biology
29120 Penicillin: Alexander Fleming’s accidental discovery of the first antibiotic

In all likelihood, you’ve probably heard of Alexander Fleming (1881-1955), the Scottish physician, pharmacologist and medical microbiologist. Made a Fellow of the Royal Society in 1943, knighted in 1944 and awarded the Nobel Prize in 1945, Fleming made one of the most significant accidental discoveries in the history of biology: the discovery of a substance called penicillin.

By isolating, naming and concentrating this antibacterial substance secreted by a Penicillium mould, Fleming effectively discovered the first modern antibiotic and enabled the creation of many subsequent antibiotics which are used to cure infections caused by bacteria: infections which were untreatable (and potentially fatal) prior to this. In this manner, medical science was utterly transformed by Fleming’s accidental breakthrough.

Following his death in 1955 his fame continues: 1999, he was named in Time magazine’s list of the 100 Most Important People of the 20th Century and he was voted the third ‘greatest Scot’ by the Scottish television channel, STV, only behind Robert Burns and William Wallace.

Of course, the fair attribution of these ‘breakthrough’ moments in science is never as straightforward as it seems – just think of the case of Rosalind Franklin who, for reasons which are still under debate, was not awarded the Nobel Prize for her work with Watson and Crick on discovering the structure of DNA – and Alexander Fleming himself was keen to highlight other scientists, such as Howard Florey and Ernst Chain who took the next steps from his discovery and transformed his petri-dish substance, ‘penicillin’ into actual drugs which were mass produced and which could be used to treat and cure bacterial infections.

But, you might be wondering, how did this accidental discovery take place, and how did that turn into the antibiotics which modern medicine relies on? Read on to find out!

The Discovery

In 1927, Alexander Fleming was studying the properties of the bacteria staphylococci whilst working at his laboratory in Paddington, London. Well-known and respected within the research community of the time for his earlier work, including the discovery of the enzyme lysozyme, he also had a reputation for untidiness as he tended to leave his laboratory in a mess. True to form, before going on holiday with his family in August 1928, he left the colonies of staphylococci stacked in a pile of petri dishes in the corner of his laboratory.

After returning from holiday in September, he noticed that one bacterial culture was contaminated with a fungus which had grown into a fungal colony, and that the colonies of staphylococci immediately surrounding the fungus had been destroyed, whereas other staphylococci colonies farther away were normal. Based on this, Fleming determined that the fungus must be producing a substance which was slowing down the growth of the bacteria. After growing this mould in a pure culture, he found that it produced a substance which killed a number of pathogenic bacteria – a substance which he originally called ‘mould juice’ and then named ‘penicillin’, in 1929, after the fungus on the petri dish, Penicillium notatum (Penicillium chrysogenum).

During the next 12 years, Fleming grew, studied and distributed the original mold and found that the substance had clear antibacterial effects on many organisms. In particular, it affected gram-positive bacteria (bacteria which have very thick walls made of peptidoglycan and show up positive in the Gram stain test) which cause conditions such as scarlet fever, pneumonia, meningitis and diphtheria. In addition, penicillin also affects Neisseria gonorrhoeae, which causes the infection gonorrhoea, even though this bacterium is gram-negative.

The Consequences

Although Fleming published his discovery in the British Journal of Experimental Pathology in 1929, it received little attention at the time. After continuing his investigations into the 1930s, Fleming found the Penicillium mould to be difficult to cultivate and that it was even more difficult to isolate the antibiotic agent.

Fleming also concluded that, due to the slow speed of its effects, penicillin could not be overly significant as a substance used to treat infections, especially as he believed that it would also not last long enough in the human body to effectively kill the bacteria causing these infections. With his clinical trials in the 1930s mainly producing inconclusive results, Fleming largely abandoned his work on penicillin.

Thankfully for us today, his work was picked up by a large team of scientists both in the UK and abroad, including Howard Florey, Norman Heatley and Ernst Boris Chain at the Radcliffe Infirmary in Oxford, who took up research to isolate and mass-produce penicillin, with funding provided by both the British and US governments. The Oxford biochemical research team developed a method of purifying penicillin to its effective first stable form in 1940, with several clinical trials following which were hugely successful and which resulted in the team developing methods for mass production and mass distribution by 1945.

