Death In The 1600s

17th century London had a problem: people were dying. A lot of people. The city was growing rapidly, leading to poorer areas becoming overcrowded. Sanitation was practically non-existent and, crucially, people were living in close proximity with animals. Plagues – that is to say, diseases that are both fast spreading and deadly – don’t generally arise from the evolution of pathogens that infect humans. For a pathogen, being deadly can only really be an evolutionary disadvantage, as dead hosts are much worse at spreading disease than live hosts, if they spread it at all. It is also unlikely for a human pathogen to develop a single mutation that suddenly makes them truly deadly. Rather, humans and our immune systems evolve and adapt alongside our diseases over thousands of years. This also means that there will always be a proportion of the human population that has acquired immunity against a disease, slowing down the spread of any new variants.

But what happens when a disease that only infects animals, in which it is not fatal, manages to jump over to humans? The disease doesn’t ‘know’ it is in a human, and will use whatever strategies it has evolved over thousands of years to overcome the immune defences of the animal. Unfortunately for the human host, those defences haven’t had a chance to develop. Suddenly, you have a disease that human immune systems have never ‘seen’ before, and that could potentially be extremely deadly. Combine this with overcrowded cities and a lack of sanitation, and you have a perfect recipe for plague.

In London and many other European cities, this had been happening on a regular basis since the 1300s. In London, there were around 30,000 deaths due to the plague in 1603, 35,000 in 1625 and 10,000 in 1636. This culminated in the Great Plague of London in 1665, which killed an estimated 100,000 people – around 25% of the city’s inhabitants (on an unrelated note, the Great Fire of London happened the next year – it really wasn’t a great century to be a Londoner).

We take the fact that we know these numbers for granted, but at the time, the recording of these deaths was actually a relatively recent development. This responsibility was given to parishes throughout London, since they oversaw burials of the dead. ‘Bills of mortality’ began to be published on a weekly basis in 1603, though it wasn’t until 1629 that a crucial piece of information – the cause of death – began to be included. Reading these bills, we can gain insight into an era in which human death was very different.

Some Olde English translation might be in order here. This bill is for the plague year of 1665, and reports a total of 97,306 burials, of which 68,596 were deemed to represent deaths caused by bubonic plague. Some of the other disease statistics are fairly self-explanatory; 617 ‘abortive and stillborne’, 625 ‘childbed’, and 46 ‘kild by severall accidents’. 4808 died from ‘consumption and tissick’ (consumption refers to tuberculosis, while tissick is cough), 2614 from ‘teeth and worms’ (teeth referring to children that died while teething), and 1288 from ‘griping in the guts’ (abdominal discomfort). 5 died because they were ‘distracted’, 23 from being ‘frighted’, and 14 from ‘spleen’.

While not the most rigorous or scientific of data, these numbers clearly demonstrate the dominance of infectious diseases and infant deaths as a cause of mortality, even when you ignore the plague. Today, death statistics are dominated by age-related diseases: 32% of global deaths from heart diseases, 18% from cancers, 6 % from diabetes and 5% from neurodegenerative diseases. These proportions are even higher when looking specifically at developed nations. Yet in 1665, no attempt was made to break down age-related deaths – it is simply marked that 1545 died ‘aged’. Of course, some of those recorded as dying from other diseases were likely to have been elderly – age at death still didn’t start to be recorded until the 1700s. However, it probably says something about attitudes at the time – those who died ‘aged’ were the lucky ones, able to live a full life (at least by the standards of the time) and were expected to die. Figuring out what they were dying of was not a particularly pressing concern compared to all of the early deaths that were taking place.

We are now living in an unprecedented time in human history, in which most people can expect to live long enough to get age related diseases. This is largely thanks to advancements in the last 100 years or so that made deaths from infectious diseases less prominent – improved sanitation, antibiotics, vaccines and so on. However, with this problem overcome, a new problem presents itself: an increasing proportion of the population is living with debilitating age-related diseases.

It was at one point hoped that these age-related diseases would be dealt with in the same way as infectious diseases – cured one by one, allowing people to live longer and longer. Unfortunately, unlike an infection, removing the disease from the body does not address the underlying cause. Removing a tumour from the lungs of a 70 year-old does not address the underlying biology of ageing that caused that cancer in the first place, and that person is likely to get cancer again unless something else kills them first. As a result, as treatment for these diseases improves, people are living longer but are spending those additional years of life in increasingly poor health. Lifespan has improved, but healthspan has not kept up.

To solve this problem, a primary goal of modern medicine should be to compress these years of poor health into a smaller proportion of total lifespan. The most efficient way to do this is to target the biology of ageing directly. This is because if the biology of ageing could be slowed or reversed, such that the aforementioned 70 year-old’s body had the biological function equivalent to that of a 60 year-old, then we would expect rates of cancer, heart disease, dementia, and all other age-related diseases to decrease to match those of a 60 year-old. We know this is possible in theory, as it is generally accepted that different people age at different rates, with a mix of genetic and lifestyle factors playing a role. Some people develop multiple age-related diseases in their 60s, while others can live into their 80s or 90s without any age-related diseases at all. So far, there is no drug or other therapy proven to slow ageing in humans, but there is a diverse range of promising strategies under investigation, and many are only just now entering human clinical trials.

Ageing has always been an inevitability of life with no treatment options, and it’s easy to be pessimistic about the prospects of this ever changing. Yet it’s hard to imagine that the people in 1665 London, many of whom had lived through multiple plagues already, were particularly optimistic about putting an end to plague. Yet just a few years later, microorganisms would be observed under a microscope for the first time, and the slow march towards the development of germ theory a few hundred years later would begin. And when the solutions arrived, they turned out to be relatively simple considering the scale of the problem, leading human global life expectancy to more than double over the course of 100 years. By comparison, we have a far greater understanding of the biology of ageing than the thinkers of the 17th century had of infectious disease, and the pace of scientific advancement is far greater. We can only hope that our own ‘bills of death’ will eventually look as strange to the historians of the future as those of 1665 appear to us.