Site hosted by Angelfire.com: Build your free website today!

Immortality and Medical Advancements

I am trying to follow along as best as I can with most of my things as I read them from the following website : Ant-Aging Firewalls, however not all information is from there that shows up on this page. Also, again, this page is mainly for my own learning benefits as my own way of taking notes and having them up to share as I progress helps to spread health and news I feel. The more I learn, the more I can word things in my own way better, and change things accordingly to eventually end up with a page mostly in my own words. If there is anything considered plaigarised to the extent of causing problems, let me know. My brain learns best from doing things this way that I've explained. Otherwise, the same disclaimer that applies to images on the index page also apply here to the notes I've made, and put up to share. I have actually started adding in a few references to things here and there if they are less obtrusive to my own learning.

 

What is Immortality?

Immortality (or eternal life) is the concept of living in a physical or spiritual form for an infinite or inconceivably vast length of time.

As immortality is the negation of mortality—not dying or not being subject to death—it has been a subject of fascination to humanity since at least the beginning of history. The Epic of Gilgamesh, one of the first literary works, dating back at least to the 22nd century BC, is primarily a quest of a hero seeking to become immortal. This story seems to have correlation between other stories told by other cultures with their varying religions and passing of stories over time. What form an unending human life would take (as well as whether it is subject to incapacitation), or whether the soul exists and possesses immortality, has been a major point of focus of religion, as well as the subject of speculation, fantasy, and debate.

It is not known whether human physical immortality is an achievable condition. Biological forms have inherent limitations which may or may not be able to be overcome through medical interventions or engineering. As of 2009 though, natural selection has developed biological immortality in at least one species of creature on this planet, though. So, there is ‘some’ hope to gain immortal life for some individuals, and science will hopefully lead to the answers that they are seeking.

What things cause aging? (14 theories of aging here. Not all are necessary here)

               There are multiple ideas out there on reasons why aging exists. Some could very well be correct, and others could be incredibly wrong. Some lack some proof due to the fact that science still doesn’t know some parts about the world’s and universe’s religious and nonreligious history, and also the fact that they don’t know if the human race did actually have any interactions with some other race of people or ‘gods’. Some ways that can be accepted though, as a hope or belief as well as factual in some of the cases are the Hayflick limit, the possibility that this could have been introduced or sped up by outside dna interactions, mutation accumulation which is selection of genes for evolution rather than keeping a person younger, and the disposable soma which allocates energy to repair still even in the lack of food although calorie restriction itself can raise NRF2 levels. In women, calorie restriction can lead to osteoporosis though. There is one other thing that somewhat works above any of these ideas to a degree though, and that is flow of time in a seemingly one way continuous direction, and perhaps maybe even under the rules of what is known as entropy, which states that the universe continuously favors moving from an organized state to a disorganized one. To a degree, we can see this as a person ages, and see how things unwind to form disorganization with the body’s workings, leading it to age faster and slowly die.

Cell death and telomere shortening, when discussing them in a religious or alien sort of way, may have originally become noticeable after the other set of beings (Gods) took a typical creature from earth and injected some of the being dna into them in order to increase the evolutionary change of the creatures which became a more modern man and have them take on more of an image of the ‘creators’. Something in this either caused longer life or for aging to be rapidly progressed from what it was. Either way, there was a change in lifespans of people during these times that these beings were supposedly here.

Mutation accumulation is another theory that was formulated by a Peter Medawar in 1952 in order to explain how evolution would select for aging. Essentially, ageing is never selected against, as organisms have offspring before the mortal mutations surface in an individual.

The diposable soma theory is another possible reason for aging and was proposed in 1977 by Thomas Kirkwood, which states that an individual body must allocate energy for metabolism, reproduction, and maintenance, and must compromise when there is food scarcity. Compromise in allocating energy to the repair function is what causes the body gradually to deteriorate with age, according to Kirkwood. This theory will most likely be discarded some day due to the fact that we have found that a certain level of calorie restriction, or not eating, can be good when conditions are favorable to fair eating at other times, or eating low calorie items. Otherwise, simply starving would probably negate any positive things that can come from calorie restriction.

Lastly, the progression of time perhaps is also a reason for aging as well if looking at it from the view of one of the rules of entropy. There are multiple parts to entropy, however the main one would be that nature tends from order to disorder in isolated systems. Scientists are still searching for answers regarding whether or not this is true.

What are telomeres, telomerase, and how do they relate to what’s known as the Hayflick limit?

A telomere is a region of repetitive DNA at the end of a chromosome, which protects the end of the chromosome from deterioration. Telomeres protect a cell's chromosomes from fusing with each other or rearranging (abnormalities which can lead to cancer) and normally destroy cells when their telomeres are consumed. Most cancers are the result of "immortal" cells which have ways of evading this programmed destruction and that are brought on by abnormalities in a cell. Telomeres do shorten automatically under normal conditions during each cell division due to the nature of the chromosome replication mechanism which normally limits cells to a fixed number of divisions, and animal studies suggest that this is one reason possibly responsible for aging and sets a limit on lifespans.

There is however an enzyme, called telomerase, that elongates the telomere and can thus retore it. On thefreedictionary.com, telomerase is defined as an enzyme that preserves the length of telomeres across cell divisions in germ cells, stem cells, and most cancer cells. It is a kind of reverse transcriptase, an RNA-containing enzyme that synthesizes the DNA of telomeres by reverse transcription. It is active during DNA replication and is thought to play a role in the proliferation and apparent immortality of cells in which it is present. In cells that lack telomerase (that is, in most somatic cells of the body), the telomeres of chromosomes shorten and eventually disappear over repeated cell divisions. The term somatic (from the Greek σωματικός) refers to cells of the body. Somatic can also defined as relating to the wall of the body cavity, particularly as distinguished from the head, limbs or viscera. It is also of or relating to the portion of the vertebrate nervous system which regulates voluntary movements. The inhibition of telomerase in cancer cells is being investigated as a method of killing cancerous cells.

In most cells, except cancer cells and perhaps some stem cells, telomerase is turned off naturally. In fact, one of the steps in a cell becoming cancerous is activation of telomerase, but this usually happens after the cell has already gone bad in some way or another if it is going to be cancerous. As of today, there is no way to activate telomerase in a controlled fashion in skin cells or other normal cells in order to escape what is known as the Hayflick limit. An increased amount of telomerase can protect cells and stop the 'caps' from being broken down slowly off of dna and perhaps lead to an extended and healthier lifespan, however telomerase is also turned on in a very similar way when cancer forms. Telomerase is found in embryonic stem cells, and only in the cells that need to divide in adults, unlike with embryos they are creating everything and therefore found in all parts.

Diet and exercise are ways that have been shown to raise telomerase levels. As a side note, they can raise NRF2 molecule levels as well. Telomerase, in one test, was boosted by 30 percent in prostate cancer patients who followed a plant-based, whole-grain diet with very little fat or sugar for three months. The men also took fish oil supplements (able to be achieved by the right types of actual fish products as well), did daily 30-minute bouts of exercise, and practiced yoga or meditation for an hour a day. "Telomerase turns up those genes associated with disease prevention and turns down the genes associated with heart disease, diabetes, and cancer," explains Ornish. These things are very similar to those that also raise NRF2.

As far as any tests go, in April 2007, Geron Corporation licensed New York-based company TA Sciences to conduct human trials on a molecule called TA-65, a derivative of Astragalus propinquus, that acts as telomerase activator.[9] Astragalus, however, has been found to lower NRF2 levels. In November 2007, Sierra Sciences announced that they had discovered a compound called C0057684 that caused the expression of even higher levels of telomerase activity in somatic cells[10] and, in 2009, announced that they had discovered an additional 62 compounds that cause telomerase activation. Telomerase is a protein that helps maintain the protective caps at the ends of chromosomes. A team of researchers at the Spanish National Cancer Centre (Madrid) tested the hypothesis on mice. It was found that those mice which were genetically engineered to produce 10 times the normal levels of telomerase lived 50% longer than normal mice. A trick with cancer cells is that this is turned on indefinitely for cells that have already gone bad. If telomerase is turned on inside the telomere before a cell goes bad, then it increases the length of telomeres on dna strands back out. Telomeres are currently what are considered the biological countdown clock to death. Once the telomeres have reached their limit (Hayflick) and can no longer cause cell replication and replenishment, then death comes. If lengthened back out, it causes longer life span and increases health and looks.

What is the Hayflick Limit?

Programmed cell death and the telomere "end replication problem" are found even in the earliest and simplest of organisms. Telomere is a 'cap' on the ends of DNA that help cells to split and recreate. These eventually wear down and at that point a cell actually dies because it can no longer replicate itself anymore. This is known as the Hayflick limit.

The "Hayflick limit" is a finding by Dr. Hayflick, many years ago, that fibroblast cells, in culture, will only have a finite number of doublings, after which they stop dividing and become senescent (dead). However, a fibroblast is a somatic(of the body) terminally differentiated cell which produces collagen. In contrast, all tissues which make extensive use of fibroblasts, including skin, bone, etc., are also well well supplied with fibrocytes.

Fibrocytes are undifferentiated stem cell versions of fibroblasts. They are not yet functioning to produce anything. When you were young, they continually produced replacement skin cells for no other reason other than the fact that they could. But, with increasing age, fibrocytes, and other stem cells become more and more likely to just sit there, waiting, in your skin, and elsewhere. Sometimes they may wait for many years, until some kind of serious damage is perceived by the body. This might include peeling by acids, lasers or otherwise. In the face of massive injury, the fully differentiated fibroblasts generate large numbers of signalling molecules, chemicals such as cytokines, which tell the fibrocytes "It is time to come out of slumber. You need to make new fibroblasts."

Generally, the fibrocyte will then divide, producing one fibroblast destined copy, and one fibrocyte to replace itself. Depending on how bad the damage is, and how persistently the existing fibroblasts call for help, this same process may repeat itself, over and over again, until many eventual fibroblasts may be produced by one fibrocyte. But, always, one replacement fibrocyte will remain. Like all stem cells, fibrocytes produce a certain amount of telomerase, and we are able to measure this in skin, after injury. Telomerase is an enzyme that acts to elongate the chromosomal "caps" called telomeres/ In mitosis, other enzymes, which stimulate division and duplication of the chromosomes, bind to each chromosome by holding it at the telomere. As a result, the particular nucleotides are blocked, and they cannot be copied. This results in a progressive shortening of the telomere caps.

Thankfully, there is a lot of telomere, at least to begin with. And, furthermore, the telomeres don't code for any needed proteins. So, losing a bit of nucleotide sequence is not devastating to the cell. However, the telomeres are essential for chromosomal stability. A measurable length of telomeric nucleotides are sacrificed with each population doubling. The telomere eventually becomes so short there is barely anything left for the mitosis enzymes to latch onto, and the cell stops dividing. That is called senescence, and the maximum number of times that a fibroblast can divide is called the "Hayflick Limit”.

What is Something Thought to Possibly combat the Hayflick Limit?

Fibrocytes, unlike fibroblasts, produce a sub-optimal amount of telomerase. This enzyme functions to add back sections to the telomere after mitosis, restoring the chromosomes to the pristine state it once enjoyed, prior to the time that the cell divided itself. I say sub-optimal because adult stem cells do not produce enough telomerase to quite equal the rate of telomere shortening. Unlike embryonic stem cells, therefore, adult stem cells do, eventually, become senescent. The time it takes for that to happen, however, is so far beyond the so-called "Hayflick Limit", that an adult stem cell is essentially "immortal," when we are talking about people who currently live to a maximum life span of about 120 years. We have enough skin stem cells, producing enough telomerase, to last a lifetime of well over 1,000 years.

How can this be? Well, as stated, your existing stock of stem cell fibrocytes are sufficient to regenerate your skin for 1,000 years. Indeed, if you believe the quasi-historical accounts in the Bible, people, like Methuselah, once did live that long. We could, potentially, even lengthen stem cell productivity far beyond that. All you would need to do is, somehow, figure out how to upregulate the production of telomerase in adult stem cells. If you did that, successfully, you would have the potential of eternal life, and eternally renewing skin. You could do as much peeling as you wanted, and never ruin your skin. We actually have some idea on how to upregulate the transcription of telomerase, in individual cells. It has been done in the laboratory, most recently by the Geron Corporation. The most important hurdle to achieving eternal life is not in upregulating telomerase. What we don't understand is how, why, and what signaling mechanisms are involved in causing the normally quesient stem cells to activate to the point where they replace worn out somatic cells, as they do when we are young.

It has been shown that blood, from a young animal, transfused into an older animal, stimulates stem cell activity, and replacement of somatic cells, especially in areas of the body that have been injured. Scientists have shown that the healing response, of old animals, can be restored to the level of youth, simply by transfusing young blood into them. Conversely, by transfusing old blood into younger animals, healing can be retarded.

