If you are wondering how your cells age, look no further than the ends of your chromosomes. Special structures called telomeres keep a close eye on the damage that accumulates in our cells and signal when it is time for them to retire.
The cells in our bodies take quite a beating throughout our lifetimes. Environmental factors, such as ultraviolet rays, poor diet, and alcohol, as well as psychological factors including stress, are putting our cells at risk of significant damage.
These factors cause damage to the DNA in our cells, predisposing us to cancer and other diseases.
Luckily, however, we have sophisticated biological systems to counteract this damage. One of these mechanisms is involved in cellular aging, ensuring that individual cells live for a certain amount of time before dying.
Telomeres are stretches of DNA and proteins at the ends of our chromosomes. Each time a cell divides, these stretches naturally get shorter. Once telomere length reaches a particular cut-off point, the cell becomes senescent, meaning that it can no longer divide and will subsequently die.
How do telomeres work? And why do some people age quicker than others?
Protective caps
As aforementioned, telomeres are structures at the ends of the chromosomes that consist of stretches of DNA and proteins. When a cell divides, chromosomes are replicated and each daughter cell inherits an identical pair.
But our cells have a major problem with replicating DNA. The enzymes responsible for this process, called DNA polymerases, can easily replicate one strand of DNA in the chromosome, but replication of the other strand is much more complex.
The reason for this phenomenon is that the DNA molecule is directional, meaning the two strands of the double helix run in opposite directions.
DNA polymerases can produce a continuous strand of DNA running in the forward direction, but when this machinery has to work backward, it gets in a tangle. Instead, short fragments are produced in the forward direction, which are then joined together by other enzymes.
When it comes to the far ends of our chromosomes, the very last stretch of the reverse, or lagging, strand cannot be replicated. Scientists call this the "end replication problem." The result of this is a progressive shortening of the telomere DNA stretch with every round of cell division.
It also means that one strand of DNA is slightly longer than the other. This is actually a good thing; it allows the free DNA strand to curl and tuck into the existing double-stranded DNA, forming a protective loop.
With progressive telomere shortening comes cell senescence. Scientists think that this is a natural defense mechanism that stops cells that have accumulated too much damage from turning into potential cancer cells.
Factors that influence biological age
Telomere length can be used to indicate an individual's biological age (which is different from chronological age). Scientists now know that many factors - including physical exercise, sleep, depression, and certain gene mutations - are associated with reduced telomere length, and, by extension, can lead to premature biological aging.
For example, a recent study published in the journal Pediatrics demonstrates that children who had lost their fathers had significantly shorter telomeres.
Likewise, a systematic review published in the September 2017 issue of the Journal of Psychiatric Research also shows an association between adversity during childhood - including violence, institutionalization, and poverty - and shorter telomeres.
Whether telomere length is a marker of biological aging or a cause of it remains to be seen. But limiting the factors that are negatively associated with telomere length is likely to contribute to a more youthful biological age.
It's often hard to talk about these things because they sound so 'remote' & technical. Another closely related subject is 'Epigenetics'.
Some evolutionary scientists are discussing the possibility that it is the 'Epigenome' which is the main trigger in 'Natural Selection', - Not mutation. Natural selection is better described as the ability (or not) to 'adapt' to changing environments. People use the term: "Survival of the Fittest" but that really refers mostly to 'breeding behaviour'. Typical that people mix up sex with survival ! (I digress).
So, about thirty years ago micro biologists discovered that the DNA has an extra 'buffer zone' or layer which protects the genes from damage, particularly during cell splitting. Apparently mutation is most likely during the process of splitting (is that mitosis - I forget)?
So, life has evolved this epigenetic defense, plants have it too, so it's very ancient. Where there are 'external impacts' on the genetic material beyond a certain valence, a system of biochemical methylation (& acetylation) occurs which protects the genes from harm BUT (& it is a big BUT) it does change the gene expression, or should we say the 'gene function'. This process happens from conception, though gestation, particularly birth (which can be very traumatic) up to the age of about three years old.
Psychologists call this 'Imprinting'. Imprints can be virtually anything, particularly 'UN MET NEED'. Poisoning in the womb from alcohol / tobacco etc etc. Also prescribed or unprescribed drugs, again particularly at birth if there are traumatic complications for the fetus. Also lack of adequate nutrition, stress in the mother and so on. These imprints define the gene function at the brainstem level which in turn define how the Limbic system develops (how we feel) and then later what we think and believe. Developmental neurologists now tell us these different brains unfold in us SEQUENTIALLY. Thus un met need during gestation and infancy can lead to all kinds of illnesses later on. Particularly depression. Infact some researchers are now saying that unmet need / trauma in the womb & during birth, then compounded in infancy / childhood is the single cause of many different diseases later on in life.
