Since the dawn of humanity, 200,000 years ago in East Africa, we have been subject to the harsh and unrelenting realities of nature. Our lives begin with the unforgiving shock of leaving the warm embrace of a mother’s womb into an alien world of blurred images, sounds, and sensations, followed by a lifelong struggle to learn, grow, and gain experience. Yet, we are constantly overshadowed by the subconscious realization that our bodily life will come to an end. Sometimes, this end comes slowly and there is ample time for thoughtful preparations. At other times (in the majority of cases), death comes suddenly and without warning.

Though this brief adventure of life has expanded from a mere 20-30 years in the Neolithic Age to a contemprary average of 79 years, it is still relatively short and almost never easy. Nonetheless, many humans are determined to fight against the process of aging and in recent times, groups such as the transhumanists have been seriously discussing the possibility of extending human life to 1,000 or even indefinitely. Are such conceptions the sign of an unhinged mind or are they worthy of deeper consideration? In order to answer this question properly, we must first seek to understand what aging is as a natural, biological process.

According to modern estimations, life on Earth began 3.8 billion years ago and was primarily constrained to single-cell organisms. Scientists speculate that these organisms divided indefinitely via the process of mitosis, thereby achieving immortality. Signs of aging did not begin to appear until these cells began interacting with each other, combining, morphing, and developing into more complex organisms. Individual cells continued to divide within their new and evolving lifeforms, but the structure and continued existence of that lifeform became senior to the immortality of its cellular parts. In order for complex organisms to maintain consistency, it was necessary for cells to develop senescence, or “aging”, so that cellular clutter might be prevented. In modern times, we call cellular immortality in complex organisms (i.e. humans or animals) cancer, because they have disobeyed the directive of the host to make way for new cells produced through division. In this way, they continue to survive and divide.

So it could be said that aging evolved without consideration of the emergence of conscious self-awareness but rather as a natural, logical maneuver to ensure the stability and persistence of lifeforms. Unfortunately, the more cells and interactions there are, the more such complexity gives rise to the potential for unsychronized biological activity. These biological missteps appear as a loss of function in the host, including vulnerability to disease, a decline in fertility, and overall degradation of its parts. In such a state, cells age and die to make way for their replacements, but those replacements are quickly outnumbered, and one or more processes lead to complete failure.

Immortality Defined

Not all organisms experience senescence at the same rate. As a matter of fact, one organism, in particular, is thought to be a contemporary example of immortality: the hydra! These simple but extraordinary creatures are able to reproduce asexually, can recover indefinitely from injury, and have been observed to continually divide without any signs of cellular aging or death. Not only are they capable of surviving unforgivingly harsh environments, but their entire body may grow back after being partly consumed by predators or damaged by the forces of nature. It is postulated that a Hydra’s cells proliferate at a rate that cannot be overtaken by cell turnover processes, thus allowing it to achieve potentially infinite longevity and avoid physiological deterioration1https://www.ncbi.nlm.nih.gov/pubmed/25012456. More importantly, some scientists also believe that the Hydra may oscillate between self-maintenance and cell regeneration, leading to the theory that any organism, including humans, may be able to disconnect molecular processes from physiological ones, opening the door to biological immortality.

The Problem of Human Longevity

The primary issue with immortality in human beings (among countless others), is the manner in which our cellular biology has evolved. In 1961, Leonard Hayflick of the Wistar Institute in Philadelphia demonstrated that human fetal cells would divide 40-60 times before they begin to show signs of aging. For every time a cell divides, the telomere caps on the ends of DNA strands shorten, decreasing the potential for cell division. It is important to understand, however, that the “Hayflick Limit” of cell division defines only helper cells in the human body. These helpers comprise the majority of cells in our bodies and are responsible for feeding and reproduction. But they are, in fact, only the children of the germ or stem cells that contain our genetic code. In this way, helper cells serve the purposes of cellular and metabolic processes in the body while stem cells only die after the body has served its biological purpose. Stem cells are the last to go!

It could, therefore, be said that stem cells are the remnants of the primordial, immortal cell line that is the progenitor of all life. In human beings, they are located in female egg cells and male sperm-forming cells. When the egg and sperm unite, the stem cells combine into a cluster that is used to produce an entire human body containing its own, immortal cell line. It is for this reason that contemporary scientists have put a great deal of attention on the possibilities of age reversal using the secrets hidden in the germ cell line.

Regardless of the presence of such immortal cell lines in our bodies, immortality of the human body, as a whole, has remained elusive. Nonetheless, we see rare examples of individuals that have lived far beyond the average modern lifespan of 79 years. For example, an Indoesian man by the name of Sodimejo was recently reported to have died at the age of 146. Born on December 31, 1870, according to his identification card, Sodimejo, though cited to be the oldest living human being in history, was more than ready to pass on. His last words were, “All I want is to die.”2https://www.usatoday.com/story/news/world/2017/05/02/longest-living-human-ever-maybe-but-hes-dead-146/101190074/ So though we have examples of frank longevity in the human record, it is clearly still tainted by the ravaging effects of senescence, an apparent byproduct of the relentless cycle of life and death.

The Flux of Life and Death

You see, in order to understand immortality as a human conception, we must come to terms with the ebb and flow of life as it is appearing at all eschalons of our planet, even our entire cosmos. Immortality, simply defined, is persistence; a constant in an otherwise entropic play of energy that is constantly changing, re-shaping, and evolving. In the world as we currently understand it, all complex structures appear to be subject to the eventual process of degradation. This chemically assisted degradation, in terms of the human body, is merely a more complex, multi-tiered form of a similar process happening at the cellular level. And though our origins may have been in a plasma of single-celled organisms dividing endlessly through mitosis, the emergence of more complex lifeforms over and against limited planetary space, has given way to natural evolutionary processes which realize change by tearing down old structures to make way for newer, more complex ones.

The processes by which this transformative, evolutionary change takes place are called autophagy and apoptosis. Autophagy is that very process by which cells disassemble unnecessary or dysfunctional components that have accumulated in their cytoplasm. It is a “housecleaning program” to maximize the life of the cell. Without it, life could not be sustained for any length of time. Eventually, when a cell’s usefulness has run its course, the body invokes apoptosis, which takes the cell out of commission to make way for newer cells. This process of “cellular death” occurs between 50 and 70 billion times per day in an average human adult, without which dysfunctional cells would quickly overtake the body and cause death.

So we are able to support a consistent, stable presence in the world because of the persistent, unrelenting processes of cell clean-up and programmed death that are happening billions of times per day in every conceivable area of our bodies. Apoptosis, in particular, is tightly regulated, and is only invoked when either cells sense stress internally or externally from other cells. When the body loses control of apoptosis, there is mass cell death and atrophy of organs and muscles. And when there is too little apoptosis, cells are allowed to proliferate without restraint, leading to cancer. This is, of course, the invocation of immortality for a cell, but extremely problematic for the host organism. In simpler lifeforms of a more primitive self-awareness, such runaway biological processes are not suffered so profoundly. This leads us, however, to an important consideration: the imposition of human consciousness on the non-human, natural processes of life and death.

Homo Sapien Consciousness

It is my opinion that Homo Sapiens, as a complex multi-cellular lifeform, is not the apex of planetary evolution, nor is it the beginning of self-awareness. Nonetheless, it is the most advanced form of self-aware, conscious life on Earth at this time and, therefore, the limiting factor in understanding what ultimately defines consciousness. According to our own simplistic definitions, consciousness is commonly presumed to be the state or quality of awareness. In human terms, it is the awareness of the cohesive, integrated whole that is the human body and its identification with a particular point in time and space. This is the subjective “self”, the presumed owner and dispatcher of all cells and cellular processes that are part and parcel to the human body. Regardless of the endless descriptions humans have devised for consciousness, we have not yet cognized what it is or how it has appeared. There is an extremely deep reason for this, but before we delve into that consideration, we should ask the question, “where, in the complex evolution of organisms on planet Earth, did consciousness first arise?”

There is a hidden presumption in modern science that only higher lifeforms are conscious3https://www.psychologytoday.com/blog/animal-emotions/201208/scientists-conclude-nonhuman-animals-are-conscious-beings. Such prejudices are based in an objective scientific observation of the subjective qualities of consciousness as we perceive and experience them – via the Homo Sapien brain. We presume that self-awareness is required for consciousness, simply because self-awareness is a hallmark of human consciousness. We thereby extend these qualities to the domestic animals and higher lifeforms with which we share our lives presuming that they, also, experience the world in a similar fashion. To the degree that lifeforms do not display the outward signs of self-awareness, we deem them “less conscious”. This paradigm is deeply flawed and does not concur with my own understanding and experience.

