Ageing occurs virtually to all  organisms in the world, the only thing that differs between species is the rate that we age. For this reason, the concept of ageing is already very complex and what causes ageing is difficult to understand.  How can we know what causes ageing if it occurs differently in all organisms? Even within species there are differences, this is shown by studies done in Danish twins, which will be discussed to develop a stronger argument for either environmental factors that cause ageing, or genetic factors that cause ageing- based on the results of the study4. Ageing is thereby thought of as being ‘schochastic’ which means there is a random probability distribution of it occurring, because even within one mammal its different tissues age at different rates 1. 

Ageing is significant because it happens all over the world and every second of the day, for years the concept of reversing ageing and becoming more youthful has been imagined , and sometimes even experimented by scientists such as Belmont at the Salk Institutute in America just recently (2016) where 4 genes known as the Yamanaka genes were turned on, these are known to turn adult cells into embryonic like cells ( cells that have not been specialised). By doing  this they found that the mice with a syndrome known as Hutchinson Progederia, (which mean’t they aged faster,) lived 30% longer than mice with the same condition 2. This is only just a segment of the vast amount of research that has been done to show that genetics could possibly be the cause of ageing. 
Ageing can be thought of in numerous angles; such a biological ageing , chronological age, social age and psychological age 7. This essay will mainly be focussing on the definition used for chronological age, which  refers to ageing as , ‘ the number of years that have elapsed since a person’s birth…Age is merely a crude marker for the processes that influence behaviour over time’.

By researching both the genetic factors and the environmental factors a wider understanding of ageing and what causes ageing can be met. This is important for health professionals to try and reduce disease and death caused by ageing such as Alzheimers which increases in risk as we grow older.Plus, although not ethical and highly unlikely due to regulations ,it may be even possible to completely eradicate deaths associated with ageing if we knew what caused it. Once we have discussed both the environmental factors that cause ageing and the genetic factors that cause ageing the factors will then be compared with each other to see which has the greater impact on ageing. By doing this, scientists can more easily target problems such as Alzheimers and loss of eye sight because it is widely known that as we get older these risks can increase, for example, after the age of 65 the risk of Alzheimers increases by 50% every 5 years after the age of 65 8.
However, the focus of this report will not be on the risks associated with ageing but the factors that cause ageing, to make this task obtainable the factors will be spilt into genetic factors and environmental factors.

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Environmental theories can otherwise be known as causes of ageing which are caused by errors5, the major theory that will be discussed linked to this is the free radical theory, which is considered as an error theory. The term ‘Free radical’ is vital to understanding ageing and so its  important to note that free radicals are a toxic by product of our cellular metabolism, they miss an outer electron, causing them to be highly reactive. Hence, causing them to remove them from our cells. It is believed that free radicals can cause ageing , for example, through mitochondrial DNA damage6, which increase signs of ageing such as a decrease in stamina, this essay will go into further detail on how free radicals may be the cause of ageing.

 However not all factors that could cause ageing have enough evidence to support it or there is contradictory evidence, for this reason some of the factors discussed will merely be theories , but  some theories do have outstanding evidence to support them and so will be considered as factors. Examples of these theories that will be discussed are; the wear and tear theory, the free radical theory, the DNA repair theory , the evolutionary theory and the waste product accumulation theory3. After explaining the factors this essay will make a critical conclusion as to which factors are the most substantial based on the evidence they have and any contradictory evidence there may be.



 As already stated in the introduction, a free radical is highly toxic and is missing an outer electron. This causes free radicals to remove them from our cells instead, meaning they are highly toxic to our cells.Free radicals are a major source of reactive oxygen species which can cause the DNA in our mitochondria to mutate. As we age the bodies ability to repair the damaged DNA decreases and so cells enter senescence the damaged cells that do not die may secrete cytokines which contribute to ageing23.I.As a result our mitochondria ( which is the an important organelle in our body- because it is the sight of aerobic respiration and produces energy in the form of ATP) becomes damaged. This means that there is a decreased energy output from the mitochondria, which may be the cause of ageing leading to signs such a decrease in stamina and a loss of eyesight 15. Evidence that these free radical reactions cause ageing is shown by studies that found that restricting someones diet by eating less minimised the amount of free radical reactions in the body and hence  the life span can increased by as much as 5-10 years-however the right amount of nutrients must be taken in 16. 
More evidence that supports the theory is that scientists purposefully mutated the mitochondrial DNA because we already know that it is able to produce reactive oxygen species. When mutated the mitochondria accumulated more mutations and mice lived for less than a year rather than their expected life span of 2-3 years11,obviously showing that mutations to the mitochondria does cause ageing.
However, there is already lots of evidence against the free radical theory, for example, enzymes which blocked the reactive oxygen specie production did not increase the life span in mice23. Plus, an increase in mitochondrial reactive oxygen species actually extended the life span of yeast(Cell Metab,13:668-78, 2011).

