Posts Tagged ‘ Biology ’

The Risky Business of Hunger

We like to think of ourselves as rational actors when it comes to making decisions, we take in information, process it and choose the path that we think will lead to a desirable outcome (if we aren’t deep-seated masochists I suppose). Regular readers of this blog and others that espouse a sceptical viewpoint will know that this isn’t really the case. We are influenced by a large number of factors from implicit biases, to environmental factors, and errors of thinking. The hope is that if we are aware of these factors we can go some way toward mitigating their effects and making choices that are both rational and lead to improving our lives.

Well, here’s another one for you. You may have guessed by the title of this post that it involves food and risk taking behaviour. A paper published last month in PLoS ONE out of the University College London looked at how hunger and food intake affected choices that had a monetary reward. The actual experimental design ran something like this, subjects fasted for 14 hours they then performed tasks that in effect were an idealised lottery, the tasks were performed before, directly after and an hour after a standardised meal. Over this time the subjects also had blood samples taken to measure hormones that correlate with hunger and energy reserves.

The task subjects had to perform consisted of choosing one of a pair of “lotteries” where there was a 25% chance of receiving one of four monetary amounts. Each pairing was designed so that there was always a difference in risk between the two  (see the picture it’s hard to explain).

Paired Lottery doi:10.1371/journal.pone.0011090.g002

How the subjects performed on the tasks was measured to determine the amount of risk aversion. In other words, humans have a tendency to normally prefer less risky choices. The effect of of hunger and especially immediate satiation (right after eating the meal) is to decrease this risk aversion and to make the subjects more risk neutral.

This way of referring to the subject matter is a little counter intuitive and can take a bit of getting used to, the bottom line is that the researchers looked for the point at which the subjects were equally likely to choose the “safe” bet which promised an certain average reward, and a “risky” bet that may lead to a higher average pay off but a lower chance of receiving it. Thus risk aversion has been reduced. By varying the reward amounts the researchers can measure the degree of risk aversion in each subject as the trial proceeds.

Actually the correlation is more complex than I would have thought, not only is the fact that calories are received taken into account but also the amount of calories. It seems that the size of the meal (in terms of calorific intake) is assessed to determine if it meets the rate of food intake required to meet baseline energy requirements. If it does risk aversion is increased (less risky behaviour) if not the risk aversion is decreased.

In hormonal terms this meant that a greater drop in the hormone associated with hunger was correlated with greater risk aversion but a smaller drop meant an increase in risk taking behaviour. The study authors also note that the adiposity of an individual (eg higher BMI) correlated with the size of the hormonal decrease after eating with higher BMI subjects experiencing a smaller drop and a corresponding greater increase in risk taking behaviour.

In effect we not only look at the reward in terms of the gain we will receive compared to our external resources (cash in the bank, say) but also in relation to our internal resources (metabolic requirements for example). This makes sense if we consider that for most of our history true advantage was not measured in abstract accumulation of “wealth” which we would recognise today but in available energy, including that within our bodies. That’s just a speculation of course, I’m no expert in this area.

What is the take home message of this research then? Well first off we should be careful to realise that risk taking behaviour is not limited to single domains in our lives. If you take away from this that only financial decisions are affected then that is too narrow an interpretation. In the final analysis though, no matter our eating habits or body size, we should endeavour to think over important decisions carefully and be aware of the changeable nature of our biology and it’s effects on our thinking.

Symmonds M, Emmanuel JJ, Drew ME, Batterham RL, & Dolan RJ (2010). Metabolic state alters economic decision making under risk in humans. PloS one, 5 (6) PMID: 20585383

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Ravens and Empathy: The Role of Bystanders After Conflict

ResearchBlogging.orgAt the same time as we were learning that Vegetarians and Vegans might be more empathic than Omnivores we were also discovering the nature of empathy in Ravens. Published in PLoS One recently was a paper called “Do Ravens Show Consolation? Responses to Distressed Others” looking at the behaviour of Ravens and the implications for the emotional lives of these birds.

I’m always interested in these sorts of studies as they show that each facet of human capability is not unique and the variation seen between humans and the rest of the animal kingdom is usually only a matter of degree. For some reason I find this immensely satisfying, an emotional connection with the rest of the life on this planet that I rarely encounter in the suburban environment that I inhabit.

So how do you determine empathy among Ravens?

Well, it’s tricky. Essentially you have to determine a particular behaviour that occurs under particular circumstances indicating that an element of recognition of stress in one bird triggers behaviour to reduce that stress in another bird. Follow that? I’m not sure I did. What I’m saying is that definitions matter, if you want to infer a mental state from behaviour you have to be very clear on what that behaviour is to protect against confounding factors.

In this case the behaviour investigated consisted of monitoring the interactions of the birds for ten minutes after conflicts (either chase-flight, hitting [high intensity]  or forced retreats [low intensity]) and determining whether the interactions occurred more quickly than in the corresponding ten minute time frame on a following day. In this way normal interactions could be controlled for and allow interpretation of the post-conflict interactions.