Consciousness, as we will discuss in progressively more depth in future articles, is the essence and foundation of the entire universe. It pervades and exists in and as every animate and inanimate lifeform and, thereby, expresses itself via the “creation” of atoms, molecules, organelles, cells, tissues, organs, organisms, populations, communities, ecosystems, and ultimately, our biosphere. The microbes in our bodies are every bit as conscious as we are and contribute, in integrated fashion, to the complex self-aware consciousness of the body as a whole. Similarly, the apparently separate consciousness of every human being contributes to the greater entity of the biosphere, though few in our time are capable of stretching their imaginations to conceive of this possibility.

Homo Sapiens, as a species, is a temporary delineation of infinite consciousness which, by the creation of lifeforms, forever reflects upon itself through expansion, multiplication, and evolution. On the basis of this knowledge, it should become clear that our apprehension of aging and death is based on the presumption that the human body is the final, consummate expression of consciousness, whereas in reality, we are but a level in a greater, more complex hierarchy. This hierarchy may be described as an infinitely evolving entity which is a far more conscious in relation to us as we are conscious in relation to our own molecules and microbial populations.

So it is extraordinarily important to understand what consciousness is, in human terms, in order to rightly consider the concepts of anti-aging and immortality. Simple misunderstandings can lead to a lower level of the hierarchy preempting or “taking over” a higher one, as we see with cancer cell lines which become immortal to the great detriment of the human body that contains them. It should be obvious that before we can determine what aging should mean to us in the process of our personal evolution, we must first understand how our perceptions of reality in the realm of nature can mislead us to limited and ultimately unproductive conclusions.

Systems in the Realm of Nature

Since the appearance of Homo Sapiens 200,000 years ago, our perception and understanding of nature and its biological characteristics have been evolving with each generation. While it could be said that the behavior of atoms, molecules, and the fundamental building blocks they comprise has remained consistent since the dawn of time, our perception of those forms has certainly changed. And with each change in perception came a simultaneous shift in our conscious experience of reality. For example, in Aristotle’s time, there was the prevailing notion of the “spontaneous generation” of living organisms from inanimate matter. Lifeforms such as insects were thought to sometimes manifest from putrefying earth or vegetable matter and up until the discovery of airborne spores by Louis Pasteur, such microbes were thought to appear out of thin air. Though we have come a long way since even the time of Pasteur, our need to categorize the phenomena of our perception is a persistent characteristic of our conscious bias in interpreting the processes of aging and death.

Categorization of systems is a human cognitive artifact and one that has all but guided the path of science up to the present day. Understanding how the brain interprets sensory input is crucial to revealing the ways in which our internal mental categories give us a false sense of “scientific security”. One recent study, in particular, provides a key to this understanding. Using an MRI machine, researchers at the University of California, Berkeley studied blood flow in the brains of human subjects as they watched two hours of movie trailers. Each trailer had been characterized by their objects and types of motion in order to determine how the brain categorizes visual information. Using regression analysis, they mapped 30,000 regions in the brain with 1,700 types of objects and actions. The resulting map represented what the scientists referred to as the brain’s “continuous semantic space”. It revealed that the brain, instead of mapping particular objects and their categories to specific regions in the visual cortex, was actually overlapping associations in multiple regions, including those outside the visual cortex. These regions comprised approximately 20% of the entire brain.4http://news.berkeley.edu/2012/12/19/semanticspace Such a discovery shows us not only that more of the brain is involved in the process of categorization than we originally presumed, but also that such categories aren’t as linear as we thought.

Given that we make sense of the perceived world using categories and their relationships, this naturally gives rise to the question of how such delineations influence our perception of aging and the concept of biological immortality. The field of systems biology may hold an answer. This burgeoning field deals in the apprehension of nature as a series of systems, each level of which is greater than the sum of its parts. In such terms, the human body is seen to be a complex network of biological systems that may only be understood as a whole as opposed to analyzing its individual components. Systems biology attempts to step outside of the linear constraints of human cognitive categorization by using machine learning, artificial intelligence, bioinformatics, and quantum physics. These tools help us to better understand how hierarchies of systems change and influence each other over time. In this way, we are improving our ability to visualize new perspectives on disease, genetics, and the process of aging.

Ultimately, our tools will far outstrip our ability to cognize the solutions we propose. Before that happens, it would be useful to conclude that the “systems” perspective of aging inevitably leads to the realization that all lifeforms are interference patterns in a singular, infinite continuum. These patterns may be likened to the ripples and waves in the ocean and their interplay. What humans perceive to be the appearance, transformation, and disappearance of a lifeform is, in fact not in any sense a finite entity any more than cells of the human body are divided unto themselves, autonomous and independent of the being that they comprise. In this sense, the decisions we make as our technology and knowledge advance should keep ever present in mind the reality that humans are but one level in a vast and unimaginably complex hierarchy. And we would do well to understand our place in that eschalon before deciding to make our primitive, category-bound minds a persistent artifact in the ever-evolving continuum of the cosmic tapestry of which it is a part.

The American quantum physicist, David Bohm, understood this “continuum of hierarchies” better than many of our contemporaries. After a successful career at the University of California (Berkeley) and Princeton’s Institute of Advanced Studies, Bohm went on to become a professor of theoretical physics at Birkbeck College of the University of London, where he combined his formidable knowledge of science with his profound intuitions as a physicist. During that time, he proposed a radically different model of reality called the implicate order in which, “elementary particles are actually systems of extremely complicated internal structure, acting essentially as amplifiers of information contained in a quantum wave.” Such elements, in his opinion, could potentially reveal detailed information about every other element in the universe. In his own words, we exist in an “unbroken wholeness of the totality of existence as an undivided flowing movement without borders.”

Bohm’s vision of reality was one in which all elements in the Universe are instantaneously in communication with each other, regardless of their apparent distance or location. This is possible by virtue of the fact that every element contains within it the entirety of the whole, thereby being in contact with every other element simultaneously. In this sense, it could be said that the total content of the Universe throughout all time and space – a veritable infinity – is “enfolded” into all lifeforms, including human beings. Not only are human beings the interference patterns in the Universal hologram of reality, their very cells are as well. From the point of view of that pattern – the lifeform, itself – it would seem there is autonomy and individual sovereignty, but they are not ultimately distinct.

Therefore, although it is of supreme importance to Homo Sapiens at this time in our history to understand our most pressing problems, eradicate illness, and improve our experience of life, we should feel passionately obligated to go beyond ourselves in order to comprehend the vastness of the Universe in which we live. And though we will discuss in this article the means by which we can grapple with the process of aging and extend our lives, we should not forget that we may be, in the larger scheme of things, no more than the components of a greater order of existence. And that greater order is inaccessible to human consciousness at this time given the primitive way in which we perceive and categorize reality.

The evolution of our species may seem a prolonged affair from our point of view, but it is actually only a fraction of time relative to the 4.6 billion years our present universe has supposedly been in existence. If we contract the scale to a mere 46 years, humans have existed for only 4 hours. We truly are only at the beginning of a vastly larger evolutionary process which most certainly will not end with Homo Sapiens or the parameters of its mind. What we experience as aging and death, generation after generation, is none other than a cycle of conscious expression limited by “the materials at hand”. That these materials lose cohesion over time is only a problem to the self-aware organism. In this way, aging as an undesirable outcome is entirely a human conception.

The Human Conception of Aging

It should be apparent at this point that lifeforms are appearing and disappearing in a vast hierarchy, and it is within the lower levels of this hierarchy that we, as humans, create categories and their conceptions. In reality, aging, as perceived by human consciousness, is the transparent filtration of an endless, immortal continuum of life into distinct lifeforms. It is this filtration that allows us to conceive of objective categories in nature and impose upon it the quality of our self-awareness. Though these categorizations are necessary in order for our survival in the world, they inevitably lead to the ideation of a threat to apparently individual existence.

But as we delve deeper at the cellular level of the human body, we see trillions of microorganisms that outnumber human cells by 10 to 1, without which we would not be able to digest food, absorb nutrients, fight disease, or even produce neurotransmitters.5https://www.nih.gov/news-events/news-releases/nih-human-microbiome-project-defines-normal-bacterial-makeup-body We have only begun to scratch the surface of how vital this microbial population is to our health and well-being, and the greatest secret of all lies just outside the boundaries of scientific reason. You see, not only do these organisms drive critical processes in the human body, but they comprise the sum total of consciousness that makes each human unique. I am not talking exclusively about the microbial populations that produce neurotransmitters such as serotonin or dopamine but rather the very appearance of self-awareness itself by virtue of trillions of microscopic fully conscious entities. This is not to say that microbes are self-aware, but their presence in the human body, along with the 10% of human DNA that comprise the remainder, collectively confers the sensation, via brain-assisted apprehension, of a collective whole – the “I” that identifies each individual.

