of Master Qius favorite students explaines his secret of longevity as following:

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Center for Personalized Medicine | Founder & Director …

Posted: November 30, 2016 at 2:50 am

At the Center for Personalized Medicine we specialize in customized treatment plans for each patient. We are dedicated to help you achieve your wellness objectives.

We understand the importance of your wellness. To achieve your wellness objectives, you have come to expect the highest levels of service and patient care. As a result, we continuously commit ourselves to meeting and exceeding your expectations. To us, providing a total healthcare experience means dedicated and friendly staff, flexible and convenient hours, and the highest quality care available.

Services Offered

At the Center for Personalized Medicine we specialize in prescription natural hormone replacement for both women and men. We can also customize a vitamin program for you. Your nutritional needs are as unique to you as your fingerprint.

At the Center for Personalized Medicine we can also help your memory stay sharp, help your skin stay more youthful, and show you safe and simple ways to increase your growth hormone level. We also have nurses and nutritionists who will meet with you to develop your own individualized weight management program to help you achieve maximum weight loss and keep the weight off.

Have our doctors show you how to lower cholesterol without a prescription. We help cancer patients with nutritional support. If you have diabetes, let us show you new treatment options. In short, at the Center for Personalized Medicine we will take a functional medicine approach to your health care needs.

Whether you want to maintain your current good health, or if you have a disease, we will look at how your body works and design a treatment plan for you and you only. We do not mask your symptoms with medications, we instead try to fix the cause of the problem and use medications only when necessary.

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Fight Aging! Reports from the front line in the fight …

Posted: November 30, 2016 at 2:50 am

Today is Giving Tuesday: if you Favor a Long, Healthy Life for Everyone, then Make a Donation to Support the Work of the SENS Research Foundation


Following the commercial shopping days of Black Friday and Cyber Monday is the day for non-profits and charitable donation, Giving Tuesday. It is a young idea, first announced in 2012, but a great idea, and one that has seen considerable adoption. Of this cluster of marked days, I expect Giving Tuesday to be the cultural phenomenon that will produce the greatest long-term change for the better. Just focusing on support for medical research, it is clear that very few people put any thought into where therapies come from and how progress in medicine happens. Every opportunity to explain to the public at large that the most important early stages of medical research are largely funded by philanthropy is an opportunity to increase that funding and speed progress. Yes, most people will ignore the request for help, but every year the communities focused on research for specific diseases grow. Every year more people realize that we live in the midst of a revolution in biotechnology, and medicine can and will make enormous progress in the decades ahead. In our case the disease is aging: addressing the root causes of aging will, to the extent that it is comprehensive and effective, halt and turn back all of the hundreds of named forms of age-related disease, as well as the frailty and degeneration that is currently thought of as normal.

For Giving Tuesday 2016 I ask you to make a donation to the SENS Research Foundation or Methuselah Foundation, organizations that have done more than any other over the past fifteen years to advance the state of rejuvenation research. They have pushed the scientific community towards developing much more of the basis for therapies capable of repairing the cell and tissue damage that causes aging, and funded many of these programs. They have removed roadblocks and enabled other groups to make significant progress. Indeed, the entire culture of the scientific community has changed over that time, from one in which it was career-threatening to talk about extending human life spans to one in which many researchers talk openly and publish papers on this topic. Now the biggest argument is over how to proceed. That, again, has a lot to do with the years of advocacy carried out by the SENS Research Foundation, Methuselah Foundation, and their allies. Fifteen years ago, next to no work on repair of the causes of aging was taking place. Now there is at least some funded research in every important line of work, and some are well funded indeed. This has come to pass because over this time a great many people have made charitable donations to the SENS Research Foundation and Methuselah Foundation, and those organizations made very good use of that money.

Until the end of 2016, all single donations made to the SENS Research Foundation will be matched, dollar for dollar, by the generosity of Michael Greve, who has put up a $150,000 challenge fund. Similarly, Josh Triplett, Christophe and Dominique Cornuejols, and Fight Aging! have put up another $36,000 challenge fund that will match the next year of donations for anyone who signs up as a SENS Patron to make monthly donations to the SENS Research Foundation. What are you waiting for?

This is a great time for progress in rejuvenation research and development, and a great time to reinforce that progress. The first class of therapies based on the SENS vision for rejuvenation, clearance of senescent cells, is in active development by a number of startup companies, including Oisin Biotechnologies, seed funded by the Methuselah Foundation and SENS Research Foundation, and UNITY Biotechnology, where the principals have raised more than $100 million to date to bring this therapy to the clinic. Other types of rejuvenation therapy that address other forms of cell and tissue damage are within a few years of that tipping point, given sufficient funding for continued research. Researchers focused on breaking down the cross-links that cause arterial stiffness and loss of elasticity in other tissues have made great strides in building the necessary tools thanks to SENS Research Foundation funding, and are presently engaged in the search for drug candidates. Removal of the amyloids that build up in old tissues is showing progress also in recent years, with a successful trial of clearance of transthyretin amyloid and the first trial in which amyloid- was cleared in Alzheimer’s disease patients. There is much more to tell, but you get the picture. Things are moving, the wheel is turning, and this is in large part due to our support for the SENS Research Foundation and Methuselah Foundation in past years.

We, the everyday philanthropists who dare to dream big, have helped to make these successes possible. We have pushing things past the first, hardest part of the bootstrapping process, and brought the end to frailty and disease in aging that much closer. We light the way, by our participation and advocacy attracting those who are more wealthy and conservative in their donations, and who were waiting for signs of support before stepping in. By donating today to the SENS Research Foundation and Methuselah Foundation, you help to set the foundation for the successes of the 2020s, for the widespread clinical availability rejuvenation therapies that, given the funding, will come to pass in that decade.


Rates of obesity and high blood pressure, or hypertension, follow the increases in wealth and comfort that have spread through much of the world over the past 60 years. Regions that are in the process of transitioning from predominantly poor agricultural populations to a level of wealth and mix of occupations that looks much more like Europe or the US, with South Korea as a good example of the full span of such a transition, see rising life expectancy as well as a rising level of lifestyle conditions. High blood pressure drives the development of cardiovascular disease, and is made worse by excess fat tissue and lack of exercise. Though at present we can’t do much about the root cause of age-related increases in blood pressure, which is loss of elasticity in blood vessels, other than fund the most promising research that offers a path to meaningful therapies, we can adopt lifestyle choices that avoid making the problem larger than it has to be. Further, the past 20 years have seen some surprisingly effective advances in controlling high blood pressure through medication, surprising since these results have been achieved without doing much to address the underlying causes, but the very widespread use of these therapies has yet to spread to some of the regions that are now seeing increased incidence of hypertension.

In the past 40 years, there has been a large increase in the number of people living with high blood pressure worldwide because of population growth and ageing – rising from 594 million in 1975 to over 1.1 billion in 2015. The largest rise in the prevalence of adults with high blood pressure has been in low- and middle-income countries (LMICs) in south Asia (eg, Bangladesh and Nepal) and sub-Saharan Africa (eg, Ethiopia and Malawi). But high-income countries (eg, Australia, Canada, Germany, Sweden, and Japan) have made impressive reductions in the prevalence of adults with high blood pressure, according to the most comprehensive analysis of worldwide trends in blood pressure to date.