In many ways this is not surprising, we all know a bad start in life is not good. But what is exceptional here is in finding the actual mechanism. This proves how important it is to get a good start in life; something which people have trouble fully realising before they become parents themselves. I am no exception here by the way, I have a disabled son, his mother was a serious drug addict and it's not rocket science to see where his problems originated.I also had a very traumatic start in life, abuse later on and that's the cause of my depression and complex PTSD
But perhaps most interesting of all & particularly to the so called 'Mental Health Professions' is the 'maladaptive' process we call neurosis. The fact that it appears to be a mechanism for adaption in the evolutionary process. What has not yet been ascertained is the connection between this methylation process and what we call : "Repression". Very serious traumas are hard to remember, ie: our system has found a way to hide the worst from us as a defense.
Currently the idea that we might try to remember, to sense what went wrong during those really early months in order to re connect to them and re gain sanity has been met with horror. Currently we try to persuade traumatised people to 'forget' or 'put their problems in a box'. That is the essential theory of CBT. That and taking Antidepressants, which merely boost the serotonin system.
Serotonin is called a neurotransmitter but actually, according to some clinical professionals it is a neuro inhibitor. Serotonin blocks messages from the unconscious inside us so that we do not feel the terror of early imprinted trauma. That explains why serotonin and other inhibitors such as endorphine (morphine) and various painkillers help us to feel better. This is all very controversial and needs more research.
Telomeres: What causes biological aging?https://www.carenity.co.uk/forum/other-discussions/news-from-the-media/telomeres-what-causes-biological-aging-19112017-08-15 14:53:48
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The cells in our bodies take quite a beating throughout our lifetimes. Environmental factors, such as ultraviolet rays, poor diet, and alcohol, as well as psychological factors including stress, are putting our cells at risk of significant damage.
These factors cause damage to the DNA in our cells, predisposing us to cancer and other diseases.
Luckily, however, we have sophisticated biological systems to counteract this damage. One of these mechanisms is involved in cellular aging, ensuring that individual cells live for a certain amount of time before dying.
Telomeres are stretches of DNA and proteins at the ends of our chromosomes. Each time a cell divides, these stretches naturally get shorter. Once telomere length reaches a particular cut-off point, the cell becomes senescent, meaning that it can no longer divide and will subsequently die.
How do telomeres work? And why do some people age quicker than others?
Protective caps
As aforementioned, telomeres are structures at the ends of the chromosomes that consist of stretches of DNA and proteins. When a cell divides, chromosomes are replicated and each daughter cell inherits an identical pair.
But our cells have a major problem with replicating DNA. The enzymes responsible for this process, called DNA polymerases, can easily replicate one strand of DNA in the chromosome, but replication of the other strand is much more complex.
The reason for this phenomenon is that the DNA molecule is directional, meaning the two strands of the double helix run in opposite directions.
DNA polymerases can produce a continuous strand of DNA running in the forward direction, but when this machinery has to work backward, it gets in a tangle. Instead, short fragments are produced in the forward direction, which are then joined together by other enzymes.
When it comes to the far ends of our chromosomes, the very last stretch of the reverse, or lagging, strand cannot be replicated. Scientists call this the "end replication problem." The result of this is a progressive shortening of the telomere DNA stretch with every round of cell division.
It also means that one strand of DNA is slightly longer than the other. This is actually a good thing; it allows the free DNA strand to curl and tuck into the existing double-stranded DNA, forming a protective loop.
With progressive telomere shortening comes cell senescence. Scientists think that this is a natural defense mechanism that stops cells that have accumulated too much damage from turning into potential cancer cells.
Factors that influence biological age
Telomere length can be used to indicate an individual's biological age (which is different from chronological age). Scientists now know that many factors - including physical exercise, sleep, depression, and certain gene mutations - are associated with reduced telomere length, and, by extension, can lead to premature biological aging.
For example, a recent study published in the journal Pediatrics demonstrates that children who had lost their fathers had significantly shorter telomeres.
Likewise, a systematic review published in the September 2017 issue of the Journal of Psychiatric Research also shows an association between adversity during childhood - including violence, institutionalization, and poverty - and shorter telomeres.
Whether telomere length is a marker of biological aging or a cause of it remains to be seen. But limiting the factors that are negatively associated with telomere length is likely to contribute to a more youthful biological age.
MedicalNewsToday.com