At the cellular level, there is no suffering or existential crisis as a result of the ebb and flow of life through autophagy and apoptosis. But the collective whole that has become a self-reflective human body is sentient enough to endure the degradation of function as nature decomposes and re-assigns molecules and atoms. And it is specifically at the human level that the sentient desire for long or even infinite life has become an ideology. Since our appearance on the planet, our cultures have dealt with the conscious awareness of aging and death in different ways. While most people in developed countries consider aging as undesirable due to the loss of physical beauty and breakdown of the body, there are yet other cultures in the world that embrace it as a transition, based on their beliefs about the larger cosmic hierarchy of life.

Regardless of how each particular culture has come to grapple with the aging process, every human, if they live long enough, will eventually experience the same loss of bodily function and personal opportunity in the world. Depending on one’s circumstances, this can either be a peaceful time of life or one fraught with psychological hardship and frustration. It may be said, therefore, that the desire to overcome the “problem” of aging is ubiquitous the world over, and without our ability to reverse its symptoms, extending life in any fashion does not hold meaning. For this reason, we must first and foremost find sustainable solutions for all symptoms of aging that would limit enjoyment of life. These include all manner of heart conditions, neurodegenerative disease, delirium, depression, loss of urinary and bowel function, arthritis, insulin resistance, breathing problems, loss of coordination, sleep disruption, macular degeneration, cancer, and decreased body mass, to name the most prominent.

The list of symptoms is truly endless, and finding solutions to each problem separately is not a logical approach to reversing or stopping senescence entirely. Clearly, regardless of our cultural perceptions and biases on the aging process, we can all agree that enduring the degradation of the human body as a fully conscious human being is the main problem we are looking to resolve. So let’s go deeper and deconstruct this problem in an attempt to move towards a higher understanding of what healthy aging should mean in the coming decades and even centuries.

Deconstruction of “The Problem”

So we have established that aging is simply an impartial and natural dis-coordination of multiple systems that leads to biological failure. It has no concern for the human emotional perception of its mechanism since the mechanism itself is operating from a vantage point higher in the cosmic hierarchy. We, as human bodies, operate in exactly the same way irregardless of the fates of the cells that comprise us. While it may seem that our cells are not sentient, it should be easy to imagine that the cosmic hierarchy that contains human beings may perceive us to be equally as inconsequential. Lower in the hierarchy, from the point of view of human consciousness, nature’s forces appear to be brutal and cold. In reality, the apparently impartial demeanor of nature is the result of how self-awareness has developed in parallel with evolution. The animation of matter from the void did not plan for self-awareness. It could be said it has been an unexpected development, similar to if the cells in our body were to wake up and realize their own vulnerability and mortality.

As self-awareness developed in nuance and complexity throughout the course of human history, we began to look at the processes by which our bodies had evolved and formed. And we saw one basic problem which is senior to all others: biological processes have been shaped and guided by the geometrical limitation of the planet on which they arose. As the Earth is (according to our current understanding) of finite volume and mass, so are its constituents. When the playing field of life is boxed, nature must find a way of continuing evolution without stepping on its own feet. It does this by regulating cellular and organismal survival and mitigating overcrowding. At the cellular level, these are the processes of autophagy and apoptosis. At the organismal level – ageing and death.

When these regulatory processes are disrupted, the ability to inhibit overcrowding through regulation of cell survival is destroyed, and such cells are no longer marked for “termination”. In this way, they become “immortal”, causing potentially devastating effects higher up in the hierarchy – in the human body. The prevalence of cancer has increased in modern times, primarily because human beings have devised ways, through medical and biological innovations, to live longer. In this way, we have expanded the window of time in which internal processes may breakdown. You see, nature constrains the timeline for cells and their activity in order to maintain the stability of the higher-order organism. Our very form, from bones to muscles, to nerves and brain, have developed through careful control and guidance without which, we would have no hope for survival.

Nature is not programmed to allow for cellular immortality in complex organisms, and we shouldn’t presume that extending human lifespan indefinitely is not on par with cancer for higher levels of the cosmic hierarchy; levels yet beyond our comprehension. Ultimately, nature’s plan is not for immortality but for transformation, through which it gains momentum to evolve in depth of expression. My understanding of consciousness in nature is that it is eternally striving for the realization of its entirety in every part – the implicate order of which David Bohm conjectured. The biological mechanisms for actualizing this realization are secondary. With this understanding, we must ask the question – is immortality of the human organism simply an ideology of cognitive self-preservation? What does this mean for future evolution?

Transcend Genomics’ perspective on aging is one of both an evolution of human awareness and the eradication of all suffering and limitation at all stages of life, including in advanced years. It is our tenet that if a human being lives long enough, he or she will eventually come into resonance with higher levels of the cosmic hierarchy and gain the ability to consciously transition at the time and place of choosing, rather than as a random function of biology. To embrace such a paradigm, we will require a deepening recognition of the larger hierarchy within which we live in order to understand, most fundamentally, the need for transcendence of our biological “cocoon”. This awareness must be realized by every future human being such that the death transition is fully understood and embraced rather than feared and avoided. This leaves us with the resolution of the “real problem” – the issue of extending life to a sufficient enough degree to allow this “evolution in consciousness” to take place, without being prematurely disrupted by biological death. And it cannot happen without creating a solid physiological foundation, including boundless energy and stamina, development of superhuman cognitive capabilities, and the complete mastery and control over all biological processes that make us human.

So how do we extend and improve life such that we can realize greater continuity with the “larger organism” of which we are a part while not disrupting its inherent totality and order of existence? Let’s discuss the mechanisms of breakdown in human senescence as science understands them presently.

Mechanisms of breakdown

Up until very recently, medical science has been focusing almost exclusively on the ways in which metabolic processes degrade and cause cellular and molecular damage in our tissues and organs. The proposed solutions have centered primarily around drugs that can slow down those processes, thereby mitigating their effects on our cells. We have seen the advent of drugs that lower cholesterol, regulate blood pressure, and control glucose levels, but they come with a staggering number of side effects that, ultimately, can end up reducing lifespan or, at the very least, reducing quality of life.

Medicine, today, is defined by a constant struggle with the ravages of aging and in the majority of cases, it is simply operating in crisis mode, prolonging life by only weeks and months or, if the patient has robust genes, a few years. The truth of the matter is that the very metabolic processes that sustain our life and maintain our vitality in youth eventually work against us as they become deregulated and unsynchronized. And blocking their activity or interfering in their influence in any manner often leads to unforeseen consequences, given the complexity of the human system as a whole. Fortunately, developments within the last decade have taken the originally optimistic, new science of rejuvenation biotechnology into the realm of actionable methodology.

Biotech is now approaching the aging conundrum with the intention of removing, repairing, and replacing damaged cellular and molecular machinery as opposed to trying to affect the metabolic processes that alter and damage them. This will allow us to not only slow down the aging process but, more importantly, restore the characteristics of youthfulness to aged cells and tissues even after aging has entered advanced stages. There are several mechanisms of breakdown that have become the targets for research in this burgeoning field. We will briefly review the most promising of them.

Mitochondrial Mutations

Inside each of our cells exists two forms of DNA: the code in the cell nucleus that comprise our human genes and the DNA inside the mitochondria, also called mtDNA. In the early stages of evolution, our cells did not contain mechanisms to make their own energy and gradually acquired this capability by symbiotically absorbing the bacteria-like structures of mitochondria. As a result, human and mitochondrial DNA have remained separate, even though they exist within the same cell.

Mitochondria behave similarly to power plants, taking in raw materials from food and converting it to energy in the form of ATP. In the process of energy generation, byproducts called free radicals are created which can potentially damage cell structures. Further, because free radical production is so close to the source of energy production, the mtDNA can also be damaged, hindering its ability to properly signal.

As a result, mitochondria become mutated and instead of producing ATP, generate even greater levels of free radicals, altering signaling within the cell itself. Soon, the cell begins to confuse mutant mitochondria with healthy ones and, in delirious fashion, discards the good ones in favor of the bad. As levels of mutant mitochondria rise, they eventually compromise the integrity of the human cell within which they reside, causing membrane degradation and releasing their byproducts directly into circulation. This causes further oxidative stress throughout the body and, over time, organ breakdown and aging.