Both elevated systolic (higher than 140 mmHg; first number in blood pressure reading) and diastolic (higher than 90mmHg) blood pressure can be used to make a diagnosis of high blood pressure. Recent research suggests that the risk of death from ischemic heart disease and stroke doubles with every 20 mmHg systolic or 10 mmHg diastolic increase in middle and older ages. Over the past four decades, the highest average blood pressure levels have shifted from high-income western countries (eg, Norway, Germany, Belgium, France) and Asia-Pacific countries (eg, Japan) to LMICs in sub-Saharan Africa, South Asia, and some Pacific island countries. High blood pressure remains a serious health problem in central and eastern Europe (eg, Slovenia, Lithuania). The findings come from a comprehensive new analysis of global, regional, and national trends in adult (aged 18 and older) blood pressure between 1975 and 2015. This includes trends in average systolic (the maximum pressure the heart exerts while beating) and diastolic blood pressure (amount of pressure in the arteries between beats), as well as prevalence of high blood pressure. The Non-Communicable Disease (NCD) Risk Factor Collaboration pooled data from 1479 population-based studies totalling 19.1 million men and women aged 18 years or older from 200 countries (covering more than 97% of the world’s adult population in 2015).

“High blood pressure is the leading risk factor for stroke and heart disease, and kills around 7.5 million people worldwide every year. Most of these deaths are experienced in the developing world. Taken globally, high blood pressure is no longer a problem of the Western world or wealthy countries. It is a problem of the world’s poorest countries and people. Our results show that substantial reductions in blood pressure and prevalence are possible, as seen in high-income countries over the past 40 years. They also reveal that WHO’s target of reducing the prevalence of high blood pressure by 25% by 2025 is unlikely to be achieved without effective policies that allow the poorest countries and people to have healthier diets – particularly reducing salt intake and making fruit and vegetables affordable – as well as improving detection and treatment with blood pressure lowering drugs.”



Researchers here investigate a class of drug that blocks interleukin-1 receptor activity, something that has been found to reduce cell death and improve regeneration following stroke. This form of interference in cellular metabolism lowers the level of inflammation, but that may or may not be the most important mechanism in the outcome for stroke patients; it is plausible, but the details remain to be determined conclusively at this point.

The pro-inflammatory cytokine interleukin-1 (IL-1) is a major driver of inflammation, with well documented detrimental effects in multiple preclinical models of systemic inflammatory disease as well as in cerebral ischemia. To this end, the selective, naturally occurring competitive inhibitor of IL-1, interleukin-1 receptor antagonist (IL-1Ra) has shown potential as a new treatment for stroke. More specifically, in a number of experimental stroke paradigms IL-1Ra reduces infarct volume and improves long term functional outcome, including in co-morbid animals. However, exact mechanisms by which IL-1Ra is neuroprotective are yet to be fully established.

While much research has focused on limiting ischemic damage in the initial stages of acute reperfusion, it is also important to understand mechanisms that underpin brain repair following injury and develop strategies that enhance reparative endogenous processes, including adult neurogenesis. Ischemic injury elicits a robust neurogenic response by stimulating production of neuronal progenitor cells (NPCs) in distinct neurogenic regions, which include the subventricular zone (SVZ) and the subgranular zone (SGZ), to generate new functional neurons. Though mechanisms underlying post-stroke neurogenesis and the influence of inflammation on these processes are still poorly understood, it has been observed in young and aged animals that inflammation impairs both basal levels of neurogenesis and attenuates the neurogenic response triggered by central nervous system (CNS) injury via induction of the pro-inflammatory cytokines. IL-1, for example, reduces the proliferation and differentiation of NPCs to neurons in pathologies such as stress and depression, effects reversed by administration of IL-1Ra.

Here, we explored how inhibition of IL-1 actions by clinically relevant, delayed administration of subcutaneous IL-1Ra affects stroke outcome and neurogenesis up to 28 days after experimental ischemia, in aged/co-morbid and young rats. All experiments were performed using 13-month-old male, lean and corpulent (Cp) rats and 2-month-old Wistar rats. Cp rats are homozygous for the autosomal recessive cp gene (cp/cp), and spontaneously develop obesity, hyperlipidemia, insulin resistance, glomerular sclerosis, and atherosclerosis. Delayed IL-1Ra administration at 3 and 6 hours reperfusion in aged lean, aged Cp and young Wistar rats induced a significant reduction in infarct volume at 24 hours and 7 days of reperfusion, and a significant reduction in cortex loss at 28d in young Wistar rats. Reductions in infarct volume at 24 hours of reperfusion were 37%, 42% and 40% in aged lean, aged Cp and young Wistar rats respectively. IgG staining at 7 days reperfusion revealed a reduction of 40%, 48% and 46% in blood-brain barrier (BBB) damage in IL-1Ra treated aged lean, aged Cp and young Wistar animals respectively, versus their placebo-treated counterparts. A reduction of 26% was also observed at 14d reperfusion in young Wistar rats treated with IL-1Ra versus their placebo counterparts.

Our findings demonstrate that subcutaneous administration of IL-1Ra is neuroprotective in young and aged animals with multiple risk factors for stroke and increases post-stroke neurogenesis. It has previously been observed that delayed administration of IL-1Ra exerts neuroprotective effects at acute time points following experimental ischemia. Here we extend these findings to show that the early beneficial effects of IL-1Ra persist for at least 7 days in aged/co-morbid animals and for 28 days in young/healthy animals. Our data show that although 13-month-old corpulent rats had a plethora of stroke associated co-morbidities, infarct volumes were of a similar size to aged leans, suggesting that the extent of ischemic damage was close to maximal and that no further increase was possible. Conversely, younger rats were more resistant. This suggests that age is the primary variable that increases the brain susceptibility to infarction following an ischemic stroke. However, despite reaching maximal levels of infarction, tissue is still salvageable under these circumstances if IL-1Ra is administered within a therapeutic window.

Furthermore, our results indicate that although the delayed administration of IL-1Ra (3 and 6 hours from reperfusion onset) reduces infarct volume, it produces an increase on cellular proliferation and migration of immature neurons versus placebo counterparts in the SVZ following stroke in young and aged/co-morbid rats, suggesting that a reduced inflammation of the tissue fosters a more efficient repair of the damaged tissue. We also show that IL-1Ra increases the number of new integrated neurons in areas surrounding the infarct lesion in young animals compared to placebo groups a result that correlates with improvements in motor and behavioral sub-acute outcomes. The benefits of IL-1Ra are therefore not limited to inducing neuroprotection, but also favor and promote neurorepair mechanisms. We conclude that further studies are required to fully elucidate the mechanisms through which IL-1Ra may be mediating its beneficial, neurogenic effects.



In the paper I’ll point out today, researchers map an efficient form of protein quality control from stem cells and recreate it in somatic cells, producing extended life in nematode worms as a result. Proteins are large, complex molecules, and their correct function depends on the assumption of a precise three-dimensional arrangement after creation, a process known as protein folding. Proteins can and do misfold, however, and in doing so many become actively harmful rather than merely unwanted clutter. A baroque system of chaperone proteins assists in correct folding, as well as identification and removal of misfolded molecules. The presence of misfolded proteins is effectively a form of damage: some of the molecular waste that accumulates with age and contributes to the development of age-related disease consists of misfolded proteins, such as the various forms of amyloid, for example. The gradual failure of cellular recycling systems, such as declining lysosomal function caused by the presence of metabolic waste that is hard for the body to break down, or similar failures in the proteasome, also contribute to rising levels of damaged and dysfunctional proteins. Since aging is nothing more than the accumulation of damage and the reactions to that damage, more efficient operation of chaperone and other quality control systems in cells should slow aging: the less damage there is at any one time, the less of an opportunity that damage has to spread and cause secondary issues. It is probably not a coincidence that increased quality control activity is observed in many of the methods shown to modestly slow aging in laboratory animals, and that some forms of slowing aging cannot work without that quality control boost.