Across the pond, between 1941 and 1943, a team at the USDA Northern Regional Research Laboratory (NRRL) in Peoria, Illinois, United States, managed to isolate higher-yielding strains of the Penicillium fungus and also developed methods for industrialised penicillin production. As a consequence, survivors of the Cocoanut Grove fire in Boston in December 1942 were the first burn patients who were successfully treated with penicillin. After the bombing of Pearl Harbour, mass production of the antibiotic began, and, by D-Day in 1944, enough penicillin had been produced to treat all of the wounded in the Allied forces.

Impact Today and Wider Implications

As previously noted, Fleming himself was modest about his contribution to the development of penicillin, calling his fame ‘the Fleming Myth’ and attributing the success to Foley and Chain for their work in creating penicillin drugs. That said, as the famous cell biologist, Sir Henry Harris said in 1998, “Without Fleming, no Chain; without Chain, no Florey; without Florey, no Heatley; without Heatley, no penicillin.” Fleming’s discovery by chance and subsequent isolation of penicillin in September 1928 can truly be said to mark the start of modern antibiotics.

Finally, considering Fleming’s discovery can also allow us to reflect upon one of the most significant issues facing medicine in 2019: bacterial resistance to antibiotics. It should be noted that during Fleming’s research he found that bacteria would develop antibiotic resistance if too little penicillin was used in treatment or when it was used for too short a period. As early as 1940, Chain and Edward Abraham noted the first example of antibiotic resistance to penicillin, an E. coli strain that produced the penicillinase enzyme: an enzyme capable of breaking down penicillin and thus completely negating its antibacterial effect.
Fleming himself was outspoken on the issue and cautioned that penicillin should not be used unless there was a properly diagnosed reason, and that it should never be used for too short a period, or in too small quantities, as these are conditions in which bacteria become resistant to antibiotics. In the modern world, the number of bacteria resistant to penicillin is increasing, and, according to the Centres for Disease Control and Prevention, at least 2 million people in the US per year fall ill due to an antibiotic resistant infection.
As Fleming himself warned, “the microbes are educated to resist penicillin and a host of penicillin-fast organisms is bred out … In such cases the thoughtless person playing with penicillin is morally responsible for the death of the man who finally succumbs to infection with the penicillin-resistant organism. I hope this evil can be averted.”

That said, despite the risks posed by resistance today, penicillin has saved, and is still saving the lives of millions of people around the world. Research into antibiotic resistance continues today and scientists are working to develop more effective strains of penicillin-based and other antibiotics. By studying both the causes and mechanisms of antibiotic resistance, modern scientists can tackle the problem and keep one step ahead of these pathogenic bacteria.

Categories: Articles Tags: , , 26533 The Biologist’s Haven: Downing Site

Of all the sciences, I find that biology seeps into a place with more enthusiasm than most others. Even here, in this widowed hotel on the frayed edge of Rome, as I eat my soup with plastic fork and pretend those gunshots are fireworks. Even here, biology is taking hold.

Life creeps greenly into car park cracks while also, since the sky sparkles not, bleeding out onto a floor. But, living subjects aside, can the science itself inhabit a place over time? Can the study of living processes become as embedded in a place as the ant colony in my hotel en-suite?

Why, yes. Yes it can. And the horde of Cambridge students cycling daily to the Downing Site will agree with me. Well, they should anyway. It’s only through work done here that we can understand what’s going on in that scurrying millipede of cycling legs. Sir Bryan Matthews’ oscillograph laid the foundations for measuring the nerve activity, while the pioneering electrophysiology work of Hodgkin and Huxley helps us understand what those measurements actually mean!The construction of Downing Site itself signalled an attempt by the University to take the sciences seriously. Even before the site was built, the wild, boggy marshland of the Pembroke Leys would portend the coming focus on the life sciences. Death arrived first though, as the place was fertile hunting ground as early at the 1780s. Then, as the 19th century rolled around, it was bought for the construction of Downing College. But, as is often the case when discussing the colleges of Cambridge and their grand projects, the money soon ran out and the northern reaches of the Leys we left unused. Eventually, between 1895 and 1902, the University would purchase this land for the construction of laboratories, to ease the overload of scientists in the New Museums Site across the road. Despite the prospect of some elbow room, this proposed move was met with some outcry because surely the scientists didn’t need that much space. It was only biology, after all. And rocks, I suppose – but that’s an article for another day.Soon afterwards, the biologists came in their droves, bringing their new ideas with them. First, in 1904, the botanists came to set up their labs and their… leaves. And on their leaves, they penned some of the most influential work in the taxonomy of British and European flora in the last century. In addition, the blossoming field of plant physiology saw great strides here. For example, the great Frederick Blackman proved that leaf absorption of carbon dioxide occurred almost wholly through the stomata; published his theory on the limiting factors of photosynthesis; and originated the idea that separate reactions occur in the light and dark to sustain plant life. Students of Blackman included CS Hanes, who elucidated the structure of plant starch and Robin Hill who, after the biochemists’ arrival in 1924, shed yet more light on the reactions of photosynthesis. Another biochemist, Frederick Sanger, would sequence the insulin protein at Downing Site, before going on to sequence DNA itself, later in his career.Soon after, the early education of the medics and vets of Cambridge was cemented in Downing Site. After the Physiology laboratory made its new home there in 1914, the human anatomists would muscle in after 1938. The veterinary anatomists doggedly followed in 1958. The study of living things in Cambridge has since become synonymous with Downing Site, with many of the more modern breakthroughs – such as Bob Edwards’ early work on In-Vitro Fertilisation – taking place somewhere in that redbrick, Jacobean maze.