Future solutions for mitochondrial mutations will include the prevention of mtDNA damage and the repair of existing damage before the cascade of cellular degeneration can even begin. Unfortunately, technology is not sufficiently advanced at this time to mount such an undertaking, so we must look to techniques such as allotopic expression as a workaround6https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017613/. This approach would allow placement of mitochondrial gene copies into the cell’s nucleus, where they would be far removed from the danger zone of the free radical-producing mitochondria. Should there be damage to the mtDNA in the course of energy production, the mtDNA copies could be sourced from the cell nucleus and imported into the mitochondria using specialized transport docks in their membranes7http://www.sciencedirect.com/science/article/pii/S0167488908001456.

Cellular Junk

Another mechanism of breakdown in the aging process is the accumulation of junk inside and outside the cells. The intracellular variety occurs when the cell’s “disposal system”, the lysosome, is unable to breakdown damaged or aging components via the process of autophagy. The components, when damaged, tend to bind to one another, hindering the necessary enzymatic processes that would deconstruct and dispose of them. As a result, this cellular debris accumulates and eventually crowds out the lysosome, inhibiting or blocking its ability to dispose of the junk properly. As this crisis unfolds, the lysosome either ruptures or the cell itself sends a distress signal which leads to its destruction via apoptosis. If this apoptosis continues unabated, there is tissue breakdown and organ failure.

We can also see junk accumulating outside cells when proteins become misfolded and sticky. This causes them to stick to each other and form masses that obstruct functions body-wide. The most common form of extracellular junk is the beta-amyloid protein that forms plaques in the brains of people suffering from Alzheimer’s disease. Amyloid accumulation is a natural part of aging in even healthy humans, and it is believed that if a person lives long enough, they will die of amyloid-related organ failure sooner or later.

Some compelling solutions have been proposed for disintegration or sequestration of intra- and extracellular junk. In the case of junk inside the cells, it should be possible to use specific enzymes, many of which are present in fungi and soil-based bacteria, to bombard the debris by force, more quickly and efficiently degrading it before cellular apoptosis incurs. In order for this to work, the non-human enzymes would need to be molecularly modified for compatibility with the human lysosome. The only caveat would be delivering them to the necessary places in our cells, which would require either a delicate system of cell “stress detection” or some other means of identifying areas of crisis.

Extracellular junk requires a different approach, and proposed solutions include the use of antibodies to trap and sequester amyloid proteins. This could be accomplished using vaccines that either stimulate internal antibody production with fractional amounts of amyloid or using laboratory-derived antibodies developed in vitro. The problem with this method is twofold. First, the antibody itself may be too large to pass through the blood-brain barrier, where it would need to go to find the amyloid plaques in Alzherimer’s ravaged brains. Secondly, even if it was successfully able to cross that barrier, the antibody-amyloid complex would be even larger and may get trapped in the brain, unable to make an exit. In the best case scenario, the complex would exit via the blood-brain barrier but cause oxidative stress and inflammation along the way.

For these reasons, an alternative approach to antibody vaccines was proposed by Dr. Sudhir Paul at the University of Texas Health Science Center at Houston. His method uses antibodies with catalytic properties to breakdown amyloid proteins into smaller pieces, leaving the responsibility for their destruction and removal to the immune system.8https://link.springer.com/article/10.1007/s00281-004-0191-1 This novel approach would be more effective than the “trap and sequester” vaccine approach, since it would not require the removal of whole amyloid plaques from the brain but rather disintegrate them on contact within the brain in systemic fashion. Naturally, this approach could also be applied as well to other organs where “rogue proteins” accumulate.

Crosslinking

The human body is filled with protein structures that sustain form and function throughout an entire lifetime. Many of these structures are comprised of collagen and are critical for the integrity of a wide array of tissues such as skin, tendons, ligaments, blood vessels, the cornea of the eye, cartilage and bones, the gut, intervertebral discs, and even dentin in teeth. Sometimes, blood sugar can react with collagen without enzymatic regulation, causing the proteins to cross-link together, restricting their motion and causing disruptions in function. This crosslinking can lead to a reduction in the elasticity of tissues and organs where collagen is located, causing them to stiffen. Once proteins have become bonded in this way, inflammatory signaling may ensue, causing additional damage and, if left unabated, cancer.9https://www.ncbi.nlm.nih.gov/pubmed/16706655

The upside of crosslinking is that their resulting formations are quite different from other protein structures, making them easily identifiable in the milieu of tissues. For this reason, it should theoretically be a straightforward task to design synthetic enzymes that could locate crosslinks and sever them. The main issue with such an approach would be sourcing the necessary energy required to reverse the link between crosslinked proteins. Scientists speculate that such therapeutic enzymes could traverse cell membranes to obtain ATP without compromising cellular survival, thus getting the upper hand on the lower-energy consuming crosslinking molecules.

Apoptosis and Tissue Atrophy

As we have discussed, human cells are in a constant state of flux. As they serve their functions day in and day out, they begin to show signs of aging. Those components that can be recycled via autophagy keep some cells in commission, while other cells might instead endure excess stress from intracellular junk accumulation, and death (i.e. apoptosis) ensues.

While it is ultimately to our benefit for the body to rid itself of cells that can no longer function, those lost cells must be replaced by tapping into the immortal stem cell reservoir. Stem cells are tissue-specific and with repeated stress over time, they become less effective at repairing damage. As the more prominent tissues and organs in our body such as the brain, heart, and muscles lose cells in parallel with a dwindling stem cell reserve, they are unable to recover completely and, as the years pass, eventually fail.

So the most pressing question for aging populations is – how can we slow down or halt cellular degradation and apoptosis without triggering excessive growth processes such as cancer? Longevity experts have posited several approaches to this problem, the most popular of which has been the cultivation of complete organs in sterile, laboratory environments for the purpose of transplant. In the past, we have had to rely on donors for our high-demand transplant needs, and organs have been in scarce supply. Even after a successful transplant, the body of the recipient recognizes the organ to be foreign, and medications must be taken life-long in order to coerce the immune system into compliance. Fortunately, new biotechnologies are becoming available that would allow us to grow organs from a recipient’s own supply of cells.

This new, promising method involves taking samples of the recipient’s cells in readily available sources such as blood or skin and restoring them to their original germ-line state via the process of pluripotent stem cell induction. Such stems cells can then be freely used to create any organ or tissue imaginable. In this way, abundant cell populations such as the skin can be donors for heart, kidney, and in the near future, even brain neurons. Once the pluripotent form of the donor cells are in their target organ, they can reproduce as needed to rejuvenate the tissues.

Abnormal Cells

Another important mechanism in the process of aging is the accumulation of abnormal cells. In youth, such cells are quickly and efficiently cleared from circulation via programmed cell death. As we get older, however, the body gradually loses control over apoptosis and the number of abnormal, dysfunctional cells grows. Though this typically happens after the age of 50, it can become a problem at any age, depending on lifestyle, genetics, and environmental influences.

There are several ways in which cells become problematic for the body, the most important of which is the senescence program. This program detects changes in the expression of a cell DNA and proactively halts mitosis (i.e. division and replication) for those cells that show signs of becoming cancerous. Although this prevents overgrowth of certain dangerous cell populations, the arrested cells nevertheless continue to take up space and excrete inflammatory proteins that disrupt immunological signaling and cause oxidative stress throughout the body.

Among all cell types, fat cells tend to present the greatest challenges in an aging body. Over time, preadipocyte function begins to decline, causing a shift in the way new fat cells are formed. This results in abnormal changes in fat density and location, with some areas of the body losing fat while others accumulate it. To add insult to injury, adipose tissue macrophages (ATMs) also begin to accumulate in the fat surrounding the gut and liver in an attempt to remove dysfunctional, dying fat cells. In the process, additional inflammatory signals are produced, causing further disruption to cellular signaling in healthy fat cells. As a result, glucose uptake plummets due to a steadily declining sensitivity to insulin.

Another family of cells that are vulnerable to abnormalities in aging are the killer T-cells, which seek and destroy cells that have been overtaken by pathogens or cancer. In youth, there is a broad reserve of “naïve” cells that are appropriated to specific threats in the body as needed. Unfortunately, this reserve and their specialized progeny remain a fixed population throughout life, while the variety of bacteria and viruses in the environment can mutate. As a result, as the body ages, older “soldiers” dispatched to fight certain invaders earlier in life accumulate, while there is no room for new specialized killer cells. To make matters worse, the larger populations of killer cells also crowd out existing smaller groups, creating an imbalance in available immune reserves. This leads to an increasing inability to mount an immune response to new invaders later in life, making vaccines less effective as well.