As for any study that extends life in short-lived species in this way, it is worth noting that the life span of short-lived species is far more plastic than that of longer-lived species such as we humans. Where the research community can directly compare methods, such as calorie restriction, exercise, or growth hormone receptor mutation, it is clear that doubling worm life spans or a 40-60% increase in mouse life spans certainly doesn’t map to that much of a change in human life span – or even more than just a few years. If it did, we’ve have noticed by now, as it would leap out of the data on human health and mortality. That researchers don’t see that in the data constrains the effects to be fairly small, a handful of years at most. So for my part I believe we should look at this and other similar studies as indicators of importance, not a literal guide to building human therapies. These studies help to point out which forms of age-related molecular damage have the biggest impact, and thus are the highest priority for repair via the methods outlined in the SENS rejuvenation research proposals. It isn’t a suggestion to attempt to adopt modified chaperone systems in humans, as that would be a highly inefficient way to proceed. It would likely produce results on a par with exercise or calorie restriction: improved health, modestly slowed aging. That is far less useful than methods of repairing the damage, clearing out all of the misfolded proteins every now and again before they rise to the level of causing real issues. Periodic repair can create rejuvenation if comprehensive enough. In the near term of decades, adjusting biology to run in a different way can only modestly slow aging; it will be a long time indeed before the research community is capable of safely creating a new biology that doesn’t age in this way. That is time far better spent on the faster path to working rejuvenation treatments.

Defining immortality of stem cells to identify novel anti-aging mechanisms

With age, somatic cells such as neurons lose their ability to maintain the quality of their protein content. Pluripotent stem cells, on the contrary, do not age and have increased mechanism to maintain the integrity of their proteins. The survival of an organism is linked to its ability to maintain the quality of the cellular proteins. A group of proteins called chaperones facilitate the folding of proteins and are essential to regulating the quality of the cellular protein content. This ability declines during the aging process, inducing the accumulation of damaged and misfolded proteins that can lead to cell death or malfunction. Several neurodegenerative age-related disorders such as Alzheimer’s, Parkinson’s or Huntington’s disease are linked to a decline in protein quality control.

Human pluripotent stem cells can replicate indefinitely while maintaining their undifferentiated state and, therefore, are immortal in culture. This capacity necessarily demands avoidance of any imbalance in the integrity of their protein content. “There is one chaperone system, the TRiC/CCT-complex that is responsible for folding about 10% of all the cellular proteins. By studying how pluripotent stem cells maintain the quality of their proteome, we found that this complex is regulated by the subunit CCT8. Then, we discovered a way to increase the assembly and activity of the TRiC/CCT complex in somatic tissues by modulating this single subunit, CCT8. The increase resulted in prolonged lifespan and delay of age-related diseases of the model organism Caenorhabditis elegans. For this study we combined the results from human pluripotent stem cells and C. elegans, to have both in vitro and in vivo models, providing a more convincing approach. Our results show that expressing CCT8 as the key subunit of the complex is sufficient to boost the assembly of the whole system. It is very interesting that expressing this single subunit is enough to enhance protein quality and extend longevity, even in older animals. One of our next steps will be to test our findings in mice.”

Somatic increase of CCT8 mimics proteostasis of human pluripotent stem cells and extends C. elegans lifespan

Human embryonic stem cells can replicate indefinitely while maintaining their undifferentiated state and, therefore, are immortal in culture. This capacity may demand avoidance of any imbalance in protein homeostasis (proteostasis) that would otherwise compromise stem cell identity. Here we show that human pluripotent stem cells exhibit enhanced assembly of the TRiC/CCT complex, a chaperonin that facilitates the folding of 10% of the proteome. We find that ectopic expression of a single subunit (CCT8) is sufficient to increase TRiC/CCT assembly. Moreover, increased TRiC/CCT complex is required to avoid aggregation of mutant Huntingtin protein. We further show that increased expression of CCT8 in somatic tissues extends Caenorhabditis elegans lifespan in a TRiC/CCT-dependent manner. Ectopic expression of CCT8 also ameliorates the age-associated demise of proteostasis and corrects proteostatic deficiencies in worm models of Huntington’s disease. Our results suggest proteostasis is a common principle that links organismal longevity with hESC immortality.


The comparative biology of aging and longevity, comparing the biochemistry of similar species with different life spans, is a good way to improve understanding of which aspects of our biology are important determinants of degeneration and age-related disease. In the open access paper linked here, researchers undertake an examination of gene expression profiles in cell cultures for a range of mammalian species, for example. Despite the usefulness, as an investigative method this will, I expect, be overtaken by prototype rejuvenation therapies based on damage repair in the years ahead. Aging is an accumulation of cell and tissue damage, and the best way to determine the contribution of any one particular type of damage is to remove it. Researchers are beginning that process for cellular senescence, now that senescent cells can be selectively destroyed in an efficient manner, and other items from the SENS portfolio of rejuvenation biotechnologies will be added as they reach the stage of practical demonstration in animal studies.

The maximum lifespan of mammalian species differs by more than 100-fold, ranging from ~2 years in shrews to more than 200 years in bowhead whales. While it has long been observed that maximum lifespan tends to correlate positively with body mass and time to maturity, but negatively with growth rate, mass-specific metabolic rate, and number of offspring, the underlying molecular basis is only starting to be understood. One way to study the control of longevity is to identify the genes, pathways, and interventions capable of extending lifespan or delaying aging phenotypes in experimental animals. Studies using model organisms have uncovered several important conditions, such as knockout of insulin-like growth factor 1 (IGF-1) receptor, inhibition of mechanistic target of rapamycin (mTOR), mutation in growth hormone (GH) receptor, ablation of anterior pituitary (e.g. Snell dwarf mice), augmentation of proteins of the sirtuin family, and restriction of dietary intake. While many of these genes and pathways have been verified in yeast, flies, worms, and mice, the comparisons largely involve treatment and control groups of the same species, and the extent to which they explain the longevity variations across different species is unclear. For example, do the long-lived species have metabolic profiles resembling calorie restriction? Do they suppress IGF-1 or growth hormone signaling compared with the shorter-lived species? More generally, how do the evolutionary strategies of longevity relate to the experimental strategies that extend lifespan in model organisms?

To address these questions, a popular approach has been to compare exceptionally long-lived species with closely related species of common lifespan and identify the features associated with exceptional longevity. Examples include the amino acid changes in Uncoupling Protein 1 (UCP1) and production of high-molecular-mass hyaluronan in the naked mole rat; unique sequence changes in IGF1 and GH receptors in Brandt’s bat; gene gain and loss associated with DNA repair, cell-cycle regulation, and cancer, as well as alteration in insulin signaling in the bowhead whale; and duplication of the p53 gene in elephants. Again, it is important to ascertain whether these mechanisms are unique characteristics of specific exceptionally long-lived species, or whether they can also help account for the general lifespan variation.

An extension of this approach has been cross-species analyses in a larger scale. For example, several biochemical studies across multiple mammalian and bird species identified some features correlating with species lifespan. Longevity of fibroblasts and erythrocytes in vitro, poly (ADP-ribose) polymerase activity, and rate of DNA repair were found to be positively correlated with longevity, whereas mitochondrial membrane and liver fatty acid peroxidizability index, rate of telomere shortening, and oxidative damage to DNA and mitochondrial DNA showed negative correlation. The advent of high throughput RNA sequencing (RNAseq) and mass spectrometry technologies has enabled the quantification of whole transcriptomes, metabolomes, and ionomes, across multiple species and organs. These studies revealed the complex transcriptomic and metabolic landscape across different organs and species, as well as some overlaps with the changes observed in the long-lived mutants created in laboratory.