Membrane bound organelles are found in cells which are known as eukaryotic cells, mainly found in complex organisms. Mammals have their genetic information contained in string shaped spools of DNA , known as chromosomes. At either end of a chromosome is a telomere. Every time our DNA is replicated ( for example for growth), and our cell divides via mitosis, our telomeres shorten1 ref, because DNA polymerase is less able to replicate the DNA.In cells such as sperm, egg and embryonic cells  do not lose their capacity to use an enzyme known as telomerase to restore their telomeres(only after multiple cell divisions do they lose this capacity), but normal cells such as adult body cells do. Once our telomeres are very short there comes a point where our immune system is not able to distinguish enemy cells ( foreign cells) from cells of our body10ref. This means that our immune system starts attacking our own cells with very short telomeres-this is known as autoimmunity.Linked to autoimmunity is the idea that as we age the body ability to produce antibodies declines (needed to protect us against viral pathogens) meaning we become susceptible to diseases such as Lupus (Bengtson and Schaie, 1998).
Some of the cells with very short telomeres just enter apoptosis and enters senescence.So, as we get older the telomeres of our cells shorten each time. By having shorter telomeres  proteins known as sheliteirens are not able to protect our DNA from damage and our own proteins become confused and are not able to properly repair our DNAEMBO Mol Med, 4:691-704, 2012.
 After Telomere damage and the cell stops proliferating the signs of ageing increase23. Neourological diseases have been found to increase in mice which are definicient in the enzyme telomerase which repairs the telomeres in the hippocampus27. This could explain why chances of getting neurological diseases such as Amyotrophic lateral sclerosis increases as we age. Also, because telomere attrition causes cell senescence, it is important to note what cell senescence can cause. When our cells enter senescence their capability to regenerate is lost and their so is their role and function.This results in tissue not being able to regenerate itself and ultimately our skin becomes more wrinkled and we age more 28. More evidence to prove that telomeres cause ageing was found by Toma ?s-Loba et al who found that over expressing the enzyme telomerase which repairs telomeres increased the life span of mice notably. Even more evidence for the telomere theory of ageing is from a progeroid disease known as Werners syndrome 28.Werners syndrome stimulates rapid ageing in humans and is caused by a mutation in the WRN gene.People with Werners syndrome have increased amounts of DNA damage causing small amount of growth.This provides evidence for telomeres to be the cause of ageing indirectly, because a decreased length of our telomeres also causes our DNA to get damaged, and so could increase the rate of ageing.


Pleiotropy is used to describe an allele of gene that has an effect on more than one type of trait. This theory was used by scientists known as Medawar and Williams in the 1950s to try and explain the evolution of ageing, and demonstrate what causes ageing30.
Antagonisictic pleiotropy occurs when an allele on a gene causes a beneficial trait, but later causes deleterious effects which are negative to humans later in life30. As we already know, genes can be activated in many different tissues, meaning that a single gene can have an affect on many tissues32. An example of the pleiotropy theory in humans is the case of reproduction, for example an increase in sexual drive is beneficial for the youth as it increases their chances of reproduction, however in the long term, it can also cause ovarian cancer in females and prostate cancer in males29.This can also be known as a ‘trade off’, because notably, a positive effect is returned with a negative effect later in life. Williams believed that the combined negative effects of these initially beneficial genes are the cause of ageing. 
However, there are many unsolved questions to this theory which causes it to not be a strong argument for ageing. One of which is , if the beneficial effects are caused by evolution, why wouldn’t the negative effects be eradicated by natural selection. Although the counter argument of this is that people reproduce before they deleterious effects onset, it is shown that although not massively, natural selection does still occur in older adults32.Plus, if ageing is caused by the same genes that are able to cause beneficial effects, why would the negative effects be so different?32. Furthermore, if these genes do cause ageing, is still doesn’t explain why different organisms can have completely different life spans, even though it is very similar gene producing the deleterious effects. 
Evidence for the antonogistic pleiotropy theory stems from diseases which are known to be caused by a single gene. One case as such is Marfan syndrome 31. This syndrome is caused by a mutation on the FBN1 gene 33 and it causes a whole list or symptoms such as hyper mobility and an increased risk of heart disease, showing that single gene is able to cause many deleterious effects.
An experiment found that when two types of round worms(also known as nematode Caenorhabditis elegans) – a wild type worm and a long lived mutant were put together in natural conditions where they had to compete for their food, the wild type outlived the long lived mutant , because it had a competitive advance29,34.This shows that the long lived mutants, as they had age became less advantageous, which provides further evidence for the Antogonistic pleiotropy theory.

As cells complete many cell divisions, toxins begin to accumulate, which eventually become toxic to our cells and prevent the normal functioning of our cells and eventually our cells die. As we age and our cells accumulate waste a pigment known as Lipofucsin is produced 34. Lipofucsin is made from fats bonded to proteins, or more specifically from the auto oxidation of lipid components ( able to oxidise itself) 35,however this varies slightly within different tissues. Alternatively , and more simply, Lipofucisn is a combination of oxidise lipids, proteins and carbohydrates. Lipofucsin is mainly found in non-dividing cells such as neurones and if found to increase linearly as we age.Lipofucsin can be observed by staining it and observing its colour during light microscopy. By using this method, scientists (Hamperl 1934) found that Lipofucin was a yellow brown pigment.Evidence that these deposits of Lipofucin cause ageing is that Lipofucin increases as we age, roughly by 0.3% every decade.As well as this humans who were  centurions had their large neurones examined, and it was found that 75% of their neurones were made from Lipofucsin35.Despite this, this does not mean that Lipofusin is the cause of ageing, it could just mean that Lipofucsin increases as we age.Nonetheless, there is no concrete evidence that Lipofucsin causes ageing and some contradictory evidence. Scientists found that people with a vitamin E deficiency actually had more Lipofucsin deposits 35, but this did not increase the rate that they aged- suggesting that it is more Lipofucisn is more complex than simply Lipofucin being the cause of ageing. Thus, people who had no vitamin E deficiency weren’t found to have a prolonged life35. 


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