It is abundantly obvious that there is an unknown substance, in the blood of younger animals which is in much shorter supply, in older blood. This unknown chemical(s) stimulates mobilization of stem cells. Mobilization of stem cells, in turn, acts to maintain the organism in a youthful state. Stem cells are stimulated, to regularly replace worn out somatic cells (such as fibroblasts, in the skin). Such microscopic activity can be seen, macroscopically, by the increased turnover of skin cells and healthier looking skin of the young, compared to the aged. In a very primitive way, by utilizing techniques that burn off the outer layer of skin with acid, lasers, etc., we are trying to stimulate some of the chemicals of youth.

It would seem however, that as a person gets older, a thing called NRF2 is decreased, which apparently helps to keep energy up and repair of the body going. Without it, NFKAPPA-B increases, because the regulation goes down, and it causes inflammation in the body. The increase causes a faster rate of aging if not regulated. Most of the pathways of the body seem to continuously go back to the production of this NRF2 as a way of keeping a person younger to a degree, and in better health, however upregulating this still won’t stop a person from aging. It may explain some of the difference between older and younger though.

Theoretically, aging is an aberration that the living organisms should not be subject to. We can see, in experiment after experiment, that the human body can and should be fully capable of maintaining itself for a 1,000 years, or more, even without direct genetic tampering. Yet, this does not happen. It seems as if some very knowlegeable person (God?) has deliberately turned off the backup systems, forcing aging and death. All the talk about anti-oxidants only addresses the issue of prolonging the life of somatic cells. Stem cells, with limited exceptions, are not susceptible to being worn out by oxidation.

What about MTOR and its affect on the hayflick limit? How is it affected by NRF2?

What is NRF2?

On the Vitality and Longevity Report, Volume 1, Number 4 regarding Dr. Joe McCord’s promotion of a product called Protandim, NRF2 is said to be a master regulator of survival genes. It is a protein that can be seen as a messenger contained in every cell of your body. NRF2 is a set of molecules, that when they are upregulated, they communicate with DNA by sending signals along microtubules (message tubes) that enter in to the nucleus of a cell to turn on and instruct genes known as ‘survival genes’ in order to produce various antioxidant enzymes, such as catalase and SOD, to fight aging and oxidative stress. Upregulation of NRF2 works through antioxidant defense mechanisms, detoxification mechanisms, and immune balancing mechanisms. So, in a way, a certain level of light stress is put on to those systems of the body in order to increase the body’s protection.

There are some things that can naturally activate NRF2. One is that a certain level of coldness will activate it. Eating certain foods or taking certain supplements can activate it. Exercise also will activate NRF2. In order to make sure to get the right amount of exercise so as it remains affective in a positive way, it should not be done to a completely exhausting point. Doing exercise or taking multiple supplements or foods simultaneously, all of which can activate NRF2, may not be good though since all of them work on the that pathway. With the product Protandum, they place green tea, turmeric (curcumin), milk thistle, ashwagandha, and bacopa as optimum supplements to promote NRF2. All of them appear on the Anti-aging Firewalls list except for bacopa and milk thistle, however milk thistle has been mentioned in one of the blogs from that site.

Are multiple products required to activate NRF2 in different spots, or will just one product be sufficient in certain doses? Previous statement would seem to suggest no.

Is Telomerase upregulated by NRF2 since telomerase is an enzyme and seems to be able to be upregulated by diet and exercise also? Is it upregulated by MTOR?

What is NFKAPPA-B?

NfKappa-B is a type of protein molecule like Nrf2, and is also a ‘messenger’ which is also in every cell of the body. Its pathway consists of 5 genes (NF-kB1, NF-kB2, RelA, c-Rel, and RelB). These five genes make 7 protiens. (which ones considering nfkappa-b is considered a protein?) There is a process to release the particular protien so that it can shift in to a cell’s nucleus by way of microtubules just as Nrf2. Once inside of the nucleus, it becomes what is known as a transcription factor. However, NfKappa-b, having a different job from Nrf2, is used to tell mitochondria to turn on genes that cause inflammation, and is activated by various types of stressors. Although the NF-kB transcription factor is often thought to be pro-apoptotic, it actually regulates eight anti-apoptotic factors. Although NF-kappaB is usually labeled as the “devil of inflammation”,  NF-kappaB can also be viewed as the “savior of survival”. that share a Rel Homology domain.

What is MTOR?

We also note that mTOR inhibition is one of the few well-documented approaches to increasing mammalian longevity(ref).  This leads one to wonder if frequent exercise-induced mTOR activation might work against longevity, while at the same time contributing to muscle regeneration.  All available evidence indicates that this is not the case.  Regular exercise is associated with both increased longevity and improved muscle maintenance, probably because exercise activates mTOR very selectively, only in specific muscle tissues; it does not activate it globally.  On the other hand, global mTOR inhibition is very likely to have adverse effects on muscle mass.

What are Microtubules?

Has anyone or anything ever lived forever, bypassing Hayflick?

Jellyfish usually die after propagating (breeding/multiplying), however there is one type known as turritopsis nutricula that can return to what is known as a polyp state. After becoming a sexually mature adult, it can transform itself back into a child (the polyp stage) using the cell conversion process of transdifferentiation. Transdifferentiation is to take a cell such as a stem cell has already changed/differentiated and has a set path it is taking, but is removed from that path, mixed with other cells not of the same type, and then caused to differentiate again off from its original intentions to begin mimicking the newly introduced cells. Basically, one cell changing into another type of cell. An example of this would be in salamanders and chickens when the lens of the eye is removed, cells of the iris turn into lens cells. For this type of jellyfish, this is done through a cell change in the external screen (exumbrella). The cells revert to a different state. The medusa is transformed into a stolon and the polyps into a hydroid colony. The umbrella turns inside out; middle section and tentacles are reabsorbed before the polyp spawns. Stolons form two days before the polyps differentiate. The ability to reverse the life cycle is probably unique in the animal kingdom, and allows this type of jellyfish to bypass natural death, rendering it biologically immortal. Lab tests showed that 100% of specimens reverted to the polyp stage. Turritopsis nutricula is capable of repeating this cycle endlessly. To some extent, this is similar to what scientists are trying to do with stem cells from people. They take them and put them back to an original state (pluripotent) in order to then take them and try to convert them over from the type of cell they were programmed to be to one with other programming so as to be useful in renewing areas in the body that would otherwise not renew themselves.

Vedics and post-Vedic rishis (such as Markandeya) attained physical immortality, Sri Aurobindo state, which includes the ability to change one's shape at will, and create multiple bodies simultaneously in different locations.

Jesus (aka Yahweh) - Bible passages in Christianity are interpreted as teaching that the resurrected body will, like the present body, be both physical (but a renewed and non-decaying physical body) and spiritual. Jesus was an example of this. There are a number of myths (Greek: stories) that relate fairly heavily to the life of Jesus in ancient history, as well as myths that relate to some other stories from the bible. One of the other stories other than that of Jesus in a different manner is the supposed great flood. Egyptians, Greeks, and Romans have their versions, and if I am not mistaken even the Sumerians before them had their version. It is possible that Jesus may have been from a story brought up from the Sumerians regarding him as maybe an Annunaki.

Annunaki – The Annunaki were gods to the Sumerians. The later Egyptian, Greek, and Roman gods are said to be somewhat based off of these in personality and some other points. There was a group, the Mycenians, who came before the Greeks though, and they had a strong influence on what went in to Greek society, so therefore the Mycenians must have had a ‘more close to original’ interaction for these ‘gods’ before even the Greeks, and perhaps even before the Egyptians and the Romans. Although the latter groups did not seem to count these beings as actual entities always physically existing with people, the Sumerians had seemed to placed them in a more realistic light, as if they were real beings, and that could be interpreted today as possibly being an advanced race with extraordinarily long lives and height. This race lived much longer than people supposedly, so there is a possibility that people may have just considered these beings to be immortal.

Who were the Sumerians? Tell more about the Annunaki as well as their gods so as to show the progression of the bible and otherwise believes mixed in with greek, roman, and Egyptian beliefs in their gods. Greek and Roman and Egyptian god myths were sometimes used to represent the seasons, which is known as a ‘what?’ type of mythos?

What are some factual things being researched in science to help lengthen life?

1.      NRF2 and telomerase upregulation – These help the appearance and function of the body to hopefully lead to extended life, however they have not reached any kind of level as to be able to promote immortality.

2.      Transdifferentiated stem cells are another way of slowing down mortality and increasing life span. This will hopefully be useful for growing new organs, eyes, hands, etc. for people eventually. If worked the right way, for those wanting to experience immortality and feeling they can tolerate it, this could possibly allow a person to endlessly supply and resupply themselves with stem cells from themselves which are compatible with their own bodies.

3.      Huntington's disease - need to change two amino acids in the huntington protien. There is a small section of it that can be modified by phosphorylation, which is a chemical process in the body that alters how protiens function. This process currently may help in preventing symptoms and may eventually lead to ridding of the disease altogether.

4.      HIV –

5.     Memory impairment - Signals come in and turn on RNA in the synaps cells. A 'silencing' molecule fragments when they are turned on. This in turn begins a 'program' to create protiens that strengthen a synaps. What happens with memory loss more and more is that each time new memories are created, protiens from previous memory degrade in order to make the process of new memories happen. Eventually these get worn out. This usually effects short term memory first, as various other protiens have been used to 'cement' longer term memories. WHen short term memory is pretty much gone, the protiens from the longer term memories begin to be used in order to try to make up for the losses of short term memories.

6.      Carbon 60 Buckballs mixed with olive oil (extra virgin better?) – Tests were done on mice, and with them, their lifespans were able to be increased by 90% of where they were in typical mouse lifespans. The downside to this is that it may actually damage the mitochondria over time, and eventually may be worse off for a person. Some people are testing this as individuals, however its safety is not guaranteed. C60 Buckyballs have been researched for quite a number of years, but was never mixed with olive oil until very recently.

7.      Life extension technologies promise a path to complete rejuvenation. Cryonics holds out the hope that the dead can be revived in the future, following sufficient medical advancements. Modern cryonics procedures use a process called vitrification which creates a glass-like state rather than freezing as the body is brought to low temperatures. This process reduces the risk of ice crystals damaging the cell-structure, which would be especially detrimental to cell structures in the brain, as their minute adjustment evokes the individual's mind.

8.     Robert Freitas, a nanorobotics theorist, suggests tiny medical nanorobots could be created to go through human bloodstreams, find dangerous things like cancer cells and bacteria, and destroy them. Freitas anticipates that gene-therapies and nanotechnology will eventually make the human body effectively self-sustainable and capable of living indefinitely, short of severe trauma. This supports the theory that we will be able to continually create biological or synthetic replacement parts to replace damaged or dying ones. This is the most likely concept to try to work towards achieving and understanding, and would basically be turning a person into a cyborg of sorts, and could possibly lead to even more implants that would possibly lead to full robotic body replacement, however nanorobots should be sufficient enough until further studies done on mind transfers from human body to robot body.

9.      Spore-like stem cells - Beyond all this, we just learned a few years ago, in addition to normal stem cells, our skin, and that of all other animals, also has abundant reserves of an unusual type of stem cell, dubbed "spore-like" stem cells. We call them spore-like because, like the spores from fungus or bacteria, these mammalian spores are very basic packages of DNA, and lack most of the baggage of full developed stem cells and somatic cells.

From their structure, spore-like stem cells probably should function like a sort of emergency "backup" DVD. If the computer fails, you put this backup in, to restore the system. Similarly, if the stem cells fail, the spore like stem cells can take their place. These cells have all the same basic DNA codes of normal cells, but the DNA is tightly wound, the tiny amount of cytoplasm surrounding the DNA has a very limited number of mitochrondria, and they are coated with tough membranes, designed to withstand great stress. If called into action (and we don't know how to do that yet) spore-like stem cells can quickly absorb nutrients from the surrounding serum, multiply mitochondria to full numbers, activate their nuclei, and convert themselves from "compressed archives" into full fledged stem cells. These can then further differentiate, like any other stem cell, into terminal somatic cells, repairing damaged tissues.

 

Spore-like stem cells are highly resistent to heat. acids, radiation, etc. If we knew more about stimulating them, we could, potentially, use one single spore-like stem cell to reconstitute the entire organism.

 

For unknown reasons, at the present time, not only are spore-like stem cells "disabled", but normal stem cells stop replacing worn out parts, for unknown reasons, simply because we reach a certain age. And, humans are not the only animals that suffer from aging. All mammals, and almost all (but not quite all) other species, do, also.

 

 

What are non-factual theories ‘claiming’ as possibilities to achieve Immortality or increase lifespan?