The discoveries and developments at Downing Site have changed how the world understands and harnesses biological processes. Couples can now have children when they previously could not; crops can be genetically modified to thrive in harsher climates; millions of diabetics have ready access to insulin; and Chinese scientists recently grew the first plants on the Moon! All of these advances were built, either wholly or in part, on the results found and documented here.

For all the budding (pun intended) biologists out there: dig out your old school textbooks, go and find out where those facts came from. Much of the biology we all learned in school can be traced back to that former patch of marshland, bound on all four sides by famous Cambridge streets. The buildings bear names of those distinguished scientists, plaques commemorate their work all over the place. It almost reassures us that, yes, the secrets of life were investigated within these walls; biology lived and still lives here, in its undergrads and its lecturers and its memories of all that came before.

arrivals day Categories: Articles Tags: , , , , 10121 How Has Altruism Evolved?

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Altruism is a topic that I studied early on in my Evolution and Behaviour model. At first glance, it appears to go against everything that Natural Selection predicts. An altruistic act is one that benefits another at your own expense. As the main biological imperative of life is for genes to replicate themselves as much as possible to increase their frequency in the gene pool, why would animals act in a way to decrease their own fitness? In this situation, fitness can be measured in terms of the number of offspring an animal has since this reflects the number of times a gene has likely been passed on. The more offspring an animal has, the more successful its life has been.

There are 4 main types of social interactions with other members of an individual’s population – cooperation, selfishness, altruism and spite:

Looking at the above table we would expect most organisms only to act in cooperative or selfish ways, as these are the only ways that benefit them. Selfish actions only benefit that individual and have no effect on anyone else. Unsurprisingly, this type of behaviour is very common and includes things such as not sharing food.

Co-operation also has many advantages to an individual. Group hunting can be more effective than individual hunting and therefore result in a higher food yield per individual. Living in a larger group causes “the dilution effect”. This describes how being in a large group reduces the chance that a predator will catch an individual. Additionally, living with a larger group increases the vigilance in watching for predators.However, this only really helps if the organism that spots the predator alerts the others, which can be considered an altruistic act as it calls attention to itself and so is more likely to be targeted by the predator. A good example of this is in meerkat groups where adults will stand-watch at higher vantage points on their hind legs and alert the rest of the group if they see a predator.

Is It a Gene Thing?

If we consider altruistic acts at the level of an individual, it seems hard to imagine how altruism has evolved. An altruist in a group of selfish animals would be at a disadvantage as they would be willing to help others, but the others would not help them. This would, therefore, be strongly selected against and any genes for altruistic traits would rapidly disappear from the gene pool. In a primarily altruistic group, a selfish individual would have an advantage over the others as they may be the recipient of altruistic acts but not return them. This means that they would have a higher reproductive success and as a result the allele for selfish acts would rapidly increase in frequency within the gene pool. In Vervet monkey populations, monkeys will sound an alarm call to warn the others of the presence of a predator – this is an altruistic act as it calls more attention to themselves – making them more likely to be targeted by the predator. Surely a monkey with a selfish trait that did not warn the others would be at an advantage as it would be able to escape quietly, while the predator targeted the others? This was described by Darwin as “subversion from within” as any altruistic group will eventually give rise to a selfish individual which will be at an advantage and therefore increase the frequency of that selfish gene.

