Category Archives: Diseases

Could ‘Outbreak’ Really Happen? How Climate Change Could be Behind Spread of Deadly Diseases


As much as last summer’s Ebola outbreak was politicized after it hit American shores, it left a significant deal of damage at its epicenter in West Africa, responsible for the deaths of tens of thousands. Although several treatments have been proposed, the question is whether such an event could happen again. As climate change brings about warmer temperatures into new regions, some researchers that it may be carrying tropical diseases to new places, and ignite a series of global epidemics.

Ebola and that much unwelcome staple of summer known as the West Nile virus are only two prime examples of invasive pathogens brought to new places. Zoologist Daniel Brooks and his team propose that the rising sea levels and increased warm weather leave us much more vulnerable than we realize, in a new paper he published in a British research journal.

You might wonder why a zoologist is so concerned with global warming – but the answer is pretty apparent, and further reinforces the impact that climate change has on most bodies of science. One of the prime symptoms of climate change has been the migration of species to new regions – such as South American birds recurring in more temperate forests. These species often bring parasites with them, capable of infecting new species – either affecting humans directly or through species we may use as a food source.

“Climate change does result in species moving around, and with respect to pathogens those movements actually create an enormous number of opportunities for parasites to jump into hosts they’ve never seen before,” said Brooks in an interview with VICE News.

Prior to Brooks’ work, many researchers thought parasites were specific to only one species. The new study, however, demonstrates a number of instances in which parasites successfully transitioned themselves onto other, similar organisms. One that affects rodents could just as easily infect other kinds of rodents — and would be successful because the new host has not had the evolutionary advantage of developing resistance.

Brooks’ specialty is reconstructing genealogies of species. His work brought him to investigate the last 30 years of related research and even his previous work in identifying vector-borne diseases, some of which date back to the last Ice Age.

“These host switches don’t happen at random. They’re actually clumped at particular times,” said Brooks. The end of the last Ice Age was particularly disastrous for a number of animals after the glaciers melted, increasing sea levels and driving species to higher grounds.

The West Nile outbreaks in the early 2000s are a prime warning of what could happen – their presence being detected by songbirds as they made their way across the Western Hemisphere. Although the songbirds began developing resistance rather quickly, people have not, and the virus is now considered a chronic illness for those affected. The parasite, however, remains, continuing to evolve.

So what is the best way to avert any potential outbreaks? “As long as we think of ebola as a human-to-human problem, we’re missing the possibility that if some non-human picks up ebola we never get rid of it,” Brooks continued. “We need to pay more attention to natural history.”

At some time in the not too distant past, AIDS was a simian virus before it managed to cross species. Not much was known about phylogeny at the turn of the twentieth century, but today focusing on the pathogens in animals and their genetic history might be beneficial.

Salvatore Agosta, an assistant professor at Virginia Commonwealth’s Center for Environmental Studies, supported the paper’s claims, as parasites are a great deal more adaptive than previously thought. Another prime example is Lyme Disease – once known only in the American Midwest but in the last several decades it moved not only to the Northeast but south as well.

Ben Beard of the CDC also agrees: “The simple statement is that changes of climate will affect the environment,” he told VICE News. “What’s more difficult is to say precisely where and how.”

As critical as predicting where and how any potential outbreaks will happen is to the CDC, it often receives the least amount of attention due to its speculative nature, further complicating the problem of migrating and invasive species. Texas, in particular, has withstood several epidemics of mosquito borne illnesses – many of which, such as chikungunya, are still relatively mysterious to many health care professionals.

The CDC was hit by budget cuts last year, which significantly affected the state’s trouble with tackling the number of Ebola cases it confronted over a short period of time.

James Sullivan
James Sullivan is the assistant editor of Brain World Magazine and a contributor to Truth Is Cool and OMNI Reboot. He can usually be found on TVTropes or RationalWiki when not exploiting life and science stories for another blog article.

Why the causes of cancer are more than just random ‘bad luck’


By Darren Saunders, Garvan Institute

What causes cancer? This deceptively simple question has a devilishly complex answer. So when US researchers proposed a relatively simple mathematical formula to explain a long-standing conundrum in cancer earlier this year, it was bound to get a lot of attention.