1.      Metaphysical universals and abstract phenomena have an eternal existence, and if they can be interacted with by human beings, then a person might obtain a degree of immortality by interacting with them.

2.      Quantum immortality is not widely regarded by the scientific community as being a verifiable or even necessarily correct offshoot of the many worlds interpretation. In the many worlds interpretation of quantum mechanics, the wavefunction never collapses, and thus all possible outcomes of a quantum event exist simultaneously, with each event apparently spawning an entirely new universe in which a single possible outcome exists. In this theory, a person could hypothetically live forever as there might exist a string of possible quantum outcomes in which that individual never dies.

3.      Mind uploading is the concept of transference of consciousness from a human brain to an alternative medium providing the same functionality. Assuming the process to be possible and repeatable, this would provide immortality to the consciousness, as predicted by futurists such as Ray Kurzweil. With mind uploading, the individuals memory may be loaded to a computer or to a newly born baby's mind. The baby will then grow with the previous person's individuality, and may not develop its own personality. Extropian futurists like Moravec and Kurzweil have proposed that, thanks to exponentially growing computing power, it will someday be possible to upload human consciousness onto a computer system, and live indefinitely in a virtual environment. This could be accomplished via advanced cybernetics, where computer hardware would initially be installed in the brain to help sort memory or accelerate thought processes. Components would be added gradually until the person's entire brain functions were handled by artificial devices, avoiding sharp transitions that would lead to issues of identity. After this point, the human body could be treated as an optional accessory and the mind could be transferred to any sufficiently powerful computer.

4.      Yet another view of immortality is traced to the Vedic tradition by the interpretation of Maharishi Mahesh Yogi:

 

That man indeed whom these (contacts)

do not disturb, who is even-minded in

pleasure and pain, steadfast, he is fit

for immortality, O best of men.

 

To Maharishi Mahesh Yogi, the verse means, "Once a man has become established in the understanding of the permanent reality of life, his mind rises above the influence of pleasure and pain. Such an unshakable man passes beyond the influence of death and in the permanent phase of life: he attains eternal life… A man established in the understanding of the unlimited abundance of absolute existence is naturally free from existence of the relative order. This is what gives him the status of immortal life." This, to me, is saying that the responsible steadfast person will be able to make wise descisions and control various influences on his life well enough to be able to use them to extend life, and can make it through any circumstance with ease.

5.      Buddhism teaches that there is a cycle of birth, death, and rebirth and that the process is according to the qualities of a person's actions. This constant process of becoming ceases at the fruition of Bodhi (enlightenment) at which a being is no longer subject to causation (karma) but enters into a state that the Buddha called amata (deathlessness). The Greeks had a belief similar to the idea of reincarnation. They believed that everything would recycle itself as a whole eventually every so many years, and that everything would start anew again from the beginning rather than necessarily a continuation of life. This information came from my note taking in my Classical Myth class at PSC. To an extent, transdifferentiation could be seen as a physical birth, death, and a rebirth cycle, except without an actual death, according to how the Greeks seemed to view the life cycle of everything.

6.      Bible passages in Christianity are interpreted as teaching that the resurrected body will, like the present body, be both physical (but a renewed and non-decaying physical body) and spiritual. Jesus was an example of this. There are a number of myths (Greek: stories) that relate fairly heavily to the life of Jesus in ancient history, as well as myths that relate to some other stories from the bible. One of the other stories other than that of Jesus in a different manner is the supposed great flood. Egyptians, Greeks, and Romans have their versions, and if I am not mistaken even the Sumerians before them had their version. It is possible that Jesus may have been from a story brought up from the Sumerians regarding him as maybe an Annunaki. Honestly, with what I have read in religion, and the things I have learned, come to understand, and now believe, I feel that this was a look at the future, or at a present that was leftover from another time which fell greatly. We, as people are working towards this… to try to make heaven on earth.

What is a good plan to follow to help try to live longer?

Take these vitamins and or supplements * = not necessary when right foods are eaten:

1.      *B Vitamin Complex in correct amounts (B50) - used for homocystiene levels to avoid various older age diseases for longer. atleast 400mcg of folic acid daily if not more for memory and for controlling homocystiene levels to avoid various older age diseases for longer, and do not go over 2000mg of niacin in a day. Try not to take too much niacin, as it is more for aging.

2.      *-Vitamin C – Good as an antioxidant. It can cause kidney stones, diahrea, and other unpleasant things in too high of amounts in pill form mainly. Usually 1000mg is fine daily. It is easy to get this from right foods though.

3.      *-Calcium - Nothing over 2000mg per day.

4.      *-Magnesium - detrimental to many functions inside the body. Magnesium can help with practically all things. It lowers histamine levels in the body (what antihistamines do), which can help clear up allergy type symptoms, help with schitzophrenia, help with tmj issues, etc. If no money to purchase the vitamin, then go with okra. Take milk with this at a high enough level so there's no shortage. Calcium and magnesium are absorbed better when together, but not so well when one is higher than the other. (400 mg). Get with a multivitamin if available in right amount.

5.      *-Fish oil supplements - naturally increase telomerase production some and cuts down on the rate at which telomeres degrade, as well as find high omega fats that help control and lower weight. Make sure to get purified for mercury types and with atleast a 400mg combined between DHA and EHA. Eat 1-2 cans of bumblebee light tuna in oil for this daily if unable to get or afford supplements.

6.      *-Quercitin - inhibits the expression of HSP70 in cancer cells? Found in broccoli, raspberries, black tea, green tea, red wine, red onions, tomatos. Red onion and the teas contain the most. Eat red onion skin.

7.      *-L-Carnosine – 3 – 4 grams daily (8oz (1cup) daily of either chicken or beef). Helps slow down the methylation of dna strands and greatly increases the amount of times cells can divide, thereby inturn helping to stay younger for longer. Increases GABA in the body and can increase pain and stress tolerance. Carnosine is very abundant in protein-rich foods. Some common examples of such foods include milks, eggs and cheese. However, the best food sources of carnosine include beef, poultry and pork products. Beef has about 1,500 mg carnosine per pound. Poultry has about 2,000 mg carnosine per pound. Pork has about 2,000 mg per pound.

8.      *-L-theanine – found in green tea. If you want natural occurring l-theanine, switch over to a high grade green tea, which may contain as much as 50 milligrams per cup. High grade green tea is normally made from young tea buds harvested early spring. They need not be expensive. As far as theanine goes, my personal favorites are the Dragon Well and Biluochun tea.

9.      -cycloastragenol - replacement for astragalaside IV. Helps various stem cells as well as regular cells in the body to begin producing again instead of sitting around and doing nothing. telomerase activator by RevGenetics. 10x nire effective than astragaloside IV. take before resveratrol because it increases ability to get through blood brain barrier

10.   -Reserveratrol - orally and hold in mouth for a few minutes and let it soak through and then swallow the rest. Take max amount allowed daily once less expensive. Reduces inflammation. It can be found in red wines and /japanese knotroot for amounts that do any good. activates sirt1. Reservatrol also increases natural testosterone and helps protect the lungs from cigarette smoke to a degree. Oral administration of resveratrol (5mg/kg b.w) to streptozotocin-nicotinamide-induced experimental diabetic rats for 30 days significantly normalizes the levels of blood glucose, plasma insulin, glycosylated hemoglobin, AST, ALP, ALT, and modulates the altered activities of carbohydrate metabolizing enzymes in the liver and kidney tissus of diabetic rats. (take into account a rat’s average weight vs. human weight, and also take into consideration any notices for overdose). It was seen to increase ampk which is released during muscle stimulation, but in this case there is no stimulation in occurance. Ampk basically turns on various energy producing pathways and is also seen as life extending qualities. In a study of 123 Finnish adults, those born with certain increased variations of the SIRT1 gene had faster metabolisms, helping them to burn energy more efficiently—indicating that the same pathway shown in the lab mice works in humans. Mice fed resveratrol for fifteen weeks had better treadmill endurance than control mice. The study supported Sinclair's hypothesis that the effects of resveratrol are indeed due to the activation of the Sirtuin 1 gene. The sirtuin 1 gene basically increases the regulation by proteins against stressors and helps increase cellular longevity. These sirtuin proteins are usually produced by yeast, some of which can be found in red wines, however tests with red wines show that there is not enough available in drinking of red wine to be effective. Sirt1 genes lock onto the proteins in order to work. In mice, oral resveratrol also produced large reductions in brain plaque in the hypothalamus (-90%), striatum (-89%), and medial cortex (-48%) sections of the brain. In humans it is theorized that oral doses of resveratrol may reduce beta amyloid plaque associated with aging changes in the brain. Researchers theorize that one mechanism for plaque eradication is the ability of resveratrol to chelate (remove) copper. Nicholas Wade's interview-article with Dr. Auwerx states that the dose was 400 mg/kg of body weight (much higher than the 22 mg/kg of the Sinclair study). For an 80 kg (176 lb) person, the 400 mg/kg of body weight amount used in Auwerx's mouse study would come to 32,000 mg/day. Compensating for the fact that humans have slower metabolic rates than mice would change the equivalent human dose to roughly 4571 mg/day.

11.   -DHEA - Supplementing hormones for men not living with women. 6 months longer in mice and must be quite a bit longer in humans. Inhibits mTOR pathway which is increased with use of niacin (b3). May only mimic calorie restriction for obese people, allowing them to continue eating alot but keep an average lifespan. Can cause hairloss on rare occasions, but not with everyone and mainly women. Otherwise, this is quite safe even in higher amounts. If using synthesized DHEA, then do not take higher doses. Naturally only found in wild yam from Mexico extracts currently. Use 7 Keto DHEA if hairloss begins to be experienced with regular DHEA. If an individual's DHEA levels were healthy enough, there would be no need for estrogen, or testosterone, melatonin or other hormone replacements, as the DHEA hormone would naturally supply your body with whatever hormone your body happened to be lacking.

12.   Turmeric  / Curcumin – limit to 1 pill per day with lunch. It raises NRF2 and reduces inflammation. It can be found within turmeric spice or on its own as a spice on shelves in stores. It is a chemo preventive agent with potent anticarcinogenic activity in a wide variety of tumor cells. Curcumin inhibits cancer cell proliferation in part by suppressing cyclin D1 and inducing expression of the cyclin-dependent kinase inhibitor p21. Ground from the root of a plant (Curcuma longa L.) of the ginger family, found wild in the Himalayas and grown across South Asia. Don’t use often or ever. Causes faster telomerase shortening.

13.   -Co Q-10  or COQH (Ubiquinol) - protect mitochondria and also provides energy. This is found highest in sardines, however not enough is provided to make it of any real benefit. Supplementing with it with q-sorb or as coqh vs. coq10 is much better.

14.   -Alpha-lipoic acid - protect mitochondria. Stops unwanted cell death. Can come with carnatine. Can be found in broccoli, spinach, collard greens, and even tomatoes, however it’s effectiveness is significantly less and of no real benefit in such small amounts. Try to limit this, as ALA may work negatively on mitochondrial dna.

15.   -acytl-l-carnitine - protect mitochondria and reduce telomere shortening. Stops unwanted cell death. Can come with alpha-lipoic.

16.   -Melatonin – natural sleep aid.

17.   -Ginko biloba - activates telomerase in non-cancer cells, and helps to prevent various types of cancer. 60mg most days, and no more than 120mg ever, although up to 300mg on very rare occasions is ok. Increased level of energy and better circulation. This plant also increases circulation to the penis to achieve rock-solid erection for a better sexual performance. More blood coming into the penis results to bigger erection. 78% of men suffering from non-medically related impotence had experienced the powerful results of Gingko Biloba without any side effects.

18.   *-Vitamin D3 - histone unwrapping inhibitor - helps to prevent an item that causes inflammation, and that enters the nucleus of a cell from activating. A histone is a string down the middle of a set of dna strands. They wrap around the histone, and can unwrap as well. These must be kept wrapped around the histone in order to inhibit inflammation. Get with milk instead of a pill.

19.   -Bromelain – anti-inflammatory, and helps continue to help hair grow well. It is found in pineapples, however not in high enough amounts to do any good.

20.   -Glucosamine Chondroitin - cartilage structure and joint lubrication

21.   -Ashwagandah - cancer prevention and heart, as well as male performance sexual enhancement. It raises NRF2 levels.

22.   -Boswellia seratta - cancer prevention and heart

23.   *-Nature’s Bounty - covers C, D3, E, zinc, and other important vitamins

-cordyceps? - type of chinese mushroom that protects lungs and kidneys by making it easier to breathe and function. Can supposedly cure a few different cancers. Also increases amount of testosterone In the body.

If male, take these supplements that are good for enlarging a penis and/or atleast helping to keep function at a more nominal level :

1.      -Hawthorn berry – lowers blood pressure, but has sexual benefits.