While molecular profiling of mammals at the level of tissues may better represent the underlying biology, profiling in cell culture represents more defined experimental conditions and allows further manipulation to alter the identified molecular phenotypes. In this study, we examined the transcriptomes and metabolomes of primary skin fibroblasts across 16 species of mammals, to identify the molecular patterns associated with species longevity. We report that the genes involved in DNA repair and glucose metabolism were up-regulated in the longer-lived species, whereas proteolysis and protein translocation activities were suppressed. The longer-lived species also had lower levels of lysophosphatidylcholine and lysophosphatidylethanolamine and higher levels of amino acids; and the latter finding was validated in an independent dataset of bird and primate fibroblasts.



To what degree does regular exercise beyond the recommended minimum of 30 minutes a day improve long-term health and life expectancy? This and related questions on the shape of the dose-response curve for aerobic exercise remain open for debate. It is clear that being sedentary has a cost in terms of health and life expectancy, and the balance of evidence to date suggests that the 80/20 point for benefits due to exercise is found somewhere higher than the generally recommended level. Yet it is unclear as to whether professional athletes, who tend to live longer than the general population, live longer because of the high levels of exercise or because they also tend to be more robust individuals who would have enjoyed greater longevity regardless of profession. While it remains to put good numbers to much of the dose-response curve for exercise, this study of the Hadza people adds to the evidence for additional benefits to accrue to those who go beyond 30 minutes a day:

The Hadza live a very different kind of lifestyle – and a very active one, engaging in significantly more physical activity than what is recommended by U.S. government standards. They also have extremely low risk of cardiovascular disease. Researchers have spent several years studying the lifestyle of the Hadza. “Our overall research program is trying to understand why physical activity and exercise improve health today, and one arm of that research program aims to reconstruct what physical activity patterns were like during the evolution of our physiology. The overarching hypothesis is that our bodies evolved within a highly active context, and that explains why physical activity seems to improve physiological health today.”

The U.S. Department of Health and Human Services recommends that people engage in 150 minutes per week of moderate intensity activity – about 30 minutes a day, five times a week – or about 75 minutes per week of vigorous intensity activity, or an equivalent combination of the two. However, few Americans achieve those levels. The Hadza, on the other hand, meet those weekly recommendations in a mere two days, engaging in about 75 minutes per day of moderate-to-vigorous physical activity, or MVPA. Furthermore, and consistent with the literature identifying aerobic activity as a key element necessary to a healthy lifestyle, researchers’ health screenings of Hadza people have shown that the population has extremely low risk for heart disease. “They have very low levels of hypertension. In the U.S., the majority of our population over the age of 60 has hypertension. In the Hadza, it’s 20 to 25 percent, and in terms of blood lipid levels, there’s virtually no evidence that the Hadza people have any kind of blood lipid levels that would put them at risk for cardiovascular disease.”

While physical activity may not be entirely responsible for the low risk levels – diet and other factors may also play a role – exercise does seem to be important, which is significant because humans’ physical activity levels have drastically declined as we have transitioned from hunting and gathering to farming to the Industrial Revolution to where we are today. “Over the last couple of centuries, we’ve become more and more sedentary, and the big shift seems to have occurred in the middle of the last century, when people’s work lives became more sedentary. In the U.S., we tend to see big drop-offs in physical activity levels when people age. In the Hadza, we don’t see that. We see pretty static physical activity levels with age. This gives us a window into what physical activity levels were we like for quite a while during our evolutionary history, and, not surprisingly, it’s more than we do now. Perhaps surprisingly, it’s a whole lot more than we do now. Going forward, this helps us model the types of physical activity we want to be looking at when we explore our physiological evolution. When we ask what kinds of physical activity levels would have driven the evolution of our cardiovascular system and the evolution of our neurobiology and our musculoskeletal system, the answer is not likely 30 minutes a day of walking on a treadmill. It’s more like 75-plus minutes a day.”



Cellular senescence is one of the root causes of aging, and there are at present serious, well-funded efforts underway to produce rejuvenation therapies based on the selective destruction of senescent cells in old tissues. This progress is welcome, but it could have started a long time ago. It has taken many years of advocacy and the shoestring production of technology demonstrations to finally convince the broader community of scientists and funding institutions that the evidence has long merited serious investment in treatments to clear senescent cells. This is what it is, and now we must look to the future, for all that it has been a long, uphill battle. Cellular senescence is today having its time in the sun. Many research groups are linking the mechanisms of senescence to other aspects of aging; senescent cells are showing up in many more research papers than in past years, now that there is more of a scientific and financial incentive to search carefully for their influence. I think that declaring cellular senescence to be the causal nexus of aging, as one research group did, is going overboard a little, as there are, after all, other independent causes of aging, forms of metabolic waste and damage that would cause death and disease even if cellular senescence did not exist. Nonetheless, it is gratify to watch the spreading realization that cellular senescence plays a role in many areas of health and biology associated with aging. The advent of therapies that can remove senescent cells promises to produce sweeping beneficial effects on aging and disease.

There is a set of fairly well established threads of research that link aging with visceral fat tissue and immune dysfunction in the form of chronic inflammation. Visceral fat produces an accelerated pace of aging by generating greater chronic inflammation, producing an hostile tissue environment of inappropriate signals that attract immune cells and then cause those cells to become dysfunctional. The more fat there is the more inflammation it creates. This is thought to be the primary mechanism by which obesity increases the risk and severity of age-related disease. All of the common age-related diseases are accelerated in their progression by higher levels of chronic inflammation. The material difference between a lot of fat and a normal amount of fat is well demonstrated by a study in which researchers produced life extension in mice through surgical removal of visceral fat, but there is a mountain of data on human health to show that people who are overweight will suffer a shorter life expectancy and more age-related illness, and that this effect scales by the amount of excess fat tissue. How do senescent cells fit into this picture? One of the characteristic features of senescent cells is that they produce greater levels of chronic inflammation via the secretion of signal molecules such as cytokines. Of late, researchers have shown that senescent cells are found in the immune system, as in other cell populations. Given this, it should not be a surprise to find that cellular senescence can be implicated in the way in which visceral fat accelerates aging: their presence in visceral fat tissue and the immune cells interacting with that tissue fits right in with the broader picture of inflammation and bad cellular behavior.

Obesity accelerates T cell senescence in murine visceral adipose tissue

Visceral obesity is associated with chronic low-grade inflammation in visceral adipose tissue (VAT) and a sustained whole-body proinflammatory state, which may underlie metabolic and cardiovascular diseases. VAT inflammation associated with obesity involves a complex network of responses of immune cell components, including acquired immune cells such as various subsets of T cells and B cells and innate immune cells such as macrophages. Among these cells, CD4+ T cells have been recognized as a central regulator of chronic VAT inflammation. The number of CD4+ T cells in VAT increases as the tissue expands in obesity. Factors that drive CD4+ T cell expansion and into proinflammatory effectors in VAT during the development of high-fat diet-induced (HFD-induced) obesity may include MHC class II-associated antigens, possibly self-peptides, because the T cell receptor (TCR) repertoire of CD4+ T cells in VAT is limited, and deficiency of MHC class II protects mice from high fat diet (HFD)-induced VAT inflammation and insulin resistance. However, the obesity-associated immune background underlying chronic inflammation in VAT remains elusive.

Significant changes occur in the overall T cell populations with age. In CD4+ T cells, proportions of naive (CD44loCD62Lhi) cells sharply decline in ontogeny, with an age-dependent increase in cells of the memory phenotype (CD44hiCD62Llo). Among CD44hiCD4+ T cells, a unique population expressing programmed cell death 1 (PD-1) and CD153 actually increases with age in mice. The CD153+PD-1+CD44hiCD4+ T cell population shows compromised proliferation and regular T cell cytokine production on T cell receptor (TCR) stimulation but secretes large amounts of proinflammatory cytokines, such as osteopontin. These CD4+ T cells also show signatures of cell senescence, including a marked increase in senescence-related gene expression and nuclear heterochromatin foci, and are termed senescence-associated T cells (SA-T cells). Notably, the age-dependent development of SA-T cells, which may include autoreactive cells, is dependent on B cells. As such, the increase in SA-T cells is suggested to be involved in part in immune aging phenotypes such as impaired acquired immune capacity, increased proinflammatory traits, and high risk for autoimmunity.

