On Thursday 16th October, Professor Kenneth Kendler delivered his second (and final) Loebel Lecture, entitled ‘The dappled causal world for psychiatric disorders: implications for psychiatric nosology’. You can view it online here or listen here.
Whilst Kendler’s first lecture – summarised by Roger Crisp here - focused on empirical issues, the second lecture was more philosophical. Kendler’s key question in the second lecture could perhaps be formulated as: Given the complex aetiology of mental disorders, how can we best understand and explain how they arise? Continue reading
The Genetic Epidemiology of Psychiatric and Substance Abuse Disorders: Multiple Levels, Interactions and Causal Loops
What causes psychiatric disorders, such as depression or alcohol abuse disorders? It’s obvious that background and upbringing often play a significant role, as do life events, such as losing one’s spouse or one’s job. And we also know now that genetic propensities are important. But how do these different factors inter-relate with one another? For over three decades, these issues have been at the centre of the research of Oxford’s first Loebel Lecturer, Professor Kenneth Kendler.
Professor Kendler is one of the world’s leading, and most highly cited, psychiatric researchers. He uses a range of methods, including family studies, twin and adoption studies, and molecular genetics. He also has a serious interest in the philosophy of psychiatry. His first Loebel Lecture — The Genetic Epidemiology of Psychiatric and Substance Abuse Disorders: Multiple Levels, Interactions and Causal Loops – was presented at the Oxford Martin School on Wednesday 15 October 2014, and is now available on Youtube and as an MP3 audio file. Continue reading
Kyle Edwards, Uehiro Centre for Practical Ethics and The Ethox Centre, University of Oxford
Caroline Huang, The Ethox Centre, University of Oxford
An article based on this blog post has now been published in the May – June 2014 Hastings Center Report: http://onlinelibrary.wiley.com/doi/10.1002/hast.310/full. Please check out our more developed thoughts on this topic there!
Direct to consumer genetic testing is growing rapidly; 23andMe has hired Andy Page to help the company scale – especially since it aims at having one million members by the end at the year (currently, since its launch, 23andMe has tested over 180,000 people around the world). While most ethics discussion about personal genomics has focused on the impact on individuals (is the risk of misunderstanding or bad news so bad that people need to be forced to go via medical gatekeepers or genetics counsellors? is there a risk of ‘genomization’ of everyday health? and so on), the sheer number of tested people and their ability to compare results can result in interesting new ethical problems, as a friend found out.
For years, ‘sin taxes’ – taxes on socially undesirable and/or addictive substances/activities like smoking, alcohol and gambling – have been a source of controversy. On the one hand, they have been seen as an effective means to raise revenue and reduce consumption of addictive (and generally unhealthy) substances. On the other hand, sin taxes are generally regressive and are rather paternalistic. But beyond these typical disputes, recent research has found a new and important dimension to the sin tax debate: genetics. A study by Jason Fletcher has found that whether or not taxes reduce cigarette consumption depends on the presence of a particular genotype. This suggests an interesting and novel policy: only apply the cigarette tax to those whose genotype indicates they will respond to the tax. But is this a sound policy, or should we be keeping biomarkers out of policy debates over sin taxes? Continue reading
In an interesting article, “Why we’re the best”, Oliver Poole writing in the Evening Standard yesterday claims:
Culture, environment and genes are all cited as reasons for sporting success. But it is practice that really makes perfect.
He cites evidence that it not some genetic advantage that makes Kenyan runners so great but the fact that they run barefoot from an early age. Usain Bolt? It is not that he is biologically very different – his brilliant performances are apparently due to eating yams.
It is a mistake to draw the conclusion that genetic factors are not important in sporting performance from the fact that science has not so far identified genetic contributors to sporting performance. Our understanding of our own biology is exponentially increasing but still limited. We don’t know what most genes do or even really why humans age. How much of a sporting performance is the result of innate talent, mental determination or training is difficult to say.
It’s