At the level of the group, however, it is possible to see that groups that contain all, or primarily altruists, would have an advantage over selfish groups in bad years where food is scarce – as a result the selfish groups might all die, leaving a greater proportion of altruists in the population. However, in good years selfish groups will do better than the altruists as they can put all their resources towards producing as many offspring as possible. Darwin proposed a theory for the evolution of altruism that suggested that although self-sacrificial behaviour is disadvantageous to an individual, it might be beneficial to the group. On its own, Darwins theory does not seem sufficient to explain the evolution of something that seems like such a paradox to natural selection.

In 1964 Bill Hamilton published his theory of “kin selection” – also called inclusive fitness. If we consider fitness to mean the number of copies of a gene you cause to be passed on to the next generation we can see that as relatives are likely to share some of your genes, it may be beneficial to help them reproduce (as well as yourself). By helping close relatives, you can increase the total number of copies of your genes that are passed on to the next generation.

If we imagine a gene that increased the likelihood of an organism acting in an altruistic way such as sharing food with everyone it came across, that would provide no advantage. However, if that organism only shared food with its relatives and that extra food helped them to increase their reproductive success then we can see how an altruistic allele could increase in frequency in a population. This theory does not rely on an organism being able to recognise its relatives as in social populations relatives will normally live close together. Cuckoos have evolved to exploit this lack of ability to recognise who is actually related to them, as they lay their eggs in Dunnock nests. At first glance, seeing a dunnock feeding and looking after a cuckoo chick might seem like an altruistic act on the part of the dunnock, but in fact this is simply because the dunnock does not recognise that the cuckoo egg is not one of their own – even when the cuckoo chick hatches first and pushes the other eggs out the nest.

Hamilton’s Rule defines the conditions under which a gene promoting altruism would increase in frequency in the population:

Where A is the altruist and B is the beneficiary. If A helps B, A will suffer a cost of decreasing the number of offspring it has but B will benefit and have more offspring than it would have done without A’s help. If B is closely related to A, then B’s benefit will also benefit A since they share some of the same genes. Relatedness is the probability that one gene in an individual is an identical copy, by descent of a gene in another individual. This will, therefore, be higher in siblings (a 50% chance of sharing the same gene) than in cousins (a 12.5% chance of sharing the same gene). If the inequality described by Hamilton’s rule is met, then it is evolutionarily beneficial for A to help B at A’s own expense.

This theory of kin selection works well to explain altruistic acts within social insect populations. For example, within bee colonies, sterile worker bees spend their lives looking after the queen bee, as this is the best way for them to try and ensure some of their genes get passed on since they cannot reproduce themselves. Worker bees have stings and will attack predators that get too close to their nest – in stinging the predator, the barb gets stuck in the predator and the bee dies. The evolution of this suicidal behaviour only makes sense if we consider that the nest is full of that bee’s relatives and in protecting them they will be able to reproduce to offspring with copies of the same gene as the worker ant.

This shows that altruistic behaviour is not the paradox of natural selection it seems. If we consider kin selection, we can see that the organisms still act in a way to maximise an alleles presence in a population. The conditions for the spread of an altruistic gene are given by Hamilton’s rule and when this inequality is met it is beneficial for an individual to behave altruistically towards the other – this explains the different levels of altruistic behaviour shown to different relatives. John Haldane once said “I would gladly lay down my life for two brothers or eight cousins.”

altruism Categories: Articles Tags: , 10218 A Leaf Out of Nature’s Book

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Life first emerged on earth over 4000 million years ago, deep in the ocean in hydrothermal vents in tiny pockets formed in the rock. Since then millennia have passed and life has evolved into over 2 million different species, each adapted and moulded to fit a certain niche within their ecosystem.

Homo sapiens evolved between 350,000 and 260,000 years ago, and the industrial revolution took place within the last few hundred years. Just looking at these ridiculously different timescales suggests that the ancient wisdom of Nature has much to teach us.

In 1989, bullet trains in Japan seriously needed a redesign. These incredible feats of human engineering were fast (reaching speeds of 167 mph) but tunnels posed a problem for them. As they moved through the tunnels at high speed they pushed a wave of high pressure air in front of them, which expanded rapidly when exiting the tunnel. This made a sonic boom which could be heard 400m away. In such a densely packed country as Japan, this was unsafe for both humans and wildlife, and a solution was desperately needed.

The answer was found by turning to nature. The newly designed trains took inspiration from a graceful and streamlined hunter – the kingfisher.