2.      -Catuaba Bark Extract - all around nervous system revitalizer. It restores your nervous system function bringing about increased brain function, reduced nervousness, better sleep and improved sexual function. This is the herb that has helped the 60, 70, 80 even 90 year olds in Brazil have a healthy sex life naturally. There are no known side effects with catuaba except the occasional upset stomach and diarrhea when it is first introduced to the diet. The main concern is that you are actually purchasing real catuaba bark, as there are several exporters who export the bark as catuaba, but it is in fact from the wrong tree. There are 2 forms of catuaba tree that supplies the actual bark that is medicinally known for its benefits and the scientific names for these two is Erythroxylum catuaba and Trichilia catigua. The standard daily dose is 1000mg to 2000mg. There has not been any standardization of the extract’s concentration.

3.      -Damiana - found primarily in Central and South America. It is recorded being used as early back as the ancient Mayan civilization to prepare for lovemaking. Today it is used to relieve headaches, control bed wetting, better control of the muscles in the urinary tract, as an aphrodisiac and to enhance orgasms.

4.      -Safflower oil

5.      -Horny Goat Weed – aka Epimedium Leaf Extract. It had been found to contain icariin which can increase erectile function. It also increases blood circulation to the penis. More blood supply to the penis means a larger and stronger erection. Furthermore, it can stimulate the release of the male hormone, testosterone, which is responsible in increasing a male's libido and sexual endurance. It can come in strengths between 5% and 60%, most higher than that only being used in labs.

6.      -Cuscuta Seed Extract - increases the amount of live sperm cells of a man. It is also a known solution to premature ejaculation, a common problem among some men which greatly affects their sexual relations. A bigger, harder and more sustained erection is the male enhancement benefit of this natural ingredient. It is used in conjunction with other herbs to treat a wide range of conditions, ranging from impotence, premature ejaculation and frequent urination, to blurred vision and dry eyes. Because of its ability to reduce the loss of fluids from the body, cuscuta was once considered a "longevity herb."

7.      *Ginseng is well known as a sexual stimulant. The Chinese have long held this herb in high esteem, it is supposedly the herbal fountain of youth. It is both a stimulant and relaxant on the central nervous system and improves muscle stamina! A herb full of vitality and often used by men who have a loss of sex drive. There are cautions to take when using Ginseng. Do not take consistently and not for more than three weeks at time. Do not take during pregnancy and avoid with high blood pressure. It can be found in various liquid drinks in adequate enough amounts and with other safe additives in the drinks if correct ones chosen.

8.      -Saw Palmetto Berry - Native American Indians considered the ripe fruits of the saw palmetto a tonic and an aphrodisiac. The berries do, in fact, have a toning effect on the male reproductive system and have been employed for impotence and prostate problems. It can be used to treat prostate enlargement and cystitis.

9.      *-L-Arginine - L-arginine is converted to nitric oxide which aids in the relaxation of blood vessels. The effect is better blood circulation in the body and especially in the extremities (eg. genitalia). For this reason L-arginine helps in stimulating and maintaining erection (at least in males). Men with erectile dysfunction may benefit from intake of L-arginine rich foods or l-arginine supplement. L-arginine is a major component of ejaculate (seminal fluid and sperm) and there fore it is important for maintaining healthy ejaculate volume. Other L-arginine benefits include maintainance of nitrogen balance, removal of excess ammonia, liver detoxification, reduction of alcohol toxicity effects, wound healing, and treatment of sterility in men. 4oz to 9oz per day.

Eat these Foods - Follow mainly plant-based whole grain diet with very little fat or sugar and naturally increase telomerase production some. :

1.      Garlic powder – stimulates NRF2, acts as a natural antibiotic of sorts, and kills bad bacteria in the stomach only.

2.      Green tea – stimulates NRF2. Also, contains tryptophan, a necessary amino acid. This also inhibits the MTOR pathway. Affects metabolism and various cancer prevention. Heavy in antioxidant power. Find teas that use young leaves, as there is more natural theanine in them, and typically atleast about 30-50mg per cup. Most likely available as leaf packages rather than prepared. The theanine also helps to cancel out too much caffination. Has Quercitin. White tea is better.

3.      Cinnamon

4.      Iodized sea salt - needed for healthy synapses, but most things come with sea salt these days, so not really very necessary unless after iodine content which is generally not included in sea salt.

5.      Plain chicken or chicken added to healthier foods. Right brand of chicken nuggets is also easy prep. and decently healthy.

6.      Grapes and berries - resveratrol

7.      Peanuts or walnuts – Peanuts have resveratrol. Both have omega 3s, and they both improve memory deficits and learning skills. Both also contain L-arganine which is good for sexual function. 5.5 oz per day. Have this or peanuts for 1 day, but not both.

8.      Blueberries (frozen ones in largest bags and at about 4oz per day are best costs) – increases heat shock protein 70 (hsp70) in the brain, which is said to help work against the onset, and maybe a possible preventative to Alzheimer’s. These inhibit the MTOR pathway. They are good for cognition, neural inflammation,  alzheimer’s disease, cancer, and cardiovascular health. They are a powerful anti-inflammatory. ½ to 1 cup per day (2oz to 4oz (8oz only when have the money) per day).

9.      Salmon – Omega 3s

10.   Tuna – Containing omega 3 for weight and heart health. Occasionally have instead of beef. It’s better to take fish oil with high enough DHA and EHA amounts though, which combined should be 400 to 500mg at minimum daily. 1000 should be plenty otherwise.

11.   Fishsticks – needs to be a healthy type

12.   Eggs (I usually hard boil mine to save on using a microwave every day, i.e. slight energy saver) – Certain brands are higher in omega 3, vitamin e, and other good vitamins. 1 or 2 daily. Cholesterol contained in eggs is not bad. Eggland’s best is currently best.

13.   Fat free cottage cheese

14.   Whole grain bread (sugar free and high fructose free if possible – nature’s own usually)

15.   Dark chocolate powder or something with dark chocolate - phytochemical and caffeic acid. Have 2-3 squares per day if getting from chocolate bars depending on the brand, sugar, and fat content.

16.   Peanut butter (brand I use currently is Jif with omega 3 that includes dha and eha in it) – omega 3s no matter what, but this one adds fish oil. Possibly equivalent to eating peanuts in some respects.

17.   Tomatoes - Contain lycopene. They have low calories, so sugars should be as well. It is better to heat them up just a little, as that makes more lycopene for some reason. They have quercitin.

18.   Lean beef on occasion, but not too often. - L-Arganine which is also good for males by helping simulate and maintain erections. Offers carnosine also.

19.   Chicken has C0Q10 in it, but need to eat a fair amount of chicken to get enough. Slight ALA in it, but less than beef

20.   Extra virgin olive oil – It can increase life span by 20% from where you are at now whatever that span is. It will reduce pro-inflammatory, pro-oxidant and pro-thrombotic markers. Regular olive oil will not do. Try to make sure to get authentic EVOO which should generally be within green containers.

21.   Green pepper - Caffeic acid with anti-inflammatory properties.

22.   Cayenne pepper

23.   Rosemary

24.   Turmeric – stimulates NRF2. This item also inhibits the MTOR pathway.

25.   Grapefruit – caffeic acid, which is an anti-inflammatory

26.   Yoghurt with lower sugar, along with bifidum and acidophilus cultures. Lifeway probiotic yogurt is a good mix of blueberry, milk, and kefir (a yogurt relative). There is no added sugar. It can be substituted for atleast milk and yogurt in full. It has 12 strains of probiotics.

27.   Fat free milk – Has plenty of potassium, and calcium. Need about 1000mg daily of calcium, and can go as high as about 4000mg potassium (potassium can kill you if you have too much).

28.   Black beans/refried black beans

29.   Cereal – half the serving size of Kellogg’s Smart start is best I’ve found so far

30.   Okra or spinach – high vitamin k and supposedly having higher amounts by natural ways vs. pills is likely to cause no problems

31.   Oregano

32.   Red wine vinegar

33.   Rice of the right type (some white rice are actually fairly decent at what they provide vs. brown)

34.   Water - Metabolism

35.   Cucumbers - caffeic acid which is anti-inflammatory.

36.   Broccoli or Alfalfa Sprouts – stimulates NRF2 by way of sulforaphane. It will help delay lung cancers, help with breathing, as well as help with coagulation to cut down on blood loss. It has quercitin. Try to only do 4oz (1/2 cup per day so as to control the vitamin k).

37.   Ginger

38.   Caffeinated beverages – of the right types, caffeine is another inhibitor of the MTOR pathway. Coffee can be good for you in this way, but can act in a different way that caffeine in other products (in my experience)

39.   Red Wine - 8-16 oz per day (1 – 2 cups). Has quercitin.

40.   Baby dill pickles - don't eat more than 3 whole in a day (stops vitamin k from being as effective. vitamin k helps with blood clotting). 0 calories with right ones. Not too many, as these have vinegar in them, and vinegar is not a good product to have a lot of.

41.   Horseradish - strong antibiotic, expectorant, bronchodilatator, antibacterial, coronary vasodilatator, it increases the blood pressure, it heats up the body, stimulates the body's immune system, anti-inflammatory, antiparasitic, antianemic, antiscorbutic, diuretic. It can stimulate the appetite. It has a cardiotonic effect and is recommended to the people that suffer from high blood pressure. Also it is known that horseradish has aphrodisiacal properties.

Do these other things:

1.      30 minutes of exercise a day – This will naturally increase telomerase and NRF2 production while lowering cortisol levels. Do not over exercise, as this is actually harmful to the body. More than 30 minutes is ok, but better to do short and fast exercising in increments ( about 15 minutes multiple times a day in order to really benefit).

2.      Make a diet plan that you follow regularly such as the example one I have provided below. It’s the one I mainly follow, and can be looked at separately as just the plan itself elsewhere on the site.

3.      Follow breathing techniques on kundalini while doing meditation. It is basically the same idea as a practice so-called rebirthers take, but is done to simply relieve stress and let the energy that some people believe in to come up through the spine and give enlightenment, power, and more energy to do things. It naturally increases telomerase production and lowers cortisol levels.

4.      For sun protection, wear wide brim hats, long sleeves and pants or sunscreen. Also, wearing sunglasses that have complete UV protection will help as well.

5.      Become established in life and have understanding to it. Do not be shaken at anything, but do not give in when it is not necessary.  By doing this, a person could actually gain a title of sāttvika. A person or creature can be called sāttvika if the creature has predominantly sāttvika tendencies. The word Sattva itself means ‘pure’. A sāttvika (pure person) individual always works for the welfare of the world. He is always hardworking, alert and lives life moderately. He leads a chaste life. He eats moderately. He speaks the truth and is bold. He never uses vulgar or insulting language. He does not feel jealous nor is he affected by greed and selfishness. He does not cheat or mislead anyone. He does not even allow any evil tendencies to enter his mind. He has good memory and concentration. He also has keen interest in improving his spiritual knowledge, and spends time worshiping god or meditating. In the extreme state he may even perform penance or uninterrupted meditation. A satvic individual can be recognized if his mind, speech and actions synchronize. Manasa, vacha, karmana are the three Sanskrit words used to describe such a state. In the Indian language, these three words are together used to describe a state of consistency expected of an individual. These three aspects of an individual must synchronize. An individual is expected to speak exactly what he thinks, and do only those things that he believes in. He must not do something which his mind asks him not to do. Neither must he speak something that he does not believe in. It also means that the individual must promise exactly what he can deliver. He must not promise something that he cannot or does not intend to do. It also means that he must think before doing anything or saying something. That essentially means his mind has complete control over his body. Such a thing is not easy, and the expectation is that the individual would strive to attain such a noble ideal.

6.      Watch for updates on technological life increasing items.

7.      Have orgasms regularly, even if not to completion. This will extend life, as well as help blood flow, and possibly enlargement

8.      Keep a certain level of stress in your life. Relax, but try to keep a balance of stress. Keep a positive attitude otherwise. Chronic stress will be negative on the body though. It causes a natural hormesis, which is putting a balanced load of stress (ROS-like Stress) on the body in order to cause light stressors (Antioxident Response Elements) to trigger the stress responses and upregulate NRF2, which helps to keep a person younger for longer. (idea from anti-aging firewalls)

9.      Being cold is ok, but let yourself still be warm enough that you do not get hypothermia, and try to remain a little more comfortable with temperatures. This will also help raise NRF2. The right amount of heat will also raise its levels.

Longer Life Diet Example

This can occasionally be broken if you are really hungry or really craving something like a pizza. What’s listed below is a list of foods and supplements which I’ve read should be best for optimal health and life extending abilities, as well as a diet plan fairly close to my current plan when I’m not being homeless and have refrigerator availability. This must be adhered to the majority of days though to hopefully experience weight loss, as well as the overall health benefits that are said to extend out life longevity for you.

