Archive for April, 2012

How many genes does it take to vote…?

“2 genes predict voter turnout”

If it was as simple as that we can forego all the campaigning. That was the headline that came with a 2008 study — a watershed moment — in which in which two authors claimed that they sufficiently demonstrated that when it comes to political ideology, genes count for more than environment. The whole spectrum of political ideology and affiliation, they could distill into liberal or conservative. And, better yet, they could distill down to just two genes.

That watershed moment was probably the first in a long line of research within a growing subfield of political science known as genopolitics. Simply put, the study of genetics can be used to help us understand political behaviour and how people vote.

This follows a trend — domains and schools of thought, once the purview and authority of the human and social sciences, are now being encroached upon, infiltrated and assimilated by the harder sciences. The neurosciences has contributed more recently to the understanding of human thought than philosophers would like to admit. Throwing up conceptual issues and dilemmas that threaten to leave the philosophers behind.

The suggestion that humans exhibit inherent variability in their willingness to participate in politics is one that unlocks a whole manner of Orwellian thinking. In 2008 James Fowler and Christopher Dawes put forth that people in their study showed a gene interaction that increased the likelihood of voting. The two genes they pinpointed were monoamine oxidase (MAOA) and the serotonin transport protein 5HTT. The finding that those that had the “high” variant of the gene voted at a higher rate than those with the “low” variant.

But is it as simple as that?

The genome is a large place. The simple fact is that hundreds of genes, both in combination and permutations, have their influence on any number of social cues. This is why most studies bypass looking at the whole picture. Choosing, instead, to focus on “candidate” genes, in what is called a candidate gene association study, where gene variant is proposed to predict a given behaviour. The inherent simplicity of conducting a study in this way has, undoubtedly, shown some remarkable results. With researchers linking genes to all manner of social behaviours — from predicting voting behavior, partisanship and party identification, liberal political ideology, credit card debt, to antisocial personality, and even leadership.

The genes coded for MAOA and 5-HTT are two genes among an estimated 25,000–30,000 genes (an estimation of only protein coding genes). The two simple “high” and “low” variant polymorphisms of the two genes that the researchers looked at are simply a handful in anywhere from 3–15 million possible polymorphisms throughout the human genome. Add to this, hundreds of single nucleotide polymorphisms and structural variations, the likelihood of a specific predictive behavioural outcome becomes less and less.

In a world where every vote counts the genetics of political behaviour are becoming an increasingly interesting area of science to look at. One that straddles both sides of the fence, incorporating both social and genetic sciences. But without a more robust way of measuring genotype against phenotype (the vast array of complex behavioral traits that rely on an outdated genetic paradigm), it seems a little like robbing Peter to pay Paul.

Image — source

CHARNEY, E., & ENGLISH, W. (2012). Candidate Genes and Political Behavior American Political Science Review, 106 (01), 1-34 DOI: 10.1017/S0003055411000554

ALFORD, J., FUNK, C., & HIBBING, J. (2005). Are Political Orientations Genetically Transmitted? American Political Science Review, 99 (02) DOI: 10.1017/S0003055405051579

Fowler, J., & Dawes, C. (2008). Two Genes Predict Voter Turnout The Journal of Politics, 70 (03) DOI: 10.1017/S0022381608080638


Battlefield Theory…

Imagine the scene — from the mouth and nose, through the pharynx into the trachea, separating into the left and right main bronchi at the larynx. This is the start of your airway. This is to be the site of inflammation, or rather, the site of battle. Across the landscape that is the airways, two sides are about to go to war. Invading pathogens versus human inflammatory cells, in a war that will eventually lead to pneumonia.

To treat pneumonia we need to pin down the exact invading pathogen and treat accordingly. The most common types of infectious agents are viruses and bacteria. But of all the microorganisms that can cause pneumonia, most cases are down to only about two dozen species. Identifying the infecting agent, the actual cause of pneumonia, relies on a lengthy process; from a full patient history and examination, to imaging studies and epidemiological information, together with bacteriological tests.

Despite all of this, in up to 50% cases of pneumonia, the causative pathogen remain unidentified.

In and amongst the invading pathogens are other organisms that are just bystanders — colonizing the airway. Other commensal organisms in and amongst our instigators of war. In diagnosing pneumonia many are implicated and detecting these organisms in the airway does not necessarily mean they are the cause of infection. As such, any commensal organism that falls within a certain spread of criteria is thought to be the causative agent.

The key to all of this is the difference between colonization and infection.

To discriminate between the two types of organisms in a pneumonia infection — infectious and colonizing —  researchers from Japan came up with the “pneumonia battlefield“. The titled “Battlefield Hypothesis” allows them to be able to predict pneumonia causing pathogens.