In the present study, we demonstrate that CD153+PD-1+CD44hiCD4+ T cells are remarkably increased and preferentially accumulated in the VAT of HFD-fed mice in a B cell-dependent manner and that these CD4+ T cells show functional and genetic features strongly resembling SA-T cells that increase in secondary lymphoid tissues with age. We also indicate that the CD153+PD-1+CD44hiCD4+ T cells play a crucial role in inducing chronic VAT inflammation and metabolic disorder via secretion of large amounts of osteopontin. We demonstrated that adoptive transfer of CD153+PD-1+CD44hiCD4+ T cells, but not other CD4+ T cells, from HFD-fed spleens into VAT of ND-fed mice recapitulates the features of VAT inflammation, including a striking increase in CD11chiCD206lo macrophages and expression of proinflammatory cytokine genes. It is noteworthy that CD153+PD-1+CD4+ T cells in VAT of HFD-fed mice show features indistinguishable from those of CD153+ SA-T cells, which gradually increase systemically with age. The age-dependent increase in CD153+ SA-T cells may partly underlie the immune aging, including a reduction in acquired immunity and an increase in the inflammatory trait and autoimmunity risk. Obesity is also associated with diminished resistance against infection, chronic low-grade inflammation, and a greater susceptibility to autoimmunity. It has been suggested that the increase in CD153+ SA-T cells in chronological aging and systemic autoimmunity is attributable to a robust, homeostatic T cell proliferation, but the precise mechanism underlying the accumulation of these T cells in VAT of HFD-fed mice remains to be investigated. Nonetheless, it is an intriguing possibility that the predisposition often associated with obesity may partly be a systemic manifestation of the premature increase in CD153+ SA-T cells in VAT, since adipose tissues can constitute up to 50% to 60% of total BW in severe obesity.


Both birds and bats have great longevity for their size in comparison to mammalian species that do not fly, which has led researchers to theorize that the metabolic demands of flight lead to the evolution of cell structures that are more resistant to the damage of aging. Energy metabolism revolves around the mitochondria, the power plants of the cells, and so this in turn points to an important role for mitochondrial function and damage to mitochondria in determining aging and longevity, both across species and in individuals. There are good correlations between mitochondrial composition, the degree to which mitochondrial structures can resist oxidative damage, and mammalian life span, for example. Researchers here take a more reductionist approach to the question of why bats are exceptionally long-lived, and begin by mapping the RNA of a bat species:

Of all mammals, bats possess some of the most unique and peculiar adaptations that render them as excellent models to investigate the mechanisms of extended longevity and potentially halted senescence. They are considered the ‘Methusalehs’ among mammals due to their exceptional and surprising longevity given their body size and metabolic rate. Typically mammals that are small have a high metabolic rate (e.g. shrews) and do not live for a long time. However, despite their small size and high metabolic rate bats can live for an exceptionally long time, with the oldest recorded Brandt’s bat (wild caught as an adult) ever recaptured being more than 41 years old with a body weight of 7 grams. Indeed, to get a positive correlation between longevity and body size in mammals, bats must be removed from the analyses. By comparing the ratio of expected longevity to that predicted from the ‘non-bat placental mammal’ regression line (longevity quotient – LQ) only 19 species of mammals are longer lived than man, one of these species being the naked mole rat and the other 18 are bats. This suggests that bats have some underlying mechanisms that may explain their exceptional longevity.

MicroRNA (miRNA) are a subset of short endogenous non-coding RNA that play a significant role in post-transcriptional regulation, via repression of translation. Since the first miRNA was discovered in 1993, a multitude of miRNA have subsequently been identified, and implicated in the regulation of the vast majority of biological pathways including cell cycle regulation, metabolism, tumorigenesis, as well as immune response. However, the role of miRNA regulation in mammalian ageing and the onset of age-related diseases has only recently been established. In mammals, various miRNA have been shown to be differentially expressed during ageing, most of which appear to be generally tissue-specific. In addition to tissue-specific ageing, it is increasingly evident that many miRNA regulate gene expressions in well-known ageing pathways, most notably in the p53 tumor suppressor pathway and insulin-like growth factor signaling pathway.

Despite being the second largest order of mammals (~1200 species), there is a scarcity of genomic and transcriptomic bat resources. To date, only five well-annotated bat genomes are publically available. Phylogenomic studies of bat genomes and other mammalian species reveal that a number of genes are under positive selection in bats. These genic adaptations have been correlated with traits such as echolocation, powered flight, hibernation, immunity and longevity. For example, specific non-synonymous mutations in GHR and IGF1R, key ageing-related genes, were detected in several long-lived vespertilionid bats (M. brandtii, M. lucifugus and Eptesicus fuscus), while a large proportion of genes involved in DNA repair (RAD50, KU80, MDM2, etc.) and the NF-B pathway (c-REL and ATM2, etc.) were reported to be under positive or divergent selection in M. davidii and P. alecto. These results suggest bats may better detect and repair DNA damage. Intriguingly, positive selection was also detected in mitochondrial-encoded and nuclear-encoded oxidative phosphorylation genes in bats, which may explain their efficient energy metabolism necessary for flight. Apart from comparative genome analysis, only a small number of transcriptomic studies on bats using have been carried out, focused primarily on the characteristics of hibernation, immunity, echolocation and phylogeny. However, the molecular mechanisms of adaptations affecting longevity are still far from understood, especially with respect to gene regulation.

In the present study, we sequenced six small RNA libraries from whole blood sampled from wild-caught greater mouse-eared bats (Myotis myotis) and for the first time made genome-wide comparisons of both miRNomes and mRNA transcriptomes between bat and non-bat mammalian species (human, pig and cow). The profiling of the M. myotis blood miRNome showed a large number of bat-specific miRNA involved in regulating important pathways related to immunity, tumorigenesis and ageing. Comparative analyses of both miRNomes and transcriptomes also revealed distinctive longevity mechanisms in bats. Several up-regulated miRNA possibly act as tumor suppressors. Gene Ontology (GO) enrichment analysis of differentially expressed protein-coding genes showed that up-regulated genes in bats compared to other mammals were mainly involved in mitotic cell cycle and DNA damage repair pathways while a high number of down-regulated genes were enriched in mitochondrial metabolism. The results and data presented here show unique regulatory mechanisms for protection against tumorigenesis, reduced oxidative stress, and robust DNA repair systems, likely contribute to the extraordinary longevity of bats.



Very few genetic variants robustly correlate with longevity across different study populations, and those that do, such as variants of APOE and FOXO3A, have small effects, only visible in the mortality statistics of large numbers of people. This indicates that the genetics of longevity, the way in which variations in metabolism and the response to high levels of age-related cell and tissue damage in later life can produce modestly different mortality rates, is a matter of many thousands of tiny, interacting contributions, very sensitive to environmental factors. It appears ever less likely that there will be any easy, small number of genetic changes that can be made to humans in order to produce significant lengthening of life. Thus the study of genetics and longevity isn’t the place to be looking for cost-effective ways to produce radical life extension of decades and more. This paper is one of many recent illustrations of this point; none of the described problems would be anywhere near as much of a challenge if there was a large genetic effect on aging and longevity with simple, narrow origins there to be found. That would stand out from the data much more readily.