Since this is only a plan, it switches up, however I have taken years and years of refining foods I eat and my plan so that hopefully it works to provide optimal vitamins, fibers, amino acids without use of protein powders I used to think I might need, etc. These all apply to me the way I have them layed out, so I don’t know if these things would be right for everyone considering what they may or may not be able to eat themselves, in case anyone has allergies. I also can’t guarantee that this will be any good if the world goes completely insane and not everything is accessible, if anything. Knowing that, here ya go:

Breakfast

1.      25mg DHEA pill (7-Keto is better if you can find it anywhere) – Helps inhibit MTOR (?) path which if inhibited enough, can make an old cell new again in cell reprogramming.

2.      Acetyl L Carnatine

3.      200mg COQ10 w/ Qsorb 100mg Ubiqionol, aka COQH

4.      60mg ginkgo biloba

5.      450mg saw palmetto

6.      470mg Ashwaghanda

7.      1500mg/1200mg Glucosamine chondroiton

Wait 30 - 45 minutes

8.      4oz plain non-fat yogurt or half a container of something like Great Value light yogurt

9.      ½ cup Kellogg’s Smart Start or Great Value Multi-grain

10.   Cinnamon

11.   4-5oz peanuts or walnuts or peanut butter

12.   1tbs extra virgin olive oil

13.   4oz blueberries

14.   2 Eggland’s best egg with omega 3’s

15.   Some form of dark chocolate, but I prefer dark chocolate powder

16.   1/2 cup (4oz) of fat free milk

17.   8oz (1 cup) white tea (must be young leafed) – green tea if white is not available

18.   10-15 minutes of deeper breaths and forceful exhaling with a clear mind (Meditation). Take time.

Lunch – make a salad out of most of ingredients

1.      Turmeric

2.      Cucumber slices

3.      ½ can of spinach

4.      Jalapeno slices

5.      ½ tomato to a whole one

6.      No fat cottage cheese

7.      4oz broccoli (I don’t follow this one well because broccoli just isn’t all too great with me.)

8.      2 slices of bread

9.      ½ of a grapefruit

10.   Chicken deli slices.

11.   Water

Dinner

1.     1 hour of exercise in the late afternoon

2.     1 can of Bumblebee Tuna (Alternate to burrito with fish sticks)

3.     Just a little bit of iodized sea salt

4.     4oz non-fat refried beans or a ‘chicken’ burrito of the right brand or homemade, or just something with chicken in it that is made healthy.

5.     Garlic powder

6.     5 Fisherman’s fish sticks

7.     Little oregano

8.     Horseradish (Similar family as garlic)

9.     Some form of dark chocolate

10.  ½ cup (4oz) of fat free milk

11.  8oz (1 cup) white tea (must be young leafed) – green tea if white is not available

Before Bed

All of these should be taken around the same time with little time in between each one:

1.      10-15 minutes of deeper breaths and forceful exhaling with a clear mind (Meditation). Take time.

2.      8-12oz Red Wine

3.      5mg melatonin pill – only if can’t get to sleep naturally by 4am

Extra Notes:

The Aghori are a Hindu sect believed to have split off from the Kapalika order (which dates from 1000 AD) in the fourteenth century AD. Most other Hindus condemn them as non-Hindu because of their cannibalistic rituals. Aghoris or Aughads command extreme reverence from rural populations as they are supposed to possess powers to heal and relieve pain gained due to their intense practices.

The Aghoris distinguish themselves from other Hindu sects and priests by their alcoholic and cannibalistic rituals. The corpses, which may be either pulled from a river [including Ganges] or obtained from cremation grounds, are consumed both raw and cooked on open flame, as the Aghoris believe that what others consider a "dead man" is, in fact, nothing but a natural matter devoid of the life force it once contained. Therefore while for ordinary folks cannibalism may be seen as primitive, barbaric as well as unclean, for aghori's it's being both resourceful and subverting the common stereotypes placed on such taboos into a spiritual ascertainment that indeed nothing is profane nor separate from God, who is hailed to be all and in all. In fact, the Aghoris see it as a scientific approach in trying to discover how matter converts from one form to another.

Hindus believe that the universe destroys itself and then recreates itself every so many years, and that life always starts new and no more difficult than the last for whatever creatures come forth in to it.

 

 

 

 

Solaray Astragalus Root Extract to cover the 5 mg of astragalosides, which requires 6 x 200 mg capsules per day in a cyclic protocol

 

featuring 15 days on, then 15 days off. Although this exceeds the recommended dose according to Solaray, I believe from toxicology

 

studies that it is safe enough.

------------------------

1 (astragaloside IV)

2 (cycloastragenol),

3 (astragenol)

4 (astragaloside IV 16-one)

5 (20R,24S-epoxy-3B, 16B,25-trihydroxy-9B-methyl-19norlanost-l,5-diene)

6 (cyc1oastragenoI6-13-D-glucopyranoside)

7 (cycloastragenol 3-13D-xylopyranoside)

8 (ginsenoside RH1).

-------------------------

loreal and dopachrome tautomerase

 

 It is important because longevity of organisms, people in particular may in fact more depend more on continuing differentiation of

 

adult stem cells than on the number of times mature adult somatic cells reproduce.

 

In the decade since the telomere hypothesis of cellular aging was proposed, the two essential genes for human telomerase were cloned

 

and characterized, allowing experimental proof of the causal relationships between telomere loss and replicative senescence, and

 

telomerase activation and immortalization. These relationships were established using a variety of cultured human cell types from both

 

normal and tumor tissues, and were largely confirmed in the telomerase knockout mouse. Taken together, the data provide strong support

 

for the potential utility of telomerase detection and inhibition for cancer, and telomerase activation for degenerative diseases. The

 

specificity of the promoter for the telomerase catalytic gene and the antigenicity of the protein product, hTERT, provide additional

 

strategies for killing telomerase-positive tumor cells. Unfortunately, the strong link between telomerase and cancer has led some to

 

confuse telomerase activation with cancer, and others to overstate the cancer risk of telomerase activation therapies for degenerative

 

diseases. This review clarifies the difference between telomerase, which does not cause growth deregulation, and oncogenes, which do.

 

It also addresses the concept of telomerase repression as a tumor suppressor mechanism early in life, with detrimental tissue

 

degeneration and tumor-promoting consequences late in life. This extended view of the telomere hypothesis helps explain how telomerase

 

inhibition can be therapeutic in cancer patients, while controlled telomerase activation for degenerative diseases may actually

 

reduce, rather than increase, the frequency of age-related tumorigenesis.

 

----many of the items listed here inhibit Nf-Kappa B, an item that plays a large part in causing inflamations and various other

 

problems, especially in autoimmune diseases------

etc

 

Selective research studies like this one suggest that certain of the firewall NF-kappaB inhibitor substances like curcumin and

 

resveratrol may be comparably powerful in their anti-cancer activities as DHMEQ. The initials stand for

 

dehydroxymethylepoxyquinomicin, a powerful recently-discovered inhibitor of NF-kappaB. DHMEQ powerfully blocks expression of NF-kappaB

 

and a host of recent publications suggests that it might be useful as a therapeutic agent for several inflammatory diseases and

 

cancers.

 

SIRT1-activating nutritional supplements. suppression of mTOR signaling, activation of SIRT1, and inhibition of expression of NF-

 

kappaB.  Activating SIRT1 does all of these things

When ends of dna strands are more methylated, it takes longer to wear them down, and therefore prevents things such as cancers and

 

such from happening sooner. Example is given above.

 

 

.

 

It appears that improvements in air quality in the US, particularly in cities, added about five months to life expectancy in the U.S.

 

over twenty years.

 

 Stress and aggression are known to induce epigenetic changes in mice, and addiction does too. Cocaine exposure, for example, is known

 

to create epigenetic changes in specific areas in the brain. How a mother treats her small daughter may generate epigenomic changes

 

that condition how that girl behaves throughout the rest of her life, and also condition the behavior of her daughter’s daughter.

 

proteins like AKT which seem to play a role in both stem cell proliferation and programmed cell death.

 

Today there is much discussion of “preventive medicine,” mainly focused on educating people to avoid habits which create disease and

 

early mortality like smoking, obesity and living on saturated fats.

 

Among the small companies engaged in longevity-related R&D are Geron, Sierra Pharmaceuticals, Elixir Pharmaceuticals, Centagentix,

 

Sirtuis, DeCode Genetics, 23andMe, Juvenon, Rejuvenon, Roche Diagnostics, and Alteon.

 

Neanderthals have long been regarded as a species somewhere between the great apes and humans on the evolutionary scale. They diverged

 

from the human line of evolution around 500,000 years ago.  Neanderthal mitochondrial DNA has around 200 differences from human

 

mitochondrial genomes whereas chimpanzee mitochondrial DNA has about 1500 differences. Neanderthal brain size appears to be equal or

 

greater than that of humans.  Neanderthals were tool users but there is dispute about how well they were able to communicate by

 

speech.

 

I normally do not like to get embroiled in ethical disputes but I wonder: Would newly-minted Neanderthals be accorded human rights or

 

treated as lab animals?  Would the first new Neanderthals be provided an education, featured on TV talk shows, trained to do strenuous

 

sports, encouraged to reproduce? 

 

For one thing, it appears now that loss of species is no longer necessarily a one-way street.

 

Vince

 

Posted in Uncategorized | 2 Comments »

Oxidative damage and mitochondrial health

 

20. February 2009 by admin.

 

A well-written article relating mitochondrial health to the use of antioxidants and can be found here.  Mitochondria are particularly

 

susceptible to oxidative damage and such damage is implicated in many debilitating conditions including  cardiovascular disease,

 

stroke, Parkinson’s disease, Alzheimer’s disease, fibromyalgia, schizophrenia, dementia, bipolar disorder, epilepsy, retinitis

 

pigmentosa, and diabetes mellitus.  I continue to strongly believe that there is a central role for anti-oxidants in an effective

 

longevity regimen.  Specifically, Co Q-10. Alpha-lipoic acid and acytl-l-carnitine are important antioxidants for maintaining the

 

health of mitochondria.  An additional report came to my attention today confirming how the use of antioxidants can  support

 

mitochondrial health, this one originated at the Stanford School of Medicine. Blood samples from 20 patients with various

 

mitochondrial diseases uniformly showed depleted glutathione, indicating a lowering of those patients’ antioxidant defenses. 

 

Apparently, mitochondrial disorders generate large numbers of free radicals.  On the other hand, those patients taking antioxidant

 

supplements did not have depleted glutathione, they found, indicating stronger antioxidant defenses.

 

Posted in Uncategorized | 1 Comment »

Oxidative damage – cause or effect?

 

20. February 2009 by admin.

 

A reported study about free radicals is radical in its conclusions.  The study was based on disabling five genes in mutant

 

Caenorhabditis elegans worms.  The study’s authors suggest that damage due to free radicals may not be a cause of aging but rather is

 

a consequence of aging and suggest instead that the aging process may originate in the mitochondria.  See my discussion on the

 

Mitochondrial DNA mutation theory of aging.  It would seriously upset the anti-aging establishment’s applecart if oxidative damage

 

turned out to be only a symptom.  However, I hesitate to accept such a broad conclusion given the preponderance of evidence that

 

exposure to strong oxidative stress, such as massive doses of radiation, generates the overt symptoms of aging.  Most likely we are

 

dealing with a chicken-and-egg causative process here where it is both the case that oxidative damage contributes to aging and that

 

aging contributes to oxidative damage.  And the mitochondria play an important role in mediating the aging process.  See the previous

 

blog post as well.

 

A recent Finish study evaluated the effect of frequency of sexual intercourse on risk of subsequent erectile dysfunction.  The study

 

was based on written interview data.  A sample consisting of 989 men aged 55 to 75 years (mean 59.2 years) was followed over a 5 year

 

period.  All men were free of erectile dysfunction at study baseline.  The major finding was that the risk of erectile dysfunction was

 

inversely related to the frequency of intercourse and that regular intercourse protects against the development of erectile

 

dysfunction in men in this age range.  Men reporting intercourse less than once per week at baseline had more than twice the incidence

 

of erectile dysfunction compared with those reporting intercourse at least once per week, that is 79 versus 33.  This is yet another

 

example of use it or lose it when body capabilities of older people are concerned.

 

stem cell research is also another thing which contains experiments that could lead to immortality. There is both using the stem cells

 

from a person's bone marrow, as well as from other people and maybe animals in order to create new organs or make repairs to older

 

ones.