One other ingredient was also required. In order to assign significance to an interaction the so-called “value” of the relationship between interacting birds has to be known. Explicitly assigning value to a relationship is a bit of unusual concept in day-to-day life but, for example, friends and family would be classed as more valuable relationships than colleagues and acquaintances. So basically the researchers were attempting to determine who the birds friends were.

What was found was that birds who were the recipients of high intensity conflict (eg hitting) were more likely to receive interactions with high value bystanders. In other words, when birds got into a serious fight their friends came over afterwards. The correlation with conflict intensity implies that the “friends” knew when the victim would be more distressed and would need to be calmed. This insight further implies some level of empathy.

Further research might investigate what (if anything) the “friends” get out of comforting the victim. Perhaps the “friend” also becomes distressed and such interactions work to lower the stress of both the victim and the “friend”.

If such experiments seem dry compared to our experiences of empathic emotion remember that teasing out the mental states of humans is just as difficult by looking at behaviour. Consoling behaviour in humans may not indicate genuine empathy but a savvy use of circumstance to increase political control. Examinations of behaviour alone might not reveal the difference. Still, it’s nice to know that birds have friends too.

Fraser, O., & Bugnyar, T. (2010). Do Ravens Show Consolation? Responses to Distressed Others PLoS ONE, 5 (5) DOI: 10.1371/journal.pone.0010605

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Intelligent Design Flaws: The Evidence for Natural Selection in Our DNA

Here in New Zealand the debate between religion and evolution is a muted affair, while news on the topic regularly makes headlines in the US, here it goes almost beneath notice. That is not to say the clash does not exist here, merely that it tends not to intrude into the public sphere. Over time the form of the argument has changed but at its heart the source of the conflict has remained the same, discoveries in science have unseated the traditional view of a divinely created world in which Humans are the pinnacle of creation.

At this point I would like to make it clear that the findings of science are not incompatible with such a view.  Even so, to accommodate the conclusions of scientific enquiries into nature certain tenets that were previously held to be literal truths (such as 7 day creation) must be reinterpreted symbolically. As in any human endeavour there exists a spectrum of approaches to the religious significance of science’s discoveries. To some, science represents the deepest truth we can know about the world, provisional as it may be, and as such must also inform the religious outlook. For others revealed scripture is the ultimate authority and where this disagrees with science, well, so much the worse for science. Most people fall somewhere between these two extremes.

I seldom wade directly into this debate but recently came across a paper that outlines some of the peculiarities to be found in our genome (in particular but multicellular life in general) which was framed in the context of refuting design. The paper is “Footprints of Nonsentient Design Inside the Human Genome” written by John C. Avise and published in Proceedings of the National Academy of Sciences. Before getting to the crux of his argument Avise spends some time to give a brief history of three concepts that have a bearing on the discussion of design in nature. Touching on Socrates, Reverend William Paley’s famous work “Natural Theology” and Darwin’s own thoughts on the topic Avise gives a primer on how the natural world was considered in pre-Darwin times. From here we move onto the rise of modern Creationism and Intelligent Design, charting it’s progression from the early 1980s to the more recent strategy of proposing the concept of “Irreducible Complexity“.

Finally there is a similarly brief sketch of Theodicy, or the attempt to reconcile the existence suffering in the world with the traditional view of an all-powerful and all-loving deity (if you are playing charades I recommend doing “sounds like” and then try acting out Odysseus’ journey following the fall of Troy). This last seems somewhat out of place in a paper such as this but the relevance becomes clear once the author begins to expound on the multitude of human ailments that are the result of imperfections in the architecture and the replicating processes of our genome.

The numbers involved and breadth of disease in this section are truly staggering, to quote from the paper itself:

Various mutations are known to debilitate the nervous system, liver, pancreas, bones, eyes, ears, skin, urinary and reproductive tracts, endocrine system, blood and other features of the circulatory system, muscles, joints, dentition, immune system, digestive tract, limbs, lungs, and almost any other body part you can name.

In covering the various methods we use to keep track of genetic diseases, one of which being the reference text “Mendelian Inheritance in Man” Avise notes that “the current version of which describes thousands of human genes, of which more than 75% are documented to carry mutational defects associated with a disease condition.” and concerning another effort at documentation the “Human Genome Mutation Database” states “recent versions of which describe more than 75,000 different disease-causing mutations identified to date“.

After all of this preamble we finally get to the design flaws we have been promised, the first being “Split Genes”. Here is where things get technical. A quick “Genetics 101″, while we may think of genes as being discrete entities in our cells that code for the proteins making up our bodies, one gene to one protein, things are actually a lot more complicated. What actually occurs for many genes is a long stretch of DNA, some of which is needed for the gene and some of which isn’t. These parts are called Exons (needed bits) and Introns (extra bits), imagine reading Harry Potter and finding someone had randomly glued in pages from the dictionary. This means each time our cells want to make a new copy of a protein the extra bits need to be chopped out and the needed bits stitched back together first.