The study published in the journal Science suggested a correlation between the variation in cancer occurrence between different tissues and the number of stem cell divisions in each tissue. In other words, it said the tissues most vulnerable to cancer are those with the greatest number of stem cell divisions.

Most of the reporting about the research ran with the line that “cancer is all down to bad luck”, implying that developing the disease is out of our hands and that preventative efforts might be useless. But is that really the case?

Much of the misunderstanding seems to have arisen from the authors’ statement that a third of the variation in cancer risk among tissues is attributable to environmental or inherited factors, with the majority due to random mutations during DNA replication in normal cells. This statement about relative risk was overblown into blanket conclusions about the underlying causes of cancer.

The wonder of replication

Cancer emerges when one of the cells that make up your tissues (and organs) grows and divides without control, losing its specialised function and invading other tissue. This happens when normal control of cell growth and division is compromised through changes, or mutations, in your genome (the chemical instruction book for life).

Mutations lie at the heart of cancer biology.

The genome is made from a chemical alphabet of just four letters (A,T,G, and C) “written” into DNA. It works like a kind of computer software for our cells, with strict instructions for growth and function.

Each of the 100 trillion cells in your body contains roughly six billion letters (called nucleotides) of this code, condensed into a thin strand of DNA about two metres long. To put this into perspective, if you stretched out all the DNA in a human body it would reach around the moon and back several times.

Every time a cell divides, the genome must be copied accurately and quickly. This synthesis of new DNA is called replication, and the numbers behind it are staggering. UK researcher John Diffley has calculated that you will have synthesised the equivalent of a light-year of DNA (10 trillion kilometres) by the time you’re 50.

Words simply cannot do this amazing process justice, but this short video by award-winning animator Drew Berry will blow your mind:

DNA replication has evolved to be incredibly efficient and reliable, but random mistakes (mutations) occasionally happen. Still, they occur at a rate of less than once per genome per cell division, thanks to some impressive molecular proofreading machines, which constantly survey the newly copied DNA and correct errors.

But with so many cells dividing so often, DNA replication still represents a major source of mutations. And every cell division increases the chance of accumulating mutations in important genes, increasing the likelihood of cancer.

Other sources of mutation

Mutations can take many forms and can emerge in a number of ways – not just through replication errors. We inherit between 50 and 100 mutations from our parents at birth, for instance, and any new or de novo mutations act on this inherited genetic background.

Even normal cellular metabolism damages DNA through the production of reactive oxygen. And, in a sinister twist, many of the inherited mutations that predispose people to cancer hit genes that control the DNA proofreading and repair systems (such as the breast cancer genes BRCA1 and BRCA2). This has the effect of amplifying the rate of new mutations.

The other major causes of DNA mutation are lifestyle or environmental factors. We are exposed to a range of these in our everyday lives, such as UV radiation from sunshine, and chemicals including asbestos or from smoking cigarettes.

Lifestyle factors including diet and alcohol consumption may also contribute. Some viruses and bacteria are known to cause DNA damage leading to cancer. They include the human papillomavirus (HPV) for cervical cancer and H. pylori for gastric cancer.

Not off the hook: alcohol and diet can contribute to DNA mutations.
Erik/Flickr, CC BY-NC

Although these different agents leave unique chemical signatures in the DNA, they are still essentially random events. Random mutations are, in fact, the raw material driving evolution. And the processes of mutation and evolution are accelerated in cancer. Indeed, we are only now starting to understand the importance of evolution in driving cancer emergence and spread, as well as its resistance to therapy.

Minimising risk

Where does this leave the idea that cancer is all down to bad luck? Is modifying your lifestyle to minimise exposure to risk factors futile?

As usual, reality lies somewhere in the middle of competing narratives. Life is a kind of genetic gamble. We have to play the cards dealt us, but we can stack the odds in either direction by altering our exposure to environmental and lifestyle factors. Suggesting cancer is all down to bad luck dilutes the important message that risk can be modified by behaviour.

The cancer lexicon is littered with notions of guilt and blame. Death is often framed as “losing the battle with cancer”, for instance. And patients and their families are bombarded by gurus profiteering from various diet and lifestyle interventions. Their implicit messages can often leave people feeling that their cancer is all their own fault and wondering if there was something they could have done differently.

The fact remains that, in many cases, there isn’t.

The Conversation

This article was originally published on The Conversation.
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