The results of many genome-wide association studies (GWAS) of complex traits suffer from a lack of replication. Differences in population genetic structures among study populations are considered to be possible contributors to this problem. One aspect of population structure – the differences in genetic frequencies among subgroups of individuals comprising the population – was traditionally linked with the effects of population stratification. Another one – the presence of linkage disequilibrium (LD) in many parts of the human genome including those that contain causal single-nucleotide polymorphisms (SNPs) – was actively exploited in GWAS of complex traits. Methods of fine mapping following the “discovery” phase are used for evaluating causal SNPs. One could expect that the non-replication problem due to differences in LD patterns among study populations in GWAS would disappear if the detected marker SNP is a causal one, i.e., if it contributes to the variability of a trait. It turns out that the differences in LD levels around a functional SNP may still contribute to the non-replication problem.

The estimated associations in this case depend on whether the detected functional SNP is in LD with another functional SNP, the effects of these SNPs on the trait in the absence of LD (pure effects), and on the level of LD between corresponding SNP loci. This property has important consequences for interpretation of the results of genetic analyses of complex traits. In the presence of LD the estimated effects of a causal SNP may be spurious and may incorrectly characterize the biological relationships between the SNP and the trait. In contrast the pure effect of a given causal SNP estimated in the absence of LD with other such SNPs may correctly characterize the biological connections between the SNP and the trait. Therefore, for example, performing genetic analyses of African populations (that have lower levels of LD patterns for many SNP pairs than populations of European origin) has the potential to reduce bias in the estimated effects of functional SNPs on a trait caused by the presence of LD between functional loci. This condition is, however, not sufficient because of the possible presence of hidden gene/gene interaction effects, gene/environment correlations, and gene/environment interaction effects.

Human lifespan and many other aging, health and longevity related traits are multifactorial phenotypes, that is, they are affected by many genetic and non-genetic factors. The relationships between genes and these phenotypes have special features that distinguish them from other complex traits, influence methods of their genetic analyses, and affect the interpretation of the research results. The genetic variants that influence aging, health, and longevity related traits generate age dependent changes in the population genetic structure, i.e., changes in the frequencies of genetic variants and in the levels of linkage disequilibrium (LD) among them. This feature has important implications for studies focused on the replication of GWAS research findings: independent populations involved in such studies often have different genetic structures, due in part to the differences in the population age distribution at the time of biospecimen collection. As a result, the frequencies of the genetic variants associated with these traits and their LD patterns may differ even if the genetic structures in the corresponding population cohorts were the same at birth.

Detecting statistically significant associations of genetic variants with complex traits is not the end of the genetic analyses. One reason is that the relationship between a detected marker SNP and the complex trait of interest is not, necessarily, a causal one. More often these relationships serve as proxies for the real effect of some unobserved causal SNPs (due to linkage disequilibrium (LD) between the marker and causal SNPs), and, hence, do not have a direct biological effect on the phenotype. To generate insights about the biological mechanisms responsible for the trait’s variability one has to identify the causal SNPs responsible for the association signal. To identify such SNPs a number of efficient fine-mapping procedures have been recommended. The main limitation of existing methods is that they seek to identify a single causal variant which is independent of (not in LD with) other causal variants. Since this is not sufficiently realistic, a new approach that allows for efficient detection of multiple causal variants has been proposed. The case where two or more causal SNPs are in LD creates additional problems for interpretation of the results of genetic association studies.

In this paper we show that the estimates of the effects of a causal SNP on lifespan depend on the genetic structure of the population under study (e.g., the level of LD of the SNP with other causal SNPs). Genetic association studies of this trait using data from populations with different LD levels are likely to produce different results. We show that differences in population genetic structures can explain why genetic variants favorable for longevity in one population appear as harmful risk factors in another population. Population structure may also be responsible for the age-specific effects of genetic variants on mortality risk. Differences in genetic structures in distinct populations may be responsible for the low level of replicability of GWAS of human aging, health, and longevity related traits.



I stumbled upon an interesting open access paper a few days ago, linked below, in which the authors present their view of immunosenescence, the age-related failure of the immune system, as being in part a process wherein some cells of the adaptive immune system change their characteristics and function to become more like innate immune system cells. It makes for interesting reading, though it is worth bearing in mind that the immune system as a whole is fantastically complex, and in many ways still a dark and unmapped forest. It is easy to theorize unopposed when there is such a lot of empty space remaining on the map, making it hard to argue concretely about the relative importance of various mechanisms and observations. This poor understanding of the intricacies of the immune system is why autoimmune diseases and immune aging are largely lacking in effective treatments, and why the best of the prospective cures are those that sidestep the entire question of specific causes and mechanisms in face of the Gordian strategy of destroying the entire immune system in order to start over with new stem cells and immune cells.

As you might know, the immune system of most higher animals is two-layered. The layer that evolved first, and which remains the entirety of the immune system in lower animals such as insects, is known as the innate immune system. It reacts quickly, generates inflammation, and reacts in the same, predictable way to every threat. It has no memory and does not reconfigure its operations in response to circumstances and history. Later in evolutionary history, a second layer known as the adaptive immune system came into being, a more sophisticated set of functions resting on top of the existing innate mechanisms. The innate immune system reacts to intruders, and then the adaptive immune system records the nature of the threat and responds in its own manner, augmenting the attack. As the name suggests, the adaptive immune system maintains a memory and adjusts its operations in order to more aggressively destroy pathogens that it has encountered in the past. As anyone in the field will tell you, however, this high level picture of cleanly divided dualism is overly simplistic, however. There are numerous grey areas and incompletely understood complexities at the border between the two sides of the immune system.

Given that the adaptive immune system can adapt, its failure with aging is in large part a matter of acquired misconfiguration. There is only a small influx of new immune cells in adults, and this puts an effective limit on the number of immune cells that is supported at any one time. The inevitable problem in a space-limited system that keeps a continual record of history is that it runs out of space: evolutionary pressures produced the trade-off of a system that works very well out of the gate in young people, but fails sometime in later life. An old adaptive immune system is burdened with too many cells devoted to memory and too few cells devoted to attacking new threats. That is on top of the progressive failures that occur due to the the growing burden of the molecular damage that accompanies aging: persistent metabolic waste products such as cross-links and lipofuscin, mitochondrial damage, diminished stem cell activity, and so forth. The innate immune system has its own problems that arise from this damage, but is less prone of the issue of misconfiguration.

Understanding exactly how aging progressively harms the intricate choreography of the immune response is a massive project, and nowhere near completion. It is possible to judge how far along researchers are in this work by the side effect of the quality of therapies for autoimmune disease, which are malfunctions in immune configuration, and largely incurable at the present time. From a practical point of view, and as mentioned above, the best prospects for effective treatments in the near future involve destroying and recreating the immune system. That works around our comparative ignorance by removing all of the problems that researchers don’t understand in addition to ones that they do. Destroying the immune system can only be done with chemotherapy at the moment, which no-one would undergo unless there was no choice in the matter given that it has significant negative effects on long-term health, but once new methods of selective immune cell destruction are developed, lacking side-effects, then we can start to talk about treating immune aging by rebooting the immune system.