Kingfishers and Trains

When kingfishers dive into water from the air, they experience a large change in pressure, just like the train emerging from a tunnel. Kingfishers are able to enter the water and barely create a splash – maybe this could be imitated by the train. The kingfisher’s beak is long in comparison to its body and is sharply pointed, creating a very aerodynamic shape. A new bullet train design, based around the kingfisher, featured a tapering nose nearly 50ft long.

When different shaped noses were trialled, the one based on the kingfisher’s beak outperformed the others by far. The new design travelled 10% faster than before as well as using 10% less energy and resolving the problem of the sonic boom.

So how did this near-perfect design for pressure change just appear on the head of a kingfisher? The answer lies in natural selection. The kingfishers more likely to survive to a ripe old age and therefore pass of their genes to their offspring are the ones which catch the most fish. The ones with the streamlined beaks are better hunters who fish well, whereas their companions with flat faces splash into the water and never catch anything. So the genes which code for streamlined beaks are passed on, and the flat-faced genes are lost, as those birds cannot fish and therefore never get the chance to reproduce.

This process means that over the years, the genetics of kingfishers converge to coding for the long and graceful beak which makes them the best fishermen in the pond.

Compared to tests we could carry out in a lab, it is clear that using designs found in nature will use far more data, millions more specimens and experience beyond comprehension.

Biomimetics is possibly the laziest form of design – simply copying ideas already painstakingly refined by natural selection over millions of years – but can also be the most effective.

This isn’t a new idea – Velcro’s hook-and-loop design, invented in the early 1940s, was based on the way Burdock seeds latched onto the inventor’s dog’s fur. And even before this, ideas used by the Wright brothers came from studying the flight of birds.

But “biomimicry” as a term wasn’t first coined until 1997, by Janine Benyus. Benyus defined 3 distinct types of biomimicry.

The first is mimicking shape, just like the train and the kingfisher. This is possibly the most widely seen form of biomimetics – just this month researchers in Singapore created an underwater robot which uses motors and flexible fins to propel itself in the same way as a manta ray, one of nature’s most efficient swimmers with a unique style.

The Eastgate centre in Zimbabwe was designed after the architect watched termites building their nests. Mick Pearce was inspired by the way the insects are able to create ventilated mounds using very scarce resources. The termites create holes all over the surface of the mound to provide “passive ventilation” – using energy from the surroundings instead of typical AC or central heating systems.

The Eastgate tower’s outer “skin” takes heat from the environment during the day and absorbs it into the structure, meaning the air has cooled by the time it gets into the building. In the evening, the heat absorbed during the day keeps the air inside from getting too cool, creating a regulated temperature with minimal energy input.

The second form of biomimicry is to mimic processes. This includes things like communication between animals and how their societies behave. The communication within a colony of ants has been studied, programmed into software and could be used to control the communication of fleets of autonomous cars.

The final form is that of mimicking an entire ecosystem. In many ecosystems, waste is practically non-existent. One material or compound useless to organism one, is eagerly picked up and put into use by organism two.

Ecosystems are also extraordinarily resilient – suppose a forest fire destroys an area of woodland. In the new environment, grasses and shrubs may be better suited to the surroundings and become the dominant species, bringing in animals which feed on them and establishing a new, but still functioning and efficient ecosystem.

If we could live more like this – with no wasted by-products from manufacturing, with each old product being upcycled, reused or reinvented – we could drastically reduce waste and hugely reduce the damage we do to the environment.

Obviously, we have many lessons to learn from nature – it’s an interesting thought that when we find ourselves faced with a seemingly unsolvable problem, perhaps the answer is just outside the window.

What Is Biomimicry?
Biomimicry: Learning Design from Observing the Birds and the Bees
nature Categories: Articles Tags: , 10183 Why Do We Age?

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This is a topic that really interested me during my first year at Cambridge. The question of how we age is well covered by the media and research has led to the production of countless “anti-ageing” products. The question of why we age is less well understood. Since the most important biological imperative in life is to survive to reproduce and pass your genes on to the next generation, why would we have evolved in a way that leads to the deterioration of our bodies with old age?

The biological definition of ageing is very precise. It is the persistent decline in age-specific fitness components of an organism due to internal physiological deterioration. According to this definition, the everyday use of this word in the context of increasing age with each birthday is wrong – you do not start to age until your body begins to decline.

Surprisingly, ageing is not inevitable. There are extensive cellular mechanisms to prevent deterioration at a cellular level. There is also great variation in the rate of ageing between different species. So why would evolution select for something that involves a loss of fitness?