New approaches are being explored at this time to handle abnormal cell accumulation. Of all the proposed solutions, the most compelling is the idea to use surface patterns on the membranes of abnormal cells to identify them. This would allow us to develop molecular agents to seek, find, and destroy cells with a particular molecular surface signature. While we are currently only using this technique in cancer therapies, it could easily be customized to target ATMs in visceral fat cells or abnormal killer T-cells10https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582125/. Further, by biosynthetically engineering a fresh supply of naive cells that are cancer-resistant, abnormal killer cells could be replaced as new immune challenges arise. What’s more, those naive cells could also be programmed to enter apoptosis should they become dysfunctional, killing two birds with one stone.

Cancer

Cancer certainly needs no introduction. More than 4,500 new cases are diagnosed each day, and as of 2016, it takes the life of nearly 600,000 people each year. Though declines in specific types of cancer have been reported in recent times, the overall incidence is on the rise. Medical science has looked far and wide for answers to the cancer enigma, but the death rates prove our deep lack of understanding of what kind of adversary we are up against.

Cancer is ultimately not a disease but rather a natural program whose purpose is cellular immortality. Apoptosis exists as a means to keep cellular populations under control, but as chaos unfolds in the body’s metabolic processes, either as a result of environmental influences or through aging, the apoptotic program can fail. As a result, either cell DNA is damaged or the epigenetic mechanisms that allow genes to be turned on and off are rendered unstable. This leads to a loss of control over the cellular processes that govern cell-suicide, allowing increased replication and overgrowth.

Contrary to common belief, cancers do not develop as a result of mutations that occur later in life but rather from epigenetic modifications to DNA that occurred during our early development as embryos and children. These were the times of wild, explosive cell division and growth which, by the graces of nature, are extremely error-prone. Depending on which genes were altered during that brief window of time, our behaviors and environmental exposures will have different effects. For this reason, cancer is not exclusively a genetic story but rather one that contains a great deal of randomness. Solutions that target oncogenes (i.e. cancer promoting genes) will not be effective. We must search deeper for an answer.

Common wisdom tells us, from an early age, which behaviors and environmental exposures can be dangerous in the cancer pathology. Ingrained in our subconscious is the healthy appreciation for the risks of smoking, drinking, sun exposure, and all the other “usual suspects” which doctors and medical experts blame when a patient presents with the disease. But simple avoidance does not always lead to a clean bill of health, as is amply evident in the number of healthy people that eat properly, exercise, and avoid toxins but still succumb to cancer.

Cancer Strategy #1: Telomerase Inhibition

Cancer is not a disease that must be eradicated, but rather a natural, biologically constrained phenomenon that should be understood. If we turn our attention away from the genetic liabilities that could promote it and look, instead, to its means of existence, I believe we will be closer to answers. And one of those answers could very well lie in a cancer cell’s greatest vulnerability: its dependency on telomere renewal. Telomeres are the DNA-containing caps on the ends of our chromosomes that protect them from fraying and coming apart. The shorter the telomere cap, the less stable a cell’s chromosomes will become. As more and more chromosomes lose their telomeres, cell survival is compromised and eventually, the cell will commit suicide.

Cancer cells proliferate at a far more rapid pace than normal, healthy cells and as a result, they burn more quickly through their telomeres. Their survival depends on the ability to stretch the telomeres back out to their original length, and this requires telomerase – an enzymatic template that elongates telomeres. If the cancer cell cannot gain access to telomerase, its chromosomes will quickly fray from metabolic damage and the cell will die before it has had a chance to affect other healthy cells. For this reason, drug research involving cancer-specific telomerase inhibition is by far the most promising direction we can take at this time.

Unfortunately, targeting telomerase to inhibit cancer cell lines is not a silver bullet, as the cells are sometimes able to find “back doors” that sidestep the requirement for telomerase. Furthermore, cancer cell genetic code is constantly in flux, adapting to its environment to ensure survivability. While targeted drug therapy might eradicate the majority of cancer, it could not possibly guarantee a defense against the cells that had used evolution to evade scientific intervention. It is precisely for this reason that chemotherapy often works in the beginning but yields to newer, more virulent strains of cancer in the end.

Cancer Strategy #2: Whole-Body Telomere Lengthening

Another approach has been proposed for the eradication of cancer that does not involve telomerase inhibition. This approach involves robbing all cells, body-wide, of their ability to lengthen telomeres by destroying the genetic code that produces telomerase. The most obvious problem with this solution is that apart from cancer cells, human stem cells also share the ability to implement telomerase. The only way that this method would work is if stem cells with shortened telomeres were replaced at regular intervals to offset the senescent populations. Clearly, this would create a serious issue if there were to be, at any point, a disruption in access to clinical maintenance. Further, the entire approach hinges on the presumption that telomerase serves no other purpose in the body other than lengthening telomeres – a distinct impossibility.

While targeted telomerase-based therapy may be the brightest of opportunities on the cancer front, we will most certainly need to go deeper in our understanding of the human organism in order to prevent its occurrence in future generations. This will necessarily require a simultaneous evolution of our superconscious abilities via deeper resonance with the great hierarchy within which we live. And for this to happen, we must evolve in ways inaccessible to the average imagination.

What is Healthy Aging?

Regardless of the understanding that mechanisms of breakdown in aging involve many complex processes from mitochondrial mutations to cancer, it should be fairly clear that we currently to not have the level of intelligence, as a species, to truly grasp the larger picture. Though we have isolated many of the processes by which aging evolves, our apprehension of such processes is still limited by the fractured, incongruous categorizations of our ancient, cognitive machinery.

While we can develop solutions for the mechanisms of aging we have identified, there is no guarantee, from the perspective of primitive, Homo Sapien consciousness, that these mechanisms are the only factors.  We likely do not fully understand the myriad of hidden relationships they have to other areas of human biology. For this reason, we must leverage presently known workarounds to maximize our vitality and longevity while the medical and biological sciences evolve with the help of cognitive enhancement and artificial intelligence.

Anti-Aging Strategies

Multiple proteins – and the metabolic and cellular pathways in which they operate – have been identified as targets for anti-aging strategies. Many of these strategies, in parallel with an in depth understanding of one’s genetic liabilities, may be implemented to substantial effect now, while we are waiting on more advanced options for radical life extension. Let’s take a look at the most prominent strategies that science knows of to date.

mTOR Inhibition

Back in the 1970s a research effort on the Polynesian island of Rapa Nui discovered the bacteria Streptomyces hygroscopicus in soil samples. It was observed to have unique antifungal properties and became a subject of great interest as an immunosuppressing agent. It was later given the name rapamycin and subsequently used to treat cancer and for the prevention of restenosis following angioplasty. Later on, further research discovered the gene in mammals upon which rapamycin exerts its influence. This gene became known as “rapamycin’s target” or mTOR.

It wasn’t until 2009 that mTOR was shown to extend lifespan in mice. As research evolved, we began to understand how mTOR influenced many upstream pathways, including insulin and growth factor signaling. Today, mTOR is seen as a crucial regulator of human metabolism and physiology involving everything from muscles, white and brown adipose tissue, and the brain. It has also been implicated in the pathologies of cancer, obesity, and diabetes, making it an important part of every anti-aging strategy. Though mTOR activation can lead to desirable results such as increased muscle mass, more energy, and better neuroplasticity, the majority of people will want to work to inhibit it in order to realize longevity enhancement.

Although rapamycin is the most direct means to inhibit mTOR, it is not without side effects, and sourcing is problematic. For this reason, there are other mechanisms which can produce similar results if combined. These include HIIT (high-intensity interval training), cyclical calorie restriction, high-fat / low-carbohydrate diets and supplementation with high quality Resveratrol and Curcumin.

AMPK Activation

AMPK or 5′ adenosine monophosphate-activated protein kinase is an enzyme that inhibits synthesis of fatty acids, cholesterol, and triglycerides. It also plays a crucial role in the uptake of fatty acids and the generation of energy (ATP) via the process of β-oxidation. As such, it liberates more energy for life activities while suppressing the storage of fats.