Convergence of Innate and Adaptive Immunity during Human Aging

Aging is associated with a general decline in immune function, contributing to a higher risk of infection, cancer, and autoimmune diseases in the elderly. Such faulty immune responses are the result of a profound remodeling of the immune system that occurs with age, generally termed as immunosenescence. While the number of nave T cells emerging from the thymus progressively decreases with age as a result of thymic involution, the memory T cell pool expands and exhibits significant changes in the phenotype and function of antigen-experienced T cells, particularly evident in the CD8+ T cell compartment. Chronic immune activation due to persistent viral infections, such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV), is one of the main drivers contributing to the accumulation of highly differentiated antigen-specific CD8+ T lymphocytes that have characteristics of replicative senescence. In combination with the depletion of the peripheral pool of nave T cells, the accumulation of these terminally differentiated T cells with age skews the immune repertoire and has been implicated in the impaired immune responses to new antigens and vaccination in the elderly

Natural killer cells and CD8+ T lymphocytes are the two major cell lineages with constitutive cytotoxic activity and have a crucial role in the recognition and killing of abnormal cells. However, the paradigm for the recognition of target cells is fundamentally different between these two cell types: conventional CD8+ T cells rely on the T cell receptor (TCR) to recognize specific peptides presented by major histocompatibility complex class-I (MHC-I) molecules, whereas NK cells use a repertoire of germ line-encoded receptors to detect “missing self” or “altered-self” antigens and directly kill abnormal cells, without prior sensitization. Besides antigen specificity, the development of immunological memory is conventionally another distinctive feature between NK and T cells, categorizing them into distinct arms of the immune system and the innate and adaptive immune system, respectively.

Nevertheless, accumulating evidence supports the existence of NK cell memory, as well as evidence for TCR-independent responses mediated by CD8+ T lymphocytes, suggesting that the conventional limits between the innate and adaptive arms of the immune system may be not as distinct as first thought. NK and T lymphocytes have a common origin from a lymphoid progenitor cell in the bone marrow, and recent comparative proteomic and transcriptomic studies have demonstrated a remarkably close proximity between effector CD8+ T lymphocytes and NK cells, reiterating an evolutionary ancestry and shared biology between the two cell lineages.

An increasing body of literature reveals the existence of subsets of T cells with features that bridge innate and adaptive immunity. These cells typically co-express a TCR and NK cell lineage markers, distinguishing them from NK cells and other innate lymphoid cells, which lack the expression of a TCR or somatically rearranged receptors. Functionally, innate-like T cells respond to TCR ligation but are also able to respond rapidly to danger signals and pro-inflammatory cytokines, independently of TCR stimulation, resembling innate cells. Recently, subsets of conventional CD8+ T cells expressing NK cell markers and intraepithelial T cells have been included in this vaguely defined group of innate-like T cells. Despite the similarities in phenotype and function, there are clear differences in ontogeny and tissue distribution between them.

In this review, we will discuss recent evidence that aging is associated with the expansion of a subset of conventional CD8+ T cells with phenotypic, functional, and transcriptomic features that resemble NK cells. Such innate-like CD8+ T cells have the characteristics of terminally differentiated T cells, and the acquisition of functional NK receptors is most likely part of a general reprograming of the CD8+ T cell compartment during human aging, to ensure broad and rapid effector functions. We propose that innate-like CD8+ T cells share important features with other innate-like T cells; however, fundamental differences in origin and development separate them from truly innate cells. Interestingly, these cells are also differentially affected by aging, suggesting distinct roles in immune responses at different times of life. Evidence indicates that chronological aging is associated with accumulation of cells combining features of both the innate and adaptive arms of the immune system, most likely to compensate for functional defects of conventional NK and CD8+ T cells with age. We propose that senescent CD8+ T cells should not be seen as a dysfunctional population but instead a functionally distinct subset, which uses recently acquired NK cell machinery to maintain rapid effector functions throughout life. Contrary to the classic paradigm that peripheral TCR ligation is essential for T cell activation, this subset of highly differentiated T cells has impaired TCR responsiveness and may be non-specifically activated by inflammatory cytokines or after ligation of innate receptors. The switch to an innate mode of function may shed light on the mechanisms that allow highly differentiated CD8+ T cells to maintain functionality, despite the loss of TCR signal functions.

Our understanding of the physiological significance of the expression of NKRs on T cells is still incomplete, and the identification of the molecular mechanisms and the transcriptional regulators underpinning the development of innate features in T cells is essential. Most importantly, it will be important to understand how the intersection between innate and adaptive immune features may be manipulated to enhance immune function and to use this information to develop new approaches to improve immunity in the elderly.


There are many possible answers to the question of why women have a longer life expectancy than men, but no real consensus on which of the candidate mechanisms are the important ones. It is interesting to note that, in an age in which rejuvenation therapies are starting to arrive, the research community has a better idea of how to bring aging under medical control, and thus make natural variations in longevity irrelevant, than of how to definitively determine the mechanisms causing those natural variations between groups of humans. Fully understanding our biochemistry is a massive undertaking, far greater in scope than merely wrestling degenerative aging into submission by addressing its root causes. Biology is enormously complex, and working with statistical demographic data or evolutionary theory doesn’t tend to produce firm answers, only helping to narrow down the directions for further inquiry.

People worldwide are living longer, healthier lives. A new study of mortality patterns in humans, monkeys and apes suggests that the last few generations of humans have enjoyed the biggest life expectancy boost in primate history. The gains are partly due to advances in medicine and public health that have increased the odds of survival for human infants and reduced the death toll from childhood illness. Yet males still lag behind females – not just in humans but across the primate family tree, the researchers find. “The male disadvantage has deep evolutionary roots.”

An international team compiled records of births and deaths for more than a million people worldwide, from the 18th century to the present. The data included people in post-industrial societies such as Sweden and Japan, people born in pre-industrial times, and modern hunter-gatherers, who provide a baseline for how long people might have lived before supermarkets and modern medicine. The researchers combined these measurements with similar data for six species of wild primates that have been studied continuously for three to five decades, including sifaka lemurs, muriqui monkeys, capuchins, baboons, chimpanzees and gorillas. The data confirm a growing body of research suggesting that humans are making more rapid and dramatic gains than ever before seen in the primate family tree. For example, in the last 200 years life expectancy in Sweden has jumped from the mid-30s to over 80, meaning that a baby born today can hope to live more than twice as long as one born in the early 19th century. The data show that today’s longest-lived human populations have a similar 40- to 50-year advantage over people who live traditional lifestyles, such as the Hadza hunter-gatherers of Tanzania and the Ach people of Paraguay.

In contrast, these modern hunter-gatherers – the best lens we have into the lives of early humans – live on average just 10 to 20 years longer than wild primates such as muriquis or chimpanzees, from which human ancestors diverged millions of years ago. “We’ve made a bigger journey in lengthening our lifespan over the last few hundred years than we did over millions of years of evolutionary history.” One indicator of healthcare improvement is infant mortality, which strikes fewer than 3 in 1000 babies born in Sweden or Japan today. But it was more than 40 times higher for those born two centuries ago, and is still high among hunter-gatherers and wild primates.

The researchers also studied lifespan equality, a measure similar to income equality that indicates whether longevity is distributed evenly across society, or only enjoyed by a few. They found that, for both humans and wild primates, every gain in average lifespan is accompanied by a gain in lifespan equality. That is, for a population to be very long-lived, everyone must benefit more or less equally, with fewer individuals left behind. The researchers were surprised to find that the longevity of human males has yet to catch up with females, and the improvements in males aren’t spread as evenly. A girl born in Sweden in the early 1800s could expect to outlive her male counterparts by an average of three to four years. Two hundred years later, despite Swedes adding 45 years to their average lifespan, the gulf that separates the sexes has barely budged. The life expectancy gender gap isn’t just true for humans. Females outlived males in almost every wild primate population they looked at.



In the field of tissue engineering, this is the era of organoids. Researchers are limited in the size of tissue they can produce because of the lack of a robust method of generating the blood vessel networks needed to support large tissue sections, but are otherwise making significant progress in the generation of functional organ tissue. Initially this is producing the greatest benefit for further research and development, allowing tests to be conducted in living tissue at a much faster pace and lower cost. For many tissue types, however, organoids also offer the possibility of benefits realized through transplantation, as in many cases they are capable of integrating with existing organ tissue to improve its function.