 

Posted in Uncategorized | 1 Comment »

Melanoma and stress

 

20. February 2009 by admin.

 

Stress may increase the rate of progression of the most malignant form of melanoma, according to a report on a study conducted in New

 

Zeeland of 1600 people diagnosed with that disease.  Small wonder given what we know about stress and how stress-generated cortisol

 

suppresses the functioning of the immune system. Of course, some of the stress may come from the diagnosis itself.  This study  points

 

again to the importance of the substances in the anti-aging firewalls that encourage regular sleep and mental calm like l-theanine and

 

melatonin as well as a relaxed mental attitude that takes any problems in stride.

 

A simplistic variant of the argument from evolution is to say extending lives is not natural.  If nature or God wanted us to live to

 

150 or beyond, he or she would have set it up that way, the argument goes.  My response is: who says what is natural?  From the

 

viewpoint of the year 1600, living lives as long as the ones we enjoy now would have been seen as highly unnatural.

 

Another argument against life extension is the burden on the young argument.  It is another variant of the argument from evolution

 

stating that extending the lives of older people will lead to more and more unproductive older people, an unfair burden on the young

 

people.  My response to this is that there should be no such burden.  The young, by virtue of their requirement for a long and

 

expensive period of rearing and education are already a burden on their working parents – those in their productive years.  I am

 

arguing for further extending the productive years so as to give more time for amortizing the investments in the young and minimizing

 

the burden for those in their productive years due to having to take care of the young as well as the debilitated and unproductive

 

old.

 

Another argument against life extension is that a society consisting of much older people will lack vibrancy, stress conformity and be

 

uncompetitive compared with societies consisting of younger people.  The opposite is true.  In most countries in Africa and the Middle

 

East where the population has recently exploded, the average age is now under 25.  Educational level per capita is minimal, the

 

societies and their people cannot compete on the world stage, and there appears to be a chronic condition of poverty and social

 

hopelessness.  In those countries lives are not seen to be worth much and average life spans are relatively short.  In advanced

 

Western countries where there is large investments in education and life spans are long, lives are worth a lot.  It just takes a lot

 

of years for people to come up to speed so they can compete in the world economy today.

 

use stem cells from hair to regrow smooth muscle (parts for muscles likt the heart) or to assist in regenerating skin where wounds are

 

rather than it repairing and using up extra cells.

 

Immunosenescence refers to the gradual deterioration of the immune system brought on by natural age advancement. It involves both the

 

host’s capacity to respond to infections and the development of long-term immune memory, especially by vaccination

 

“At the same time, it was established that cytomegalovirus (CMV) seropositivity was associated with many of the same phenotypic and

 

functional alterations to T-cell immunity that were being reported as biomarkers associated with aging. It was discovered that CMV was

 

the prime driving force behind most of the oligoclonal expansions and altered phenotypes and functions of CD8 cells. Independently,

 

longitudinal studies of a free-living population of the very old in Sweden over the past decade have led to the emerging concept of an

 

immune risk phenotype’ (IRP), predicting mortality, which was itself found to be associated with CMV seropositivity.

 

Whatever the age-associated mechanisms, there are a few recurring themes in the earlier literature (pre 2006): 1.  too many antigen

 

memories producing overload,  3. Cellular senescence of T and B cells, 3. insufficient proliferation of new T cells, and 4. Decline in

 

the antigen presenting function.

 

I state “Although the mobilization responsiveness of Type C stem cells declines with age, it appears that their regenerative

 

capability can be restored through environmental messages or induction of Notch activity.”

---------------------------------------------------

The key idea is to use induced Pluripotent Stem cells (iPSCs) which are fully pluripotent and equivalent to embryonic stem cells(ref)

 

(ref)(ref) as feedstock Type A cells in adults to make the stem cell supply chain as a continuous loop process instead of a once-

 

through process.  I have described the process several times before.  1.  A few human skin, fat, blood or spit cells are corrected for

 

any known genetic diseases defect are taken from an individual, 2. These cells are reverted by known means to a state of epigenomic

 

ground-zero, that is into iPSCs for that individual, 3.  These corrected cells are replicated outside the body, and 4.  They are re-

 

introduced into the body of the same individuals so as to differentiate into vital Type B and Type C stem cells in their niches

 

refreshing the existing pools of stem cells and revitalizing the cells in them.  Because they are cells derived from the same

 

individual, there should be no graft versus host disease immune system rejection or reaction to them.  The stem cell supply chain

 

becomes closed loop. Further, the Type A source cells are free of any original genetic disease susceptibility. Steps 1-3 have been

 

tried out although many issues connected with them are still being worked out.

 

advances with these steps in mice has shown that this metod does work.

 

“Although we observed some variations in the efficiency of hematopoietic differentiation between different hiPSCs, the pattern of

 

differentiation was very similar in all seven tested lines obtained through reprogramming of human fetal, neonatal, or adult

 

fibroblasts with three or four genes

 

 

 

ap-1 and nf-b travel along the jnk pathways. if you inhibit jnk pathways, then you also stop ap- and nf-b.

 

Telomerase activity coevolves with body mass, not lifespan. where she concludes “Here we show that telomerase activity does not

 

coevolve with lifespan but instead coevolves with body mass: larger rodents repress telomerase activity in somatic cells. These

 

results suggest that large body mass presents a greater risk of cancer than long lifespan, and large animals evolve repression of

 

telomerase activity to mitigate that risk.”  Of course, we are like very large rodents in the respect that telomerase activity in our

 

somatic cells is very repressed. telomerase expression by itself does not correlate with lifespan.  Second, it could well be the

 

message of the naked mole rat is that a combination of a very powerful anti-cancer defense with activated telomerase might lead to

 

significantly greater longevity. telomerase stimulation can probably be achieved through strengthening of apoptotic mechanisms such as

 

P53, P16, P21, and nrg1.

 

nrg1 is partially associated with bipolar disorders. more nrg1 is needed in order to make more normal levels. lack of this gene causes

 

methylation, and methylation in-turn causes aging and cancers of certain cells.

 

Programmed Epigenomic Changes.  As I understand it, this view says that miRNAs are the signaling messengers and “hit men” for

 

programmed aging, progressively and systematically switching off disease-protecting genes as an organism ages.

 

Klotho on reducing hypertension. They found that by increasing the expression of the gene in laboratory models, they not only stopped

 

blood pressure from continuing to rise, but succeeded in lowering it. Perhaps most impressive was the complete reversal of kidney

 

damage, which is associated with prolonged high blood pressure and often leads to kidney failure

 

What is aging?

 

Aging is the lifelong accumulation of changes in the DNA surrounding our genes that result in changing gene expression.  These are

 

called epigenomic changes, and have to do with turning our various genes off and on so to produce the observed phenomena of aging. 

 

These phenomena can include wrinkled skin, balding hair and decreased libido.  More importantly, they include gradual but generalized

 

deregulation of body processes, degeneration of organs and increasing susceptibility to disease processes.

 

stress such as sexual abuse, or just a plain bad childhood can cause shorter telomeres in people.

 

he key point is that telomerase activation might keep telomere lengths from getting critically shorter, and that would be enough to

 

stave off cell senescence and deregulation of the epigenome and, perhaps even, much of what we know as aging. These findings suggest

 

that progressive telomere shortening and the accumulation of dysfunctional telomeres with age may constitute a unique source of DNA

 

damage, sufficient to induce global alterations in genome regulation. So, put simply, telomeric shortening at some point induces DNA

 

damage which lets loose signaling which changes the epigenome disrupting epigenetic silencing and resulting in pro-aging global DNA

 

expression.

 

Polygamy which helps men live 12% longer according to research studies

 

calorie restriction helps to activate telomerase in good cells, and to cut off 'nutrition' for cancerous cells. calorie restriction

 

can help be achieved by eating things low in sugar or with no sugar (glocose). a calorie restricted diet can stave off pancreatic

 

cancers as well.

 

A December 8 2009 Science Daily story Stem Cells Can Be Engineered to Kill HIV, Scientists Show is a this-week example.  “Researchers

 

from the UCLA AIDS Institute and colleagues have for the first time demonstrated that human blood stem cells can be engineered into

 

cells that can target and kill HIV-infected cells –.  Taking CD8 cytotoxic T lymphocytes — the “killer” T cells that help fight

 

infection — from an HIV-infected individual, the researchers identified the molecule known as the T-cell receptor, which guides the T

 

cell in recognizing and killing HIV-infected cells. These cells, while able to destroy HIV-infected cells, do not exist in enough

 

quantities to clear the virus from the body. So the researchers cloned the receptor and genetically engineered human blood stem cells,

 

then placed the stem cells into human thymus tissue that had been implanted in mice, allowing them to study the reaction in a living

 

organism.  – The engineered stem cells developed into a large population of mature, multifunctional HIV-specific CD8 cells that could

 

specifically target cells containing HIV proteins. The researchers also found that HIV-specific T-cell receptors have to be matched to

 

an individual in much the same way that an organ is matched to a transplant patient. — The next step is to test this strategy in a

 

more advanced model to determine if it would work in the human body –”This approach could be used to combat a variety of chronic viral

 

diseases,” said Zack, who is also a professor of microbiology, immunology and molecular genetics (at UCLA). “It’s like a genetic

 

vaccine.

 

buildup of levels of Ink4a/P16 associated with aging slows down the rate of differentiation of adult stem cells.

 

drinking blood of younger or having blood tranfusion techniques done by means of younger blood can lead to more youthful cells.

 

 The first studies described the use of four transcription factor proteins to create iPSCs: Oct4, Sox2, Klf4, and c-Myc, aka S.K.O.M.

 

vitamin c helps greatly with efficiency of reprogramming.

 

early 2010 - cells may not have to be taken back to a pluripotent state (state in which there is no information on what type of cell

 

it is and it can become anything), and may just be able to be changed over to the new type of cell with no in between states.

 

-DNA - genetic makeup of a person or animal.

-Telomere - ends of dna strands where multiple strands can connect together.

-Methylation - wearing down of telomeres of dna over time from attempts to correctly sequence one end of dna to an attachable other -

 

strand of dna, which eventually leads to ageing, disease, and death.

-Histone - 2 parts of a DNA strand which have come undone and produce inflammation.

-In-vivo - inside of an organism.

-In-vitro - outside of an organism.

-Glial - relating to neuroglia.

-Microglia -  cells that are part of the nervous system, mainly found in the brain and spinal cord, and are first reponse from the

 

immune system. They are constantly excavating the CNS for damaged neurons, plaques, and infectious agents.

-Epigenetics - study of changes in phenotype (appearance) or gene expression caused by mechanisms other than changes in the underlying

 

DNA sequence.

-Genomes - set of dna sequences.

-Genomics - study of the full set of dna sequences (genomes).

-Epigenomics - study of the state/appearance/changes of dna(genomes) that is carried over from 1 cell to its differentiated copies.

 

There is a possibility of keeping the stem cell supply chain active indefinitely.  The key idea is to use induced Pluripotent Stem

 

cells (iPSCs) which are fully pluripotent and equivalent to embryonic stem cells(ref)(ref)(ref) as feedstock Type A cells in adults to

 

make the stem cell supply chain as a continuous loop process instead of a once-through process. Oct3/4, Sox2, Klf4 (3 items to make

 

pluripotent or use the 4 item method)

 

We already know that the normal lifespans of nematodes of 20 days can be extended to 125 days by genetic manipulation(ref).  If that

 

life extension factor of more than six could be translated to humans, it would mean normal lifespans of around 480 years.

 

I pointed out that the cost of sequencing the entire genome of a patient is heading down to the $1,000 level probably this year and

 

will be probably at the $100 level within four years or less. If a patient has his or her genome already laid out in such a database,

 

many bad-choice drug treatments could be avoided by a simple computer check against the database, just like transfusions of the wrong

 

types of blood are often avoided now.

 

adding extra copies of a telomerase gene and a P53 gene can extend the life of mice by 26% to 40%

 

working out too much can lead to a shorter lifespan. This includes too much sex. If it leads to almost full exhaustion, then it is not

 

good for longevity.

 

Therefore, life extension, the thrust of this blog, will not get rid of aging, at least not very soon.  It hopefully will postpone

 

aging for a goodly amount but the grim reaper is still going to get all of us.

 

Less microglial cells or decreased function plays a big roll in downs syndrome, as well as alzeimer's.

 

causes of againg : oxidative damage, chronic inflammation, telomere shortening and damage, increasing mTOR signaling instead of sirt1,

 

programmed epigenomic changes - systematically articulated set of epigenomic changes including  changes in DNA methylation in cells

 

accumulated with aging, stem cell supply chain breakdown, cell dna damage,

 

Fully implementing PPPM will require genetic, genomic and other “omic” profiling on the part of increasing numbers of people,

 

something that should become commonplace in 10-15 years. - keep an eye on this as emerging technology.

 

Ku protien? - helps repair double strand dna breaks which were originally thought irrepairable.