AMPK is commonly known as the “age suppressor” due to the additional roles it plays in regulating glucose uptake, protein biosynthesis, autophagy, and mitochondrial biogenesis. Activating the AMPK gene in aging persons can have a wide array of positive outcomes in disease prevention, including:

Cancer – Inhibits tumor growth by inducing apoptosis and encouraging oxygen-utilizing pathways in place of sugar-burning11http://www.sciencedirect.com/science/article/pii/S1550413112004925

Cardiovascular Disease – Reduces plaques in arteries12http://www.jbc.org/content/286/10/7917.short, lowers inflammation in cardiac tissue13https://www.nature.com/icb/journal/v92/n4/full/icb201411a.html, reverses hypertension14http://www.sciencedirect.com/science/article/pii/S0006291X12001040?via%3Dihub, mitigates blood vessel damage by oxidized LDL15http://diabetes.diabetesjournals.org/content/59/6/1386, and reduces vascular death from heart attack or stroke16https://www.nature.com/hr/journal/v33/n1/abs/hr2009187a.html

Immune Function – enhances the ability of white blood cells to find and destroy bacterial pathogens17http://static.smallworldlabs.com/molmedcommunity/content/pdfstore/13_065_Park.pdf

Obesity – Supports weight loss18http://www.sciencedirect.com/science/article/pii/S0960894X10007080?via%3Dihub[/footnote] and induces the utilization of fats for energy[footnote]https://link.springer.com/article/10.1007%2Fs00125-012-2530-4

Diabetes – Reduces insulin resistance19https://www.thieme-connect.de/DOI/DOI?10.1055/s-0030-1263122, supports glucose transport20https://www.thieme-connect.de/DOI/DOI?10.1055/s-0030-1263122[/footnote], and lowers liver’s glucose output[footnote]https://link.springer.com/article/10.1007%2Fs00125-008-1108-7

Liver Disease – Prevents fatty liver21http://ajpgi.physiology.org/content/298/3/G364.short, increases liver mitochondria22https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4990206/, and inhibits liver fibrosis23https://www.ncbi.nlm.nih.gov/pubmed/23127227

Multiple strategies exist by which AMPK can be increased, including HIIT (high-intensity interval training), cyclical calorie restriction, exposure to cold, Resveratrol, Quercetin, Berberine, Curcumin, Astragalus, CoQ10, Olive Leaf extract, and a botanical extract of Gynostemma pentaphyllum.

p53 Signaling

Tumor suppressor p53 is a protein isoform that plays a crucial roll in the prevention of cancer. Due to its ability to block genomic mutations, it has been described as “the guardian of the genome”24http://www.tandfonline.com/doi/abs/10.4161/cc.6.9.4211. It achieves this remarkable effect through a wide array of mechanisms including senescence and apoptotic responses to dysfunctional telomeres25https://www.ncbi.nlm.nih.gov/pubmed/15865944, stabilization of the cell cycle in the DNA damage recognition stage, activation of DNA repair, and even cell apoptosis, if required.

As discussed in the section above on Cancer, our body loses regulatory control over cell division as a result of the accumulation of mutations during life. Although these mutations are commonly considered to be the primary trigger for cancer, there also exists a hypothesis that p53 function may also decline with age due to stress and other similar factors, thus leaving our cells with increased vulnerability to mutation. In one study, lifespan in mice was seen to decline in parallel with p53 activity over time26 http://www.pnas.org/content/104/42/16633.full. This would suggest that loss of p53 function during aging could contribute to increased DNA mutation and tumorigenesis.

Although apoptosis and cellular senescence programs have potent tumor suppressing mechanisms, their increasing utilization with age can lead to the depletion of our stem cell reserve. This, of course, results in a constantly dwindling supply of germ line cells that may be used in tissue regeneration and repair. It should be clear that promoting cell cycle arrest via p53 activity may encourage more efficient repair and disposal by apoptotic and senescent programs. Therefore, protecting p53 function should be a vital component of any anti-aging strategy.

The best means of ensuring p53 signaling stability is to adhere to a strict circadian rhythm in synchronization with the sun cycle. Studies abound that show the link between circadian disruption and increased cancer and tumor development. For example, it has been demonstrated that a loss of function in mPer2, a critical gene in mammalian circadian rhythm27https://www.ncbi.nlm.nih.gov/pubmed/10408444, leads to deficient DNA damage responses and increased tumorigenesis. The hypothesis is that as mPer2 function declines, p53 activity attenuates in parallel28http://www.sciencedirect.com/science/article/pii/S0092867402009613. This is a clear message that our circadian clock not only regulates biological processes such as cell proliferation, in response to environmental cues, but also plays a vital role in protecting our cells from spontaneous epigenetic threats.

NF-κB Inhibition

NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that is activated by oxidative and inflammatory stress and is responsible for regulating inflammation, cell cycle progression, cell senescence, and ultimately apoptosis. Many triggers may contribute to its activation including free radicals, bacterial or viral pathogens, oxidized LDL cholesterol, UV radiation, heavy metals, and even cocaine29https://www.ncbi.nlm.nih.gov/pubmed/14501032.

NF-κB has been observed to upregulate in aging and is frequently associated with Alzheimer’s disease, diabetes, and osteoporosis. Inhibition in mouse models has proven to delay onset of age-related symptoms and pathologies30https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3295063/. As we have discussed, damage to cellular organelles can trigger the clean-up program of autophagy, but over time, consistent cellular insult can lead to an overactivation of stress response mechanisms, such as NF-κB. For this reason, NF-κB inhibition has been proposed as a means of slowing down the aging process.

Several strategies have been proposed to achieve healthy NF-κB inhibition. The most powerful method is also the simplest: increase exposure to sunlight, without sunscreen31http://www.sciencedirect.com/science/article/pii/019096229070107S, at times of the day when there is higher UVB, which is required for Vitamin D production in the skin. Vitamin D has been shown to decrease NF-κB-mediated inflammatory response32http://www.jimmunol.org/content/184/2/965.short and multiple studies have demonstrated increased NF-κB activity in locations lacking Vitamin D receptors33http://ajpendo.physiology.org/content/291/2/E315.short.

Other effective approaches to inhibiting NF-κB expression include smoking cessation, dietary lectin avoidance, keeping a tight circadian rhythm, cyclical calorie restriction, HIIT (high-intensity interval training), diet high in DHA (preferably from natural, marine-life sources not in pill form), increasing melatonin levels naturally without supplementation, proper magnesium / zinc levels, PQQ, and Curcumin.

IGF-1 and Insulin Signaling

Insulin-like growth factor 1 (IGF-1) is a hormone with a similar structure to the insulin molecule. It is produced in the liver when stimulated by pituitary growth hormone secretions and induces the growth process in cells body-wide, including muscles, bone, nerves, immune cells, and lungs. In aging, IGF-1 signaling has been shown to decline, especially in the brain, leading to impairment in cognitive function34https://www.einstein.yu.edu/centers/aging/research/igf-1-insulin-signaling-pathways.aspx. Declining levels further manifest as decreased muscle mass, loss of bone density, and compromised immune response.

For the majority of people over the age of 40, raising IGF-1 levels with lifestyle and supplementation interventions is favorable. Its most important effect may be seen in the lengthening telomeres and thus decreased incidence of DNA mutation35https://www.ncbi.nlm.nih.gov/pubmed/19913048?dopt=Abstract. Other benefits include protection against cardiovascular disease36https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199335/, increased bone density37https://www.ncbi.nlm.nih.gov/pubmed/12435898, enhanced immune response38https://www.nature.com/articles/ncomms2484, higher insulin sensitivity39https://www.ncbi.nlm.nih.gov/pubmed/1469083, greater muscle mass40https://link.springer.com/article/10.1023%2FA%3A1015234709314?LI=true, increased neurogenesis (i.e. creation of new brain cells)41http://www.sciencedirect.com/science/article/pii/S0166223603001632, and a significant boost in antioxidant levels42https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3557755/.

Unfortunately, there are circumstances which would warrant lowering IGF-1 levels, especially in the case of cancer. It has been shown that IGF-1 promotes cell division and plays a critical role in transformation and protection of cells from apoptosis. In healthy humans, this should not present a problem, however, reduced apoptosis and sustained cell proliferation in cancer cell lines should be avoided at all costs. For this reason, it would be sensible in individuals with cancer or at greater risk for cancer to inhibit IGF-1 expression with intermittent fasting, moderate protein restriction, and liberal use of Curcumin43http://www.sciencedirect.com/science/article/pii/S0304383508002310.