Scientists report using human pluripotent stem cells to grow human intestinal tissues that have functioning nerves in a laboratory. The paper puts medical science a step closer to using human pluripotent stem cells (which can become any cell type in the body) for regenerative medicine and growing patient-specific human intestine for transplant. “One day this technology will allow us to grow a section of healthy intestine for transplant into a patient, but the ability to use it now to test and ask countless new questions will help human health to the greatest extent.” This ability starts with being able to model and study intestinal disorders in functioning, three-dimensional human organ tissue with genetically-specific patient cells. The technology will also allow researchers to test new therapeutics in functioning lab-engineered human intestine before clinical trials in patients.

Researchers started out by subjecting human pluripotent stem cells to a biochemical bath that triggers their formation into human intestinal tissue in a petri dish. The process was essentially the same as that used in a 2010 study, which reported the first-ever generation of three-dimensional human intestinal organoids in a laboratory. Intestinal tissues from the initial study lacked an enteric nervous system, which is critical to the movement of waste through the digestive tract and the absorption of nutrients. The gastrointestinal tract contains the second largest number of nerves in the human body. When these nerves fail to work properly it hinders the contraction of intestinal muscles. To engineer a nervous system for the intestinal organoids already growing in one petri dish, researchers generated embryonic-stage nerve cells called neural crest cells in a separate dish. The neural crest cells were manipulated to form precursor cells for enteric nerves. The challenge at this stage was identifying how and when to incorporate the neural crest cells into the developing intestine. “We tried a few different approaches largely based on the hypothesis that, if you put the right cells together at the right time in the petri dish, they’ll know what do to. It was a long shot, but it worked.” The appropriate mix caused enteric nerve precursor cells and intestines to grow together in a manner resembling developing fetal intestine.

A key test for the engineered intestines and nerves was transplanting them into a living organism – in this case laboratory mice with suppressed immune systems. This allowed researchers to see how well the tissues grow and function. Study data show the tissues work and are structured in a manner remarkably similar to natural human intestine. They grow robustly, process nutrients and demonstrate peristalsis – series of wave-like muscle contractions that in the body move food through the digestive tract.



The first rejuvenation therapies to work well enough to merit the name will be based on the SENS vision: that aging is at root caused by a few classes of accumulated cell and tissue damage, and biotechnologies that either repair that damage or render it irrelevant will as a result produce rejuvenation. Until very recently, no medical technology could achieve this goal, and few research groups were even aiming for that outcome. We are in the midst of a grand transition, however, in which the research and development community is finally turning its attention to the causes of aging, understanding that this is the only way to effectively treat and cure age-related disease. Age-related diseases are age-related precisely because they are caused by the same processes of damage that cause aging: the only distinctions between aging and disease are the names given to various collections of symptoms. All of frailty, disease, weakness, pain, and suffering in aging is the result of accumulated damage at the level of cells and protein machinery inside those cells. Once the medical community becomes firmly set on the goal of repairing that damage, we’ll be well on the way to controlling and managing aging as a chronic condition – preventing it from causing harm to the patient by periodically repairing and removing its causes before they rise to the level of producing symptoms and dysfunction. The therapies of the future will be very different from the therapies of the past.

The full rejuvenation toolkit of the next few decades will consist of a range of different treatments, each targeting a different type of molecular damage in cells and tissues. In this post, I’ll take a look at the likely order of arrival of some of these therapies, based on what is presently going on in research, funding, and for-profit development. This is an update to a similar post written four years ago, now become somewhat dated given recent advances in the field. Circumstances change, and considerable progress has been made in some lines of research and development.

1) Clearance of Senescent Cells

It didn’t take much of a crystal ball four years ago to put senescent cell clearance in first place, the most likely therapy to arrive first. All of the pieces of the puzzle were largely in place at that time: the demonstration of benefits in mice; potential means of clearance; interested research groups. Only comparatively minor details needed filling in. Four years later no crystal ball is required at all, given that Everon Biosciences, Oisin Biotechnologies, SIWA Therapeutics, and UNITY Biotechnology are all forging ahead with various different approaches to the selective destruction of senescent cells. No doubt many groups within established Big Pharma entities are also taking a stab at this, more quietly, and with less press attention. UNITY Biotechnology has raised more than $100 million to date, demonstrating that there is broad enthusiasm for this approach to the treatment of aging and age-related disease.

With the additional attention and funding for this field, more methods of selective cell destruction have been established, and there is now a greater and more detailed understanding of the ways in which senescent cells cause harm, contributing to the aging process. Senolytic drugs that induce apoptosis have been discovered; senescent cells are primed to enter the programmed cell death process of apoptosis, and so a small nudge to all cells via a drug treatment kills many senescent cells but very few normal cells. Researchers have established that senescent cells exist in the immune system, and may be important in immune aging. Similarly, the immune cells involved in the progression of atherosclerosis are also senescent, and removing them slows the progression of that condition. Other research has shown that removing senescent cells from the lungs restores lost tissue elasticity and improves lung function. Beyond these specific details, senescent cells clearly contribute to chronic inflammation in aging, and that drives the progression of near all common age-related conditions. The less inflammation the better. These effects are caused by the signals secreted by senescent cells: that their harm is based on signaling explains how a small number of these cells, perhaps 1% by number in an aged organ, can cause such widespread havoc.

2) Immune System Destruction and Restoration

At the present time it is a challenge to pick second place. A number of fields are all equally close to realization, and happenstance in funding decisions, regulatory matters, or technical details yet to be uncovered will make the difference. The destruction and recreation of the immune system wins out because it is already possible, already demonstrated to be successful, and just missing one component part that would enable it to be used by ordinary, healthy, older people. At present researchers and clinicians use chemotherapy to destroy immune cells and the stem cells that create them. Repopulation of the immune system is carried out via cell transplants that are by now a safe and proven application of stem cell medicine, little different from the many varieties of first generation stem cell therapy. This approach has been used to cure people with multiple sclerosis, and has been attempted with varying degrees of success for a number of other autoimmune conditions for going on fifteen years now: there are researchers with a lot of experience in this type of therapy.

The catch here is that chemotherapy is a damaging experience. The cost of undergoing it is high, both immediately, and in terms of negative impact on later health and life expectancy, similar to that resulting from a life spent smoking. It only makes sense for people who are otherwise on their way to an early death or disability, as is the case for multiple sclerosis patients. However, there are a number of approaches very close to practical realization that will make chemotherapy obsolete for the selective destruction of immune cells and stem cells – approaches with minimal or no side-effects. A combined approach targeting c-kit and CD47 was demonstrated earlier this year, for example. Sophisticated cell targeting systems such as the gene therapy approach developed for senescent cell clearance by Oisin Biotechnologies could also be turned to stem cell or immune cell destruction, given suitable markers of cell chemistry. There are quite a few of these, any one of which would be good enough.

Replacing the chemotherapy with a safe, side-effect-free treatment would mean that the established programs for immune system restoration could immediately expand to become a useful, effective treatment for immunosenescence, the age-related failure of the immune system. This is in part a problem of configuration: a lifetime of exposure to persistent pathogens such as herpesviruses leaves too much of the immune system uselessly devoted to specific targets that it cannot effectively clear from the body, and too little left ready to fight new threats and destroy malfunctioning cells. Then there are various forms of autoimmunity that become prevalent in older people, not all of which are in any way fully understood – consider just how recently type 4 diabetes was discovered, for example. Clearing out the entire immune system, all of its memory and quirks, and restarting it fresh with a new supply of stem cells is a good approach to many of the issues in the aged immune system. Not all of them, but many of them, and considering the broad influence immune function has over many other aspects of health and tissue function, it seems a worthwhile goal.

3) Clearance of the First Few Types of Amyloid

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Fight Aging! Reports from the front line in the fight …

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