When two sides go to war, the numbers of “combatants” on each side adequately reflects the current state of the war. The hypothesis reflects this principle. Within that scene along your airway and into the lungs, your body has amassed its troops to combat the invading pathogens. The ratio of pathogen cells to human inflammatory cells in the sputum is an index for the dominance of the pathogen along the pneumonia ‘‘battlefield.’’

It seems a simple tally of the numbers on each side can best identify the cause of pneumonia. And the best way to count up numbers on each side is by PCR. The polymerase chain reaction (PCR)-based test is routinely used as a complementary test in diagnosing pneumonia. Apart from its rapid nature and its sensitivity (being able to detect even a small number of pathogen cells), PCR can detect the non-colonizing, non-commensal organisms that are most likely to be the causative pathogen.

The problem lies in the fact that the test is unable to discriminate and distinguish a commensal organism that causes pneumonia and one that that is simply a bystander. In essence, the test is unable to tell infection from colonization. That is, until you apply the “battlefield hypothesis”.

When pneumonia occurs, the numbers of both the causative pathogen and human inflammatory cells increase at the inflammation site. The colonizing pathogen lags behind, making up a small proportion of the total combatants. In an infection, pathogen cells predominate the ladscape. And it’s this overwhelming ration that proves to be an indicating factor of the causative agent.

It seems, like in all great wars, it’s the numbers that count.

Image — source

Originally appearing in Australian Science Mag

Hirama, T., Yamaguchi, T., Miyazawa, H., Tanaka, T., Hashikita, G., Kishi, E., Tachi, Y., Takahashi, S., Kodama, K., Egashira, H., Yokote, A., Kobayashi, K., Nagata, M., Ishii, T., Nemoto, M., Tanaka, M., Fukunaga, K., Morita, S., Kanazawa, M., & Hagiwara, K. (2011). Prediction of the Pathogens That Are the Cause of Pneumonia by the Battlefield Hypothesis PLoS ONE, 6 (9) DOI: 10.1371/journal.pone.0024474

Can’t spell brioche without BRIC…

Upon learning that the peasants had no bread to eat Marie Antoinette declared
“let them eat cake (brioche)”
This anecdote came to mind as we learnt that the House of Lords economic affairs committee believes the government’s commitment to spend 0.7% of gross national income (GNI) on aid is inappropriate and should be reconsidered… launching the aid/blog/twitter-verse into action and spawning the #powerofpoint7.
This again, points to a back dated view of aid and development, one that many are trying to reverse . Meanwhile, the BRIC countries are reshaping the world in their image. And particuarly the global health world.

A new rise of South-South cooperation seems to be the new way forward. India is making drugs that are not only helping its citizens, but others across the developing world. Thereby, ensuring their own economic develoment. Ais simply viewed through a vested self- interest and economic point of view is liable to get you left behind. It is mainly through their global health efforts that the BRICS are forging forward. Not to mention a recent increase in scientific publishing.

A new report from Global Health Strategies, entitled Shifting Paradigm: How the BRICS are Reshaping Global Health and Development, was released in the lead-up to the 4th BRICS Summit in New Delhi, taking an in-depth look at the increasingly important roles Brazil, Russia, India, China and South Africa are playing to advance health and development in the world’s poorest countries.
Brazil, Russia, India, China and South Africa are injecting new resources, momentum and innovation into efforts to improve health in the world’s poorest countries. Coming as many traditional donors reduce or slow their spending, the report explores the expanding influence of the BRICS on global health and development.
While all five countries have been engaged in foreign assistance for decades, the report finds that the size and scope of their efforts have grown rapidly along with their economies. Although G7 donors still provide far more total assistance, the report estimates that the average annual growth in the BRICS’ foreign assistance spending between 2005 and 2010 was more than ten times higher than that of the G7.
Cake for thought.

Cholera riots…!

Sometime during the night on May 29th, 1832, a woman that went by the name of Mrs Clarke died. Her death was one of a series of events that sparked-off widespread rioting in Liverpool during the summer of 1832. A summer that played host to a number of “cholera riots” across various towns throughout Great Britain.

It all began that very afternoon, when Mr Clarke called for a doctor. The couple lived in a tiny cellar in Perry Street, in the east end of Liverpool, just along the wharf. The doctor was called in for a bout of persistent diarrhoea. At the time Mr Clarke had already been ill for several days. Mrs Clarke had just fallen ill that day but was clearly suffering more than her husband. The doctor’s diagnosis was clear — cholera. That evening Mrs Clarke was to be taken to Toxteth Park Cholera Hospital by way of a “palanquin”, essentially a makeshift cart carried and transported on the shoulders of several men.

What met the doctor and the Clarkes when they emerged from the cellar onto the street was a mob — “a considerable mob” as the Liverpool Chronicle described it in the newspaper two days later. More than a thousand people, consisting mostly of “women and boys of the lowest order” had gathered. The unruly mob gave chase as the palanquin left for the hospital.

At the hospital, Mrs Clarke was placed in a sallow room to be attended to. At this point she was not in a good state. The crowd gathered around the hospital where Mrs Clarke was close to death, throwing stones, rocks and pieces of broken bricks.

Mrs Clarke was close to death, while the windows cracked under the hail of rocks. The doctor attending to her in her final stages was forced to flee and take cover. The mob was in pursuit of the doctor. They harassed and chased out anyone else that got in their way. The doctor was their target — chanting “burker” and “murderer”. For them the good doctor was a charlatan and not to be trusted. A burker referring to the highly publicised selling of bodies for anatomical dissection that occurred in Edinburgh less than four years previously.

The situation grew more intense. It would be many hours before there were enough police at the scene to disperse the mob. By that time, Mrs Clarke had already died. She would be buried in a modest funeral the next day, with only a few mourners in attendance, under a sombre, heavy rain.

This, it seemed, was only the beginning. For the next three consecutive nights similar larger crowds gathered in the vicinity of the cholera hospital and other hospitals around town. These gatherings passed largely without incident or violence. That is, until the night of June 1st when police arrested two women and two men during a riot that delayed the removal of a cholera patient from hospital.

Add to this, incidents the same day involving a woman leaving hospital being chased by a mob. Two other more serious incidents occurred in the following days, with doctors and patients being harassed. The police had to be called in on each and every occasion.

In all, over ten days of violence and civil unrest was witnessed across Liverpool, seemingly as a result of a paranoid public — attacking and breaking palanquins, harassing and stalking the sick and medical professionals.

How did this woman, Mrs Clarke, the wife of a simple dock worker, erupt a series of violent riots across Liverpool? The truth is that the case of Mrs Clarke typifies the paranoia and fear of the time.

These were not the kind of riots that we normally associate with civil disobedience and unrest. This was a new kind of riot, borne out of a different kind of social setting. This was rioting over an infectious disease. Paranoia and fear were the primary instigators. Most of all, fear of cholera. Fear of a new and horrific disease. But more importantly, fear of a disease that the medical profession had no answer for.

We have to remember the epoch. John Snow’s description implicating contaminated water as a source for the disease was more than two decades away. So, at the time, no one knew anything.

Disease and death was on the tips of every one’s tongue. A dramatic disease with rapid death and high mortality. The general populous feared an infection that could spread in all directions. Not discriminating between the rich and the poor, the old or the young, and the weak or the physically fit. With no safe zone, no vaccines, remedies or protection, some called it the act of a vengeful God.

The Great Britain of the eighteen hundreds was one ripe for the spread of infectious diseases. The streets overflowing with sewage and rubbish into rivers and ditches that also served as a source of public drinking water. Liverpool witnessed overcrowding, poverty, and poor sanitation as a result of a city heaving under the heavy burden of industrialization.

These cholera riots about a disease no one knew anything of was related and connected to the wider relationship of doctors and the general public.

A few years earlier two men, William Burke and William Hare, were tried and convicted of murdering several people and selling the bodies on to hospitals for dissection. This was very much in the public consciousness at the time of the cholera epidemic. There was a public perception that cholera victims were being removed from the hospital to be killed by doctors.

The riots in Liverpool, it seemed, broke out on individual occasions across town. They moved from south to north in a haphazard and unorganised fashion. But many failed to attribute proper significance to what had happened. The press, the middle classes, and the doctors all ignored much public concern over the dissection issue, and also underestimated the seriousness of the cholera epidemic.

An epidemic that started the year before in Sunderland, recording the first case of “Asiatic Cholera” — peaked in the summer of 1832 and petered out by the end of the year. Leaving in its wake an estimated 21 882 deaths, public mistrust, fear, paranoia, and the consequence of an unusual social reaction to a disease epidemic.

Image — source.

Burrell, S. (2005). The Liverpool Cholera Epidemic of 1832 and Anatomical Dissection–Medical Mistrust and Civil Unrest Journal of the History of Medicine and Allied Sciences, 60 (4), 478-498 DOI: 10.1093/jhmas/jri061

Gill G, Burrell S, & Brown J (2001). Fear and frustration–the Liverpool cholera riots of 1832. Lancet, 358 (9277), 233-7 PMID: 11476860

Puntis J (2001). 1832 cholera riots. Lancet, 358 (9288) PMID: 11597715



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