In all other individuals over the age of 40, multiple strategies exist for increasing IGF-1 to healthier, younger levels. Some of these methods include adopting a diet higher in fat and lower in carbohydrates, HIIT (high-intensity interval training), and increasing protein intake. Other supplements that have proven effective in raising IGF-1 levels are CDP choline44https://www.ncbi.nlm.nih.gov/pubmed/639755, HMB, and DHEA. DHEA, in particular, has been shown to increase IGF-1 levels as much as 10-20% at doses of 50mg and above. Further, such doses have also demonstrated an immunoprotective effect by increasing the numbers of monocytes45http://online.liebertpub.com/doi/abs/10.1089/jir.1998.18.125, B cells, T-cells46http://onlinelibrary.wiley.com/doi/10.1002/eji.1830200413/full, and natural-killer cells47https://academic.oup.com/jcem/article/84/9/3260/2864512/Dehydroepiandrosterone-Sulfate-Enhances-Natural.

FOXO Signaling

Forkhead box O3, also known as FOXO3, is a protein that regulates gene expression by controlling the rate of genetic information transcription from DNA to RNA. As such, it plays an extremely important role in aging and longevity. FOXO is involved in a wide variety of processes in the body, the most important of which are the regulation of stress resistance, metabolism, cell cycle arrest, and apoptosis. Being downstream from IGF-1 and insulin signaling, it is vulnerable to disruptions as a result of issues on those pathways as well.

One of FOXO’s most significant roles as a longevity promotor is in its maintenance of protein homeostasis via autophagy. As we have discussed above, autophagy is the “recycling system” that removes and disassembles dysfunctional components in the cytoplasm of cells. By affecting the expression of the genes involved in autophagy, FOXO is able to maintain cell integrity in muscle, liver, heart, and brain48https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783344/.

In addition to autophagy, FOXO also supports cellular resistance to oxidative stress from peroxides and free radicals. Such reactive oxygen species (ROS) increase gradually with age as cell function degrades. By sensing stress in upstream pathways, FOXO responds by upregulating key detoxification enzymes such manganese superoxide dismutase (SOD2), catalase, and Growth Arrest and DNA Damage 45 (GADD45). Clinical studies have shown that downregulation or genetic mutations in FOXO can ultimately compromise the ability of stem cells to reproduce49https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783344/.

As discussed in the section Mechanisms of Breakdown, stem cells, as the immortal cell line in humans, are the single most important key to not only understanding the aging process but also our potential for radical longevity. Degradation of FOXO function has been implicated in decreased regenerative potential of the hematopoietic system which governs stem cell biogenesis. One study even showed that by deleting FOXO proteins in mice, stem cells spontaneously undergo apoptosis. Clinicians were able to restore normal stem cell proliferation in such mice by administering NAC (N-aceylcysteine), a powerful antioxidant. This suggests that stem cells may be just as vulnerable to oxidative stress as the rest of the cells in our bodies.

Since FOXO expression is primarily induced by stress, there are few strategies available that might ensure its proper function in the face of active genetic mutations. In all cases, it is important to quantify the existence of SNPs (single-nucleotide polymorphisms) in the genes upstream from FOXO, such as those associated with IGF-1 and insulin signaling, to ascertain risks for under or overexpression. Further, mutations in genes regulating response to oxidative stress such as the SOD, catalase, and GADD families will also play a major role in the protection of our stem cell line. For this reason, judicious use of NAC or SOD mimetics such as grapeseed extract could be a crucial part of any anti-aging regimen.

DNA Repair

Clearly, the most effective anti-aging strategy is one that strives to prevent oxidative damage to DNA as result of environmental stress. Unfortunately, completely eliminating such stresses is not a near-term possibility, so we must include in our collection of strategies an approach for repairing damage that has already occurred. Protein-to-protein interactions in DNA repair have long been considered worthy targets for therapeutic interventions. The most promising agent for the control of cellular oxidative stress comes in the form of an enzyme discovered over a century ago: nicotinamide adenine dinucleotide or simply – NAD+.

The coenzyme NAD is a core component of the anti-aging mechanism of mTOR inhibition. Two of the proteins known to regulate DNA repair, SIRT1 and PARP1, use NAD to accomplish their tasks. For this reason, supplemental NAD has attracted a great deal of attention lately for its ability to increase the activity of such proteins.

Though anecdotal results with NAD supplementation abound in the anti-aging community, administration of its precursor, nicotinamide mononucleotide (NMN) has been proposed as an alternative, due to its ability to cross the cell membrane with ease. Though human trials are not scheduled until late 2017, studies on mice have been very telling. NAD and PARP1 levels were shown to rise significantly in old mice given NMN-infused water for one week. Cells treated with NMN also showed a sharp decrease in the number of DBC1-bound PARP1 molecules. Final results indicated reduced markers of DNA damange, proving NMN as potentially viable therapy for aging prevention50http://science.sciencemag.org/content/355/6331/1312.

Telomerase Reactivation

Last, but certainly not least, in our consideration of anti-aging strategies are the methods for telomerase reactivation. As detailed in the section on Cancer, telomerase is the enzyme responsible for preventing DNA damage by lengthening the caps (i.e. telomeres) at the end of its chromosomes. As telomeres shorten, cells lose their ability to reproduce, leading to tissue degradation and organ failure.

In a landmark study nearly a decade ago, Harvard-affiliated researchers lenghtened the telomeres in mice, showing significant reversal of degenerative changes in as little as 30 days. Among the benefits were the outgrowth of new neurons and a regeneration of the myelin sheaths surrounding existing neurons51https://www.ncbi.nlm.nih.gov/pubmed/20336134?dopt=Abstract&holding=npg. In addition to brain rehabilitation, the mice also enjoyed higher viable sperm count, a reversal of intestinal damage, and even the return of olfactory function (i.e. sense of smell). If we were to extrapolate the results of this study to human lifespan, it would be the equivalent of returning an 80-year old to the biological age of a 20-year old.

As dicussed above, telomerase activation is not the panacea that one would hope for, ultimately. Due to the fact that cancer cells also rely upon telomerase to ensure their survival, increasing telomerase body wide could lead to potentially undesirable results in those with higher cancer risk. Nonetheless, supplements are being developed that claim to enhance expression of telomerase’s RNA gene, TERC, while simultaneously avoiding cancer promotion52http://onlinelibrary.wiley.com/doi/10.1111/j.1474-9726.2011.00700.x/full.

The most well-known of these offerings is TA-65, a purified extract from Astragalus root, specifically the Mongolian Milkvetch variety. Though this root has been used for thousands of years in Chinese medicine for its vitality-enhancing properties, it wasn’t until 2013 that its active constituent, cycloastragenol, was extracted and studied by Geron Corporation. Geron eventually sold the extract to T.A. Sciences for further development. The resulting product, TA-65 is purported to elongate telomeres and rescue damaged DNA. Fortunately, TA-65 has also been shown to increase mouse telomerase reverse transcriptase (TERT) levels and elongate dangerously short telomeres. Clinical results have demonstrated improved glucose tolerance, reversal of osteoporosis and enhanced skin quality without an increase in cancer incidence. For this reason, TA-65 should be considered another adjunct to our currently known anti-aging strategies.

The Implications of Mass Longevity

As we move forward into the 21^st century, our horizon of possibilities does seem limitless. Nonetheless, it should be obvious that our current knowledge, though quite developed and complex in comparison to what we knew at the dawn of civilization, is still riddled and contorted by our cognitive mind’s categorizations of systems, processes, and their components.

Though we have uncovered many secrets that have inspired a deeper apprehension of aging and longevity, we are still burdened by the persistent, insidious presence of degenerative disease and the suffering it entails. So our ultimate question should really be – “if we devise a way to eliminate disease and increase lifespan, what implications could it have on not only human life, but the planetary biosphere and beyond?”

Points of Transition

I have posited that our primary goal as a species, at least in the short-term, should be to mitigate and ultimately eradicate suffering at every level of our biophysical lives. This means not only complete disease elimination but also a disruption of the psycho-physiological assaults on human consciousness that aging represents. Should we achieve this noble goal, we will be confronted with a very complex consideration: in achieving disease-free, radically extended human life, are we interfering with the natural evolution of a hierarchy whose intention is the transcendence of physically expressed consciousness altogether?

Therein lies the issue. For those individuals that are grounded in their sensory perceptions with little to no experience in the higher states of consciousness, it is reasonable to assume they deny the existence of a hierarchy, let alone lifeforms that are superior to Homo Sapiens. If this is your presumption, then I urge you to look no further than the world of quantum mechanics for evidence that life is far more complex than what we perceive and our very sensory apprehensions can – and do – change the outcome of events at nanoscale.

That said, we must demand that our exploration of human consciousness and experience has been exhausted to such a degree that we can make wise conclusions about our mortality. It is my opinion that Homo Sapiens are, in fact, but one eschalon in an unimaginably vast and multi-dimensional cosmic hierarchy. And the demand, at all levels of the hierarchy, is for subordination of the lower levels to the purposes and logic of the higher.