This process is both wasteful (unnecessary copying and fixing of the gene coding regions) and harmful, to quote once again:

“An astonishing discovery is that a large fraction (perhaps one-third) of all known human genetic disorders is attributable in at least some clinical cases to mutational blunders in how premRNA molecules are processed”

Next up is is a section discussing gene regulation and surveillance of errors. I have to say, this part is too complicated for me to parse ant this late hour. So I’ll leave that one for the adventuresome. Suffice it to say that the regulation (turning genes on and off) and copying of our genes is a complicated and error prone business, too much so if we are to consider it the perfect solution to the problem of creating human life.

The next stop on our curious ride is the mitochondria, or more specifically mitochondrial DNA. You may recall the oft repeated refrain that the mitochondria is the “powerhouse of the cell”, not to be confused with midichlorians which mediate the power of the Force. The mitochondria contain the reactions that allow us to extract energy from our food, without them you would die in very short order. It is one of the more intriguing facts about our cells that the mitochondria are equipped with their own DNA, and yet this DNA does not contain all of the information required to carry out the life giving energy reactions, it is supplemented by the DNA contained in the nucleus of the cell, your genomic DNA. Not only this but the interior of the mitochondria is a poor place to keep DNA, it is after all where energetic reactions are being carried out and toxic waste products are produced. Would you keep a valuable library in a working furnace?

These facts are all but inexplicable (and a great many more are mentioned in the paper) by appeal to a perfect designer but they are relatively easily dealt with via the paradigm that mitochondria are the remnants of a symbiotic bacteria. One which long ago insinuated itself into our cells and over the millennia has shed much of it’s own genome while housed in it’s comfortable new habitat. An analogy might be the loss of certain mathematical abilities in modern students who rely on electronic devices to to the hard work of calculation for them.

The paper goes on to deal with repeating sections of DNA, the existence of duplicated genes and pseudogenes and roving DNA that copies itself around the genome. But you can read about those for yourself, this post is already more than typically verbose. I would just like to sum up with the final hopeful run-on sentence (cousins of which plague my own writing) of the author:

“The evolutionary-genetic sciences thus can help religions to escape from the profound conundrums of ID, and thereby return religion to its rightful realm—not as the secular interpreter of the biological minutiae of our physical existence but, rather, as a respectable philosophical counselor on grander matters, including ethics and morality, the soul, spiritualness, sacredness, and other such matters that have always been of ultimate concern to humanity.”

Not exactly an uncontroversial sentiment itself.

Avise, J. (2010). Colloquium Paper: Footprints of nonsentient design inside the human genome Proceedings of the National Academy of Sciences, 107 (Supplement_2), 8969-8976 DOI: 10.1073/pnas.0914609107

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Extinction Vortex of DOOM

How is it that I’ve never heard this cool phrase before? Well not so cool for the species it applies to but still, someone was having a good brain day when that one was coined. The idea of an extinction vortex has been around for almost 25 years but I’m only just hearing about it now (maybe I was asleep, I mean uh sick, that day in biology class). As the name hints an extinction vortex describes factors affecting declining species that make extinction for that species almost inevitable.

An overview of the structure of DNA.
Image via Wikipedia

The paper that brought this phenomenon to my attention is eye-catching named “Trapped in the extinction vortex? Strong genetic effects in a declining vertebrate population“, published by researchers at the University of Gothenburg, Sweden. The paper looks at the genetic factors influencing the decline of an endangered shorebird the southern dunlin, specifically the effect of reduction of variation in the species due to inbreeding.

The most significant thing about this paper for lay readers is that the primary contributing factors pushing endangered species toward extinction need to be understood in order to put appropriate counter strategies into place. In this case the effects of inbreeding, likely due to reduced population size, have weakened the species and made it more difficult to produce healthy offspring. Protection of the nests and increasing the available habitat for the species did not significantly  impact the species’ steady decline. This implies that conservation minded programs should be aware that once a species is in decline multiple strategies, including reproductive approaches, may be required to halt the decline and bring the species back to a stable population.

With currently over six thousand threatened species recognised this would seem to be an important lesson to learn. If conservation efforts are to succeed then at risk populations must be fully evaluated to determine the approach that has the best chance. As noted by the study authors, genetic damage may be hardest to see (via casual observation) when the effects are most severe: when the damage is such that embryos perish before viable individuals can be born.

I can’t sum up better than the study authors themselves so I’ll let their own words wrap things up:

“We have shown that a declining population of a long-lived, endangered vertebrate suffers from substantial negative genetic effects. Our results highlight that ignoring genetics may underestimate the extinction risk of natural populations and thus lead to inappropriate conservation measures”

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