Natural selection of ageing

At some point, all organisms succumb to some extrinsic hazard and die. The older you get the higher the chance that you would have died by that point (even if you did not age). This means that organisms will tend to be more successful in terms of reproduction when they are young– i.e. the young will contribute more to lifetime reproductive success.

The cells that make up an organism can be divided into somatic cells and germ line cells. The somatic cells are those that make up almost all the cells of your body, while the germline cells form the gametes that will pass on your genetic information to your children. This germline can be described as immortal as it does not decline in quality over time. However, this immortality has a cost and the somatic cells must pay the price by ageing. The “disposable soma” hypothesis suggests that the soma has evolved in each species to maximise lifetime reproductive success. Each time an animal reproduces, the somatic cells are damaged and therefore age due to a decline in cell repair.


This suggests that ageing is the cost of reproduction. It represents a trade-off between reproduction and other aspects of fitness. When reproduction is prevented, lifespan tends to increase – for example, Korean eunuchs tend to have longer than average lifespans. Some organisms such as the jellyfish
Turritopsis nutricula are seemingly immortal. This jellyfish is very rare in that it does not have a separate germ line and soma and therefore the soma does not age.

Splitting the cost of reproduction

When parents raise their young together, they both gain equally from the offspring they produce, but it advantageous for each to pay the lesser cost of reproduction. For example, if a male impregnates a female, both the male and the female manage to pass on their genes to the next generation. If, however, he then leaves, he is able to find another female to mate with while the female has to look after and nourish the offspring – i.e. she pays the greater cost. The “winner” of the conflict is the sex which escapes with the lowest cost.

A non-adaptive explanation of ageing

The evolution of ageing can be re-enacted in the laboratory using Drosophila (fruit flies). When the Drosophila are selected to breed early in life, their lifespan decreased. Vice versa, when flies that bred later in life were selected for, the average lifespan increased. These experiments also highlight an important phenomenon – the force of natural selection decreases with increasing age. This means that deleterious alleles that are expressed only in later life are not selected against as strongly as those expressed in earlier life when reproduction is concentrated. The expression of these deleterious alleles accounts for some features of ageing – such as Huntington’s disease. The gene that causes Huntington’s disease is rare in that it is dominant. Very few genetic diseases are caused by dominant alleles since they are strongly selected against – the presence of them often means the individual cannot reproduce. However, the Huntington’s gene is not expressed in individuals until after the prime reproductive age – by this point, they have already reproduced and passed the allele on to their children.

Mechanisms of ageing

There is still much research into the mechanisms which underlie ageing but it is agreed that multiple processes are at work at the same time.

Free radicals such as reactive oxygen species can cause significant damage to the cell. Although there are mechanisms to limit this damage, over time these are overwhelmed.

Telomeres are caps of DNA at the end of each chromosome. Each time a cell divides, a small amount of DNA is lost from the end of the chromosomes. Although the degree of shortening can be minimised, this sets a limit on the number of times a cell can divide – this is called the Hayflick limit. Eventually, the telomeres are completely degraded and the damaged DNA causes the cell to kill itself through a process called apoptosis.

The extent of investment into the development of organs in early life influences the rate at which they deteriorate in later life. For example, babies born with a low birth weight are more likely to have cardiovascular problems.

Menopause

Menopause is very unusual in most animals – in most animals, a deterioration in fertility and survival are closely linked. However, in human females (as well as killer and pilot whales) a deterioration in fertility proceeds more rapidly so that reproduction ceases at about 50, while many women live on for several more decades. Why live on when reproduction ceases?

Human children take a long time to become self-sufficient and so perhaps it is beneficial for a mother to stop having children so that she can raise the children has already had before she dies. Another possibility is that extended life after reproduction allows grandmothers to chance to increase their reproductive success through helping their kin (especially their daughters) since they have her genes.

One study of Finns and Canadians showed that women who live longest after menopause tend to have more grandchildren (and are therefore more reproductively successful) because their daughters are better at having and raising kids. The study showed that the average lifespan of the grandmother was just long enough to allow their daughters to complete reproduction – they live for as long as they are useful for raising offspring and then die.

In summary, we know that animals age through a variety of mechanisms including the shortening of telomeres and cellular damage by reactive oxygen species. There are probably both adaptive and non-adaptive reasons for ageing. In almost all animals ageing is correlated with a decreased chance of reproduction, however, human women undergo menopause after their reproductive peak so that they can help their kin to reproduce and therefore maximise their own reproductive success without the personal cost of reproduction.

ageing Categories: Articles Tags: ,