Human life as we currently know it is brief. We require quick and timely indoctrination into the knowledge of the generations that have come before us in order to maintain cultural, social, and psychological continuity, but ultimately, each individual is limited by the scope and complexity of data his brain is capable of processing at any given time. At some point, every human being, even the most intelligent of us, will encounter the desire for transcendence of human form.

Therefore, it could be said that extension of human lifespan is ultimately only a shift in the point of transition from one lifeform to another. Our now 79 average years of life is “prematurely transitioned” (in death), before we have had a chance to fully develop our capabilities. And not all of those 79 years are productive, due to degenerative aging processes. For this reason, we should imagine human longevity as the maximal lifespan required to exhaust the capabilities of the current vehicle of consciousness.

It is unreasonable to presume that augmentation of our biological structure (transhumanism) or merging with artificial intelligence (e.g. the Singularity movement) is in line with the greater hierarchy of life in which we exist. And this hierarchy may not, by its very nature, be exposed without unearthing the full potential of our current species, regardless of the technologies we have developed.

The Ever-Expanding Window

Based on this common understanding – that human beings should be obligated to fully realize the potential of their current organism, at its current stage of evolution – we are faced with the second question: “what is the usefulness of a single human life, extended indefinitely?”

As our computing power increases, and the medium for its execution stray farther away from silicon into the realm of synthetic biology and quantum technology, we are clearly moving toward a future where the power of several billion human brains could be condensed into a single processing unit. Considerations of consciousness and sentience aside, it should be obvious that we are on the precipice of a revolution in biology and science that could easily make human beings, in their current form, obsolete – at least from a purely functional perspective.

Does the advent of true artificial intelligence (AI), which can encompass the entire breadth of knowledge and conscious realization of the human race, preempt any need for personal evolution? If we expand the window of human life and augment the human organism’s capabilities without understanding its inborn potential, we will, I believe, lose an extremely precious opportunity – the opportunity to guide our evolution using transcendental wisdom, unaffected by human cognitive interpretation. And the wisdom I speak of is more than philosophy. I speak of capabilities which have been demonstrated, albeit in isolated cases throughout history, but nonetheless documented – that would indicate that humanity has a few tricks up its sleeves that may have been long forgotten.

In reality, human beings are just the incubating mechanism, in the larger cosmic evolutionary process, for something far beyond our instincts and intuition. Though we appear to be the apex of evolution on this planet, in this particular time and place, we can hardly proclaim, with any certainty, that we are the consummation of evolution universally.

The truth of the matter is that we are yet a myopic species, deeply devoid of the knowledge of how absolutely vast – truly, infinite — our universe is and how probable it is that similar civilizations to our own are scattered throughout time and space. Such civilizations are only apparently invisible due to the ineffably great distances between us. These distances could be compared to the space between cells from the perspective of sub-atomic particles.

So as we consider expanding the window of human life by manipulating our aging processes, we must consider the possibility for error in our perception of reality and its physical characteristics. More importantly, we must necessarily be open to the possibility that there is more to the Universe than we have even begun to understand. In this sense, our desire to “stick around” for as long as possible may, in absolute terms, negate the acknowledgement of a deeper reality whose purpose is the evolution of a progressively more complex, more “novel” experience in consciousness than we currently enjoy.

From Surviving to Thriving

The current paradigm of human life on our planet, regardless of its sporadic creature comforts, is still very much locked into the mode of survival. The majority of people in the world are habituated to a lifestyle that is purposed to “keeping the engine running” – the engine of human enterprise and self-pleasurization. Societies the world over have been sharply divided between those that can afford to support a hedonistic lifestyle purposed toward sensory enjoyment and those that live in constant torment of poverty, lack, and existential misery.

Nonetheless, society has been so constructed that most people are simply cogs in the wheel of a larger system in which they may or may not have any conception of from a holistic point of view. For this reason, we are now implementing new sciences such as machine learning and cognitive computing to better “categorize” our world and analyze it systematically. The ultimate goal of this endeavor, so some are claiming, is to eliminate the need for manual labor and maximize the potential for enjoyment and leisure.

There is a problem, however, with the shift from surviving to, supposedly, “thriving”. If artificial intelligence is to assume responsibility for the menial work that we consider to be “viable means of existence”, then the majority of humanity, sooner or later (but probably sooner) will need to learn how to live creatively. Even our ideas of creativity at this moment are intimately tied with solving problems and mitigating the pain of living in a limited world with limited senses. And augmenting human capabilities will not go far unless we have, as I have argued above, fully uncovered our non-cognitive capabilities.

The Big Gamble

So we have covered a lot of territory in our consideration here – from the mechanisms of our mortality to the possibility for radical life extension. Regardless of the emotions these concepts evoke for you, aging and longevity really come down, most fundamentally, to which gamble you are willing to make – an embrace of the possibility of multi-dimensional, infinite life according to Bohm’s Implicate Order … or the prolonged or eternal clinging to the presumed distinct existence of your current form, as you understand it?

We have seen that cellular immortality within our bodies leads to cancer and disrupts the entire delicate system of bodily survival. It is certainly within the realm of possibility, given the advancements in medical science I have described, that many of us alive today, especially in the younger generations, may be given a chance to radically extend life. For this reason, there is a great, pressing urgency to understand what that implies not only for humanity as a whole but to the ecosystem within which we live.

Many would not argue with me that current planetary resources are, for all intents and purposes, grossly limited, and many experts are beginning to question the potential for exceeding our planet’s carrying capacity. That is a topic for another article, but I feel obligated to point out that even if we do realize radical abundance through the development of nanotechnologies and synthetic biology, there is still a limited amount of real estate on our current planet. And intergalactic migrations aside, it should be mandatory for us to consider, prior to unleashing radical life extension on the masses, what our place is in the greater scheme of life and how we might not understand how deeply our species’ decisions can affect that scheme.

What Will Be Your Next Step?

Regardless of your opinions about longevity, I believe we can all agree, beyond a shadow of a doubt, that mitigating or, ideally, eliminating suffering and pain while our bodies are alive is of paramount importance. And this noble goal may easily be embraced by all humans alive today.

There is absolutely nothing wrong with wanting to perform, live, and exist at the most optimal level that is possible in nature. And this may be said not only within the parameters of your own individual existence, but for humanity at large. Hopefully, I have made a compelling case for why we must deeply understand our position and function in the whole before we will really be able to tackle the issue of aging in Homo Sapiens.

Ultimately, if we choose to live exponentially longer lives with greater capabilities, we should be prepared for a transformation and, necessarily, extinction of Homo Sapiens to make way for an entirely different order of human consciousness. All we know now is a “baton-passing” game from one generation to the other. And this knowledge is extremely primitive and linear in that it must be “serially” consumed by all new humans. It is frequently said that by the time you really begin to understand life, it’s already coming to a close.

At Transcend Genomics, we understand that every person has their own unique set of circumstances, genetics, and physiobiology. With each individual, it is necessary to deeply understand the factors that have the greatest impact on mental health, and this requires a constant evolution of research, testing, and experimentation. Regardless of the details, each of us deserves the opportunity to not only realize optimal, resilient health, but live as long as we each require to achieve the realization that we seek.

To this end, I have established a comprehensive program for body-mind transformation that begins with an exhaustively detailed mapping and analysis of your genetic markers. By understanding your genetic liabilities, we can establish which weak links in your body and mind that could be playing a role not only in your symptoms but also in your overall perception of reality. On this foundation, we develop a protocol for testing, diet, supplementation, and lifestyle adjustment that are conducive to longevity in your particular case.

For those of you that are in search of more detailed roadmap to overall health and cognitive perfection, consider enrollment in our Initial Client Program. Regardless of your level of participation, this program includes a deep analysis of data from DNA testing services such as 23andMe, Gene by Gene, Ancestry DNA, or any whole genome sequencing service worldwide. The data is processed and analyzed using our extensive repository of medical, biological, and genetic data. Based on your genes, diet, lifestyle, psycho-physical history, and more, a detailed protocol will be designed to address and correct weaknesses and imbalances.

To date, human science has made great strides in its comprehension of cellular biology and the mechanisms of aging. Nonetheless, we must carefully assess and consider our place in the greater hierarchy of life to which we belong if we are to embrace radical longevity as a potential for human beings. If we fail to do so, our extinction may be an imminent possibility, destroying one of the greatest evolutionary opportunities in the history of our planet.