 

MSCs can deliver oncolytic adenoviruses to metastatic tumors with very low systemic toxicity and with beneficial antitumor effects.

 

sirt 1 activators :  (TA-65, TAT2, Astragaloside IV, Cycloastragenol)

 

Moderate exercise also mimics calorie restriction by inducing mitochondrial biogenesis.

 

Stress

 

There are many forms of stress, social, physical and emotional, and these may be temporary, recurring or chronic.  Stress can result

 

from external sources like injury or loss of a relative or result from internal conditions like a disease or mood disorder.    In the

 

blog entries Stress and longevity and Hormesis and age retardation I discussed how some manageable forms of body stress can lead to a

 

hormetic response, mobilization of heat shock proteins that actually confer health and longevity benefits, while more intense or more

 

prolonged forms of stress may lead to multiple pathological conditions and premature aging.  For example, the stress of parachute

 

jumping could possibly be good for you as suggested in the publication Emotional stress induced by parachute jumping enhances blood

 

nerve growth factor levels and the distribution of nerve growth factor receptors in lymphocytes.  On the other hand, stress of

 

prolonged unemployment could be bad for you even after you find a job, as suggested in the report History of unemployment predicts

 

future elevations in C-reactive protein among male participants.  I also discussed how several dietary supplements like curcumin

 

exercise positive effects in part through activating the body’s heat-shock stress response.

 

There is a significant body of research literature associated with the negative effects of chronic or excess stress including immune

 

system dysregulation, premature immunosenescence, elevated blood pressure and cortisol response, and undetected Type 2 diabetes(ref)

 

(ref)(ref)(ref)(ref)(ref)(ref)(ref) which I will not review here.  Such stress is often viewed as associated with accelerated aging.

 

Childhood stress resulting in shorter telomeres may result in accelerated cellular aging later in life.

 

o   There is a “sweet spot” range for exercise stress within which the impact of the exercise is positive and health-producing and

 

there is no stress-related telomere erosion, even if the exercise is repeated over the long term.  The sweet spot range may depend on

 

the state of the individual.

 

o   If exercise is pursued too vigorously, to the point where it produces chronic fatigue, or pursued consistently as an endurance

 

activity, telomere erosion may ensue, at least in muscles.

 

o   Psychological stress can produce telomere erosion even within a few days, but “sweet spot” exercising can prevent such erosion.

 

 Mechanisms of Neuroprotection by a Novel Rescue Factor Humanin from Swedish Mutant Amyloid Precursor Protein: “We report a novel

 

gene, designated Humanin  (HN) cDNA, that suppresses neuronal cell death by K595N/M596L-APP (NL-APP), a mutant causing familial

 

Alzheimer’s disease (FAD), termed Swedish mutant. HN protects neurons by binding to a complex or complexes involving CNTFR/WSX-1/gp130

 

Only 1 of 20 Tg/KO mouse models tested showed a shortened lifespan as predicted by the free radical theory of aging, that model being

 

SOD-/- mice.  And there is a special explanation for the shortened lifespans in that one strain.  Survival graphs were shown for mice

 

in which CuZnSOD, Catalase, MnSOD, Gpx-4 antioxidant defenses were knocked out.  Not only did the mice have the same maximum lifespan

 

as normal mice, but also at any age roughly the same number of mice survived.  The knockouts did, however, show signs of oxidative

 

damage, increased cancers and sickness.  Inserting extra antioxidant defense genes also seemed to have no significant effects on the

 

lifespans of these mice. 

 

our antioxidant defenses through diet, supplements and lifestyle interventions might not lead us to live longer, but may well result

 

in us living healthier in old age.

 

Therefore, the consumption of flavonoid-rich foods, such as berries and cocoa, throughout life holds a potential to limit the

 

neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in

 

cognitive performance.”

 

Avacados may be better for slimmer people than resveratrol - I remark that the 30% life extension in normal mice from taking

 

mannoheptulose beats the 0% life extension in normal mice achievable from taking resveratrol.  Resveratrol appears to extend the lives

 

only of obese mice on a high-calorie diet, extending their lifespans to those of normal mice

 

“Acetaminophen improves mTOR-related signaling in aged skeletal muscles.”   “Improving” mTOR signaling as described in the poster

 

meant increasing it, not reducing it. So, I am afraid that taking acetaminophen is likely to work at cross-purposes and on the whole

 

be a negative intervention.

 

Antioxidents will not cause longer lifespans, however they will help to make a much healthier life in the right quantities. B3 should

 

be avoided mostly, and the other b vitamins should not be taken in very high amounts.

 

The researchers found that participants who performed moderate to heavy levels of physical activity had about a 40 percent lower risk

 

of developing any type of dementia.

 

You can probably expect to hear a lot about PGC-1alpha as time goes on because this remarkable substance is turning out to have a lot

 

to do with health and longevity.  It appears to be the mediator of the health benefits produced by exercise. This blog post is about

 

PGC-1alpha, about its relationship to exercise, and about efforts to stimulate it with various substances, in essence seeing if it is

 

possible to provide “exercise in a pill.”

 

bad foods to have:

Vinegar – shortens life by burning up older cells

 

Sugar - So there we have it.  It is not only the calories in calorie restriction that can delay aging, but also simply substituting

 

glycerol for glucose.  

 

 

Anti-Aging Firewalls

 

A weblog on the science and practices of living healthily very long - perhaps hundreds of years.

 

    * Home

 

Info

 

You are currently browsing the Anti-Aging Firewalls weblog archives for September, 2010.

Calendar

September 2010 M    T          W        T          F          S          S

« Aug                

            1          2          3          4          5

6          7          8          9          10        11        12

13        14        15        16        17        18        19

20        21        22        23        24        25        26

27        28        29        30         

Categories

 

    * Admin (1)

    * Blogroll (1)

    * Uncategorized (308)

    * Weekly Posts (2)

 

Latest Postings

 

    * 16. September 2010: Smurf2 in senescence, aging and diseases

    * 12. September 2010: HSP70 to the rescue – But, no, no! That’s not what we want for cancer cells

    * 7. September 2010: Valproic acid - The phoenix drug arises again

    * 2. September 2010: Antagonistic pleiotropy revisited – for the last time

    * 27. August 2010: Curcumin, cancer and longevity

    * 24. August 2010: Neurogenesis, curcumin and longevity

    * 18. August 2010: PGC-1alpha and exercise

    * 16. August 2010: Blog entries in the works

    * 9. August 2010: Skin Cancer immunotherapies

    * 2. August 2010: Contrarian research findings: newly-identified aging villain substances; calorie restriction longevity is not

 

due to calorie restriction

 

Links

 

Archives

 

    * September 2010

    * August 2010

    * July 2010

    * June 2010

    * May 2010

    * April 2010

    * March 2010

    * February 2010

    * January 2010

    * December 2009

    * November 2009

    * October 2009

    * September 2009

    * August 2009

    * July 2009

    * June 2009

    * May 2009

    * April 2009

    * March 2009

    * February 2009

    * January 2009

 

Meta

 

    *

    * Register

    * Login

    * Entries (RSS)

    * Comments (RSS)

 

Archive for September 2010

Smurf2 in senescence, aging and diseases

 

16. September 2010 by admin.

 

Smurf2 is a fascinating gene and enzyme that plays a number of key roles throughout life in people, ranging from roles in embryonic

 

development and stem cell differentiation to ones relating to cell senescence and accelerated (or delayed) aging.  It is also

 

implicated in cancers and osteoarthritis.   I strive here to summarize some of the key properties of this substance and point out why

 

it is particularly interesting from the viewpoint of aging. I was made aware of the importance of this substances by a presentation by

 

Hong Zhang at the recent Ellison Medical Foundation’s Colloquium on the Biology of Aging.  Zhang is a researcher at the University of

 

Massachusetts Medical School

 

What is Smurf2?

 

The biochemical activities and genetic activation pathway related to Smurf2 are very complex.  In super-simplified terms, Smurf2 has a

 

lot to do with key processes that go in cells including cell reproduction, apoptosis and differentiation.    Smurf2 stands for SMAD

 

specific E3 ubiquitin protein ligase 2, an enzyme that in humans is encoded by the SMURF2 gene.  One of the first documents discussing

 

Smurf2, published in 2000, was Smurf2 is a ubiquitin E3 ligase mediating proteasome-dependent degradation of Smad2 in transforming

 

growth factor-beta signaling. Decoded, this means that Smurf2 links up with ubiquitin (a small regulatory protein found in almost all

 

cells with nuclei that directs proteins for breakdown and recycling) for breakdown of Smad2  in the proteasomes (large protein

 

complexes in cells that break down and recycle unwanted proteins) as part of transforming growth factor-beta  (a protein that controls

 

proliferation, cellular differentiation, and other functions in most cells) signaling.  “SMAD2 mediates the signal of the transforming

 

growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation

 

(ref)” Whew!

 

The 2001 document Regulation of Smad degradation and activity by Smurf2, an E3 ubiquitin ligase expands further on the early

 

understanding of the actions of Smurf2.  Smad proteins are key intracellular signaling effectors for the transforming growth factor-

 

beta superfamily of peptide growth factors. Following receptor-induced activation, Smads move into the nucleus to activate

 

transcription of a select set of target genes. The activity of Smad proteins must be tightly regulated to exert the biological effects

 

of different ligands in a timely manner. Here, we report the identification of Smurf2, a new member of the Hect family of E3 ubiquitin

 

ligases.  Smurf2 selectively interacts with receptor-regulated Smads and preferentially targets Smad1 for ubiquitination and

 

proteasome-mediated degradation.”      

 

Telomere length attrition, Smurf2 and cell senescence

 

There are a number of publications further detailing actions of Smurf2, but I am focusing this discussion on longevity-related issues

 

so I move now to a December 2004 publication co-authored by Zhang Smurf2 up-regulation activates telomere-dependent senescence. 

 

“Progressive telomere shortening activates replicative senescence, which prevents somatic cells from being propagated indefinitely in

 

culture. The limitation of proliferative capacity imposed by replicative senescence is thought to contribute to both organismal aging

 

and the prevention of tumor development. Here we report that up-regulation of Smurf2, an E3 ubiquitin ligase previously implicated in

 

TGF-β signaling, is a specific consequence of telomere attrition in human fibroblasts and that such up-regulation is sufficient to

 

produce the senescence phenotype.”  In other words, telomere attrition leads to upregulation of Smurf2 which in turn drives the cell

 

into senescence.  Smurf2 upregulation is an intermediary between telomere attrition and cell senescence.

 

Telomere attrition can be due to DNA damage, oxidative stress, oncogenic activation or aging.  Continuing to quote from the same 2004

 

article, “We show that the senescence-inducing actions of Smurf2 occur in the absence of detectable DNA damage or stress response,

 

that Smurf2’s effects require a novel function distinct from its E3 activity, that Smurf2 recruits the Rb and p53 pathways for

 

senescence induction, and that while p21 is elevated by Smurf2, Smurf2-mediated senescence is independent of p21. Smurf2 is the first

 

gene found to be both up-regulated by telomere attrition and sufficient to induce senescence.”  

 

Expression of Smurf2 in fibroblasts appears to depend on telomere attrition, not on how many times a cell reproduces.  “Importantly,

 

fibroblasts immortalized by adventitious expression of hTERT and analyzed after multiple passages in culture showed no increase in

 

Smurf2 expression (Fig. 1C), indicating that up-regulation of Smurf2 is not the result of extended cell passage per se but, rather, is

 

a consequence of telomere shortening.”  And exposing immortalized fibroblasts with long and stable telomeres to Smurf2 drives them

 

directly into a senescent state.  “Smurf2 expression produces senescence in hTERT-immortalized cells   Expression of hTERT in primary

 

cultures of human fibroblasts precludes the progressive shortening of telomeres that activates events leading to senescence, resulting

 

in the immortalization of cell populations (Bodnar et al. 1998; Vaziri and Benchimol 1998; Dickson et al. 2000). In strong support of

 

the conclusion that Smurf2 expression is sufficient to produce the senescence phenotype, we found that adventitious expression of

 

Smurf2 to the level normally observed during replicative senescence induced by telomere attrition (cf. Figs. ​Figs.5A5A and ​and1B)

 

reversed hTERT-mediated immortalization of human fibroblasts. — Collectively, our findings support the argument that Smurf2 up-

 

regulation mediates one of the multiple cellular pathways that have been proposed to lead to senescence (Pereira-Smith and Smith

 

1988).”

 

These findings are clearly relevant to the 12th theory of aging laid out in my treatise Telomere Shortening and Damage.   Long

 

telomeres and even extraordinary expression of telomerase cannot protect a cell from senescence if Smurf2 is also strongly present in

 

that cell.

Anti-Aging Firewalls

 

A weblog on the science and practices of living healthily very long - perhaps hundreds of years.

 

    * Home

 

Info

 

You are currently browsing the Anti-Aging Firewalls weblog archives for September, 2010.

Calendar

September 2010 M    T          W        T          F          S          S

« Aug                

            1          2          3          4          5

6          7          8          9          10        11        12

13        14        15        16        17        18        19

20        21        22        23        24        25        26

27        28        29        30         

Categories

 

    * Admin (1)

    * Blogroll (1)

    * Uncategorized (308)

    * Weekly Posts (2)

 

Latest Postings

 

    * 16. September 2010: Smurf2 in senescence, aging and diseases

    * 12. September 2010: HSP70 to the rescue – But, no, no! That’s not what we want for cancer cells

    * 7. September 2010: Valproic acid - The phoenix drug arises again

    * 2. September 2010: Antagonistic pleiotropy revisited – for the last time

    * 27. August 2010: Curcumin, cancer and longevity

    * 24. August 2010: Neurogenesis, curcumin and longevity

    * 18. August 2010: PGC-1alpha and exercise

    * 16. August 2010: Blog entries in the works

    * 9. August 2010: Skin Cancer immunotherapies

    * 2. August 2010: Contrarian research findings: newly-identified aging villain substances; calorie restriction longevity is not

 

due to calorie restriction

 

Links

 

Archives

 

    * September 2010

    * August 2010

    * July 2010

    * June 2010

    * May 2010

    * April 2010

    * March 2010

    * February 2010

    * January 2010

    * December 2009

    * November 2009

    * October 2009

    * September 2009

    * August 2009

    * July 2009

    * June 2009

    * May 2009

    * April 2009

    * March 2009

    * February 2009

    * January 2009

 

Meta

 

    *

    * Register

    * Login

    * Entries (RSS)

    * Comments (RSS)

 

Archive for September 2010

Smurf2 in senescence, aging and diseases

 

16. September 2010 by admin.

 

Smurf2 is a fascinating gene and enzyme that plays a number of key roles throughout life in people, ranging from roles in embryonic

 

development and stem cell differentiation to ones relating to cell senescence and accelerated (or delayed) aging.  It is also

 

implicated in cancers and osteoarthritis.   I strive here to summarize some of the key properties of this substance and point out why

 

it is particularly interesting from the viewpoint of aging. I was made aware of the importance of this substances by a presentation by

 

Hong Zhang at the recent Ellison Medical Foundation’s Colloquium on the Biology of Aging.  Zhang is a researcher at the University of

 

Massachusetts Medical School

 

What is Smurf2?

 

The biochemical activities and genetic activation pathway related to Smurf2 are very complex.  In super-simplified terms, Smurf2 has a

 

lot to do with key processes that go in cells including cell reproduction, apoptosis and differentiation.    Smurf2 stands for SMAD

 

specific E3 ubiquitin protein ligase 2, an enzyme that in humans is encoded by the SMURF2 gene.  One of the first documents discussing

 

Smurf2, published in 2000, was Smurf2 is a ubiquitin E3 ligase mediating proteasome-dependent degradation of Smad2 in transforming

 

growth factor-beta signaling. Decoded, this means that Smurf2 links up with ubiquitin (a small regulatory protein found in almost all

 

cells with nuclei that directs proteins for breakdown and recycling) for breakdown of Smad2  in the proteasomes (large protein

 

complexes in cells that break down and recycle unwanted proteins) as part of transforming growth factor-beta  (a protein that controls

 

proliferation, cellular differentiation, and other functions in most cells) signaling.  “SMAD2 mediates the signal of the transforming

 

growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation

 

(ref)” Whew!

 

The 2001 document Regulation of Smad degradation and activity by Smurf2, an E3 ubiquitin ligase expands further on the early

 

understanding of the actions of Smurf2.  Smad proteins are key intracellular signaling effectors for the transforming growth factor-

 

beta superfamily of peptide growth factors. Following receptor-induced activation, Smads move into the nucleus to activate

 

transcription of a select set of target genes. The activity of Smad proteins must be tightly regulated to exert the biological effects

 

of different ligands in a timely manner. Here, we report the identification of Smurf2, a new member of the Hect family of E3 ubiquitin

 

ligases.  Smurf2 selectively interacts with receptor-regulated Smads and preferentially targets Smad1 for ubiquitination and

 

proteasome-mediated degradation.”      

 

Telomere length attrition, Smurf2 and cell senescence

 

There are a number of publications further detailing actions of Smurf2, but I am focusing this discussion on longevity-related issues

 

so I move now to a December 2004 publication co-authored by Zhang Smurf2 up-regulation activates telomere-dependent senescence. 

 

“Progressive telomere shortening activates replicative senescence, which prevents somatic cells from being propagated indefinitely in

 

culture. The limitation of proliferative capacity imposed by replicative senescence is thought to contribute to both organismal aging

 

and the prevention of tumor development. Here we report that up-regulation of Smurf2, an E3 ubiquitin ligase previously implicated in

 

TGF-β signaling, is a specific consequence of telomere attrition in human fibroblasts and that such up-regulation is sufficient to

 

produce the senescence phenotype.”  In other words, telomere attrition leads to upregulation of Smurf2 which in turn drives the cell

 

into senescence.  Smurf2 upregulation is an intermediary between telomere attrition and cell senescence.

 

Telomere attrition can be due to DNA damage, oxidative stress, oncogenic activation or aging.  Continuing to quote from the same 2004

 

article, “We show that the senescence-inducing actions of Smurf2 occur in the absence of detectable DNA damage or stress response,

 

that Smurf2’s effects require a novel function distinct from its E3 activity, that Smurf2 recruits the Rb and p53 pathways for

 

senescence induction, and that while p21 is elevated by Smurf2, Smurf2-mediated senescence is independent of p21. Smurf2 is the first

 

gene found to be both up-regulated by telomere attrition and sufficient to induce senescence.”  

 

Expression of Smurf2 in fibroblasts appears to depend on telomere attrition, not on how many times a cell reproduces.  “Importantly,

 

fibroblasts immortalized by adventitious expression of hTERT and analyzed after multiple passages in culture showed no increase in

 

Smurf2 expression (Fig. 1C), indicating that up-regulation of Smurf2 is not the result of extended cell passage per se but, rather, is

 

a consequence of telomere shortening.”  And exposing immortalized fibroblasts with long and stable telomeres to Smurf2 drives them

 

directly into a senescent state.  “Smurf2 expression produces senescence in hTERT-immortalized cells   Expression of hTERT in primary

 

cultures of human fibroblasts precludes the progressive shortening of telomeres that activates events leading to senescence, resulting

 

in the immortalization of cell populations (Bodnar et al. 1998; Vaziri and Benchimol 1998; Dickson et al. 2000). In strong support of

 

the conclusion that Smurf2 expression is sufficient to produce the senescence phenotype, we found that adventitious expression of

 

Smurf2 to the level normally observed during replicative senescence induced by telomere attrition (cf. Figs. ​Figs.5A5A and ​and1B)

 

reversed hTERT-mediated immortalization of human fibroblasts. — Collectively, our findings support the argument that Smurf2 up-

 

regulation mediates one of the multiple cellular pathways that have been proposed to lead to senescence (Pereira-Smith and Smith

 

1988).”

 

These findings are clearly relevant to the 12th theory of aging laid out in my treatise Telomere Shortening and Damage.   Long

 

telomeres and even extraordinary expression of telomerase cannot protect a cell from senescence if Smurf2 is also strongly present in

 

that cell.

 

Zhang has been concerned with the overall process of cell senescence as well as with the specific role of Smurf2 and has generated a

 

number of publications  on the topic including a comprehensive 2007review paper Molecular signaling and genetic pathways of

 

senescence: Its role in tumorigenesis and aging.  His discussions in that paper of senescence and aging, senescence as a tumor

 

suppression mechanism, and senescence and tissue microenvironment are worth reading though there has been much relevant subsequent

 

research.  

 

The 2008 paper Suppression of human tumor cell proliferation by Smurf2-induced senescence, again co-authored by Zhang, continues to

 

tell the story, this time extending the research from fibroblasts cells to a wide variety of cell types including cancer cells.   

 

“Here we report that Smurf2 up-regulation induced senescence in a wide variety of human cell types, including highly neoplastic cell

 

lines. Consistent with our previous findings, the ability of Smurf2 to arrest cell proliferation did not require its ubiquitin ligase

 

activity. Furthermore, expression of the cyclin-dependent kinase inhibitor p21 was increased in tumor cells undergoing Smurf2-induced

 

senescence, and such increase occurred independently of the transactivation function of p53. Our results, which reveal a previously

 

unsuspected tumor suppression function for Smurf2-induced senescence, suggest that modulation of Smurf2 action may be a useful

 

strategy for inhibition of cancer cell growth.”  

 

From an evolutionary viewpoint, it appears that one role of Smurf2 is protection against cancers.  Cells experiencing telomere

 

attrition are driven into senescence by Smurf2 rather than being exposed to the possibility of oncogenesis due to DNA damage that

 

could be incurred in further cycles of replication.  The upside of cell senescence is limiting the accumulation of additional DNA

 

mutations and limiting the population of cells at risk for neoplastic transformation.  The downside is limiting the renewal capacity

 

of stem and progenitor cells and negative changes in gene expression and cell secretions.

 

Valerian (strting product. valproic acid is sythesized valerian that is stronger) In conclusion, our data show that the extent of

 

GABAA receptor modulation by Valerian extracts is related to the content of valeric acid(ref).” Valproic acid (also known as valproate

 

and abbreviated VPA)  is a synthetic substance, not present in the valerian plant.  Valproic  acid (by its official name 2-

 

propylvaleric acid). VPA too is a strong modulator of the GABA receptor.  Although mostly not known to be evil, it is also strongly

 

protective. valproic acid is currently marketed as a mood stabilizer under various trade names such as Depakote and Depakene. VPA

 

presents beneficial effects in clinical depression [10], absence seizures [11, 12], tonic-clonic seizures, complex partial seizures

 

[13], juvenile myoclonic epilepsy [14], seizures associated with Lennox-Gastaut syndrome [15], migraine headaches, and schizophrenia

 

(ref).”  There are ten different branded valproic acid products sold by ten different pharma companies or their branches worldwide.

 

Valproic acid shown to halt vision loss in patients with retinitis pigmentosa.  gaba increase and hdac inhibitor. HDAC inhibitor keeps

 

a histone, a spindle around which DNA is wrapped, acetylated - which is in an unfolded state that allows relatively unimpeded gene

 

activation. prostate carcinoma cell lines by activation of multiple death pathways “Our data indicate that the use of valproic acid

 

may be a suitable therapeutic agent in the control of prostate cancer progression and its action appears particularly relevant in the

 

control of refractory stages of prostate cancer.” can be used to help treat bipolar disorder.

 

injury were transplanted with NSCs and administered a drug known as valproic acid, which is used in the treatment of epilepsy. The

 

valproic acid promoted the transplanted NSCs to generate nerve cells, rather than other brain cell types, and the combination therapy

 

resulted in impressive restoration of hind limb function. Well, medication with VPA can also on rare occasions induce dementia and

 

Parkinson’s Disease symptoms as reported in this, this and this publication.  Also VPA has been reported to induce delirium in a

 

demented patient in this publication. 

-For breakfast, take a japanese knot root resveratrol pill (Olympian labs currently).

When aging cells were engineered to express telomerase, the enzyme that restores and extends stubby telomeres, those rejuvenated cells showed histone levels reminiscent of “happy, healthy chromatin,” and a partial return to a youthful chromatin profile.” The mechanisms by which cells maintain telomere lengthening involve either telomerase or the alternative lengthening of the telomere pathway, although specific mechanisms of the latter and the relationship between the two are as yet unknown.

 

eating processed meats, foods which have long been suspected to be carcinogenic because they tend to be infused with nitrites

 

exercise can nullify erosion in telomere lengths due to psychological stress.”

 

Stem cells : take a sample from a doner of any age, fix genetical errors, reprogram the cells to forget and start as anew, and then reintroduce them into the doner.

The term somatic (from the Greek σωματικός) refers to cells of the body, rather than gametes (eggs or sperm). In humans, somatic cells contain two copies of each chromosome (diploid), whereas gametes only contain one copy of each chromosome (haploid). Although all somatic cells of an individual are genetically identical in principle, they evolve a variety of tissue-specific characteristics during the process of differentiation, through epigenetic and regulatory alterations.

Somatic is also defined as relating to the wall of the body cavity, particularly as distinguished from the head, limbs or viscera. It is also of or relating to the portion of the vertebrate nervous system which regulates voluntary movements.

 

 

-Return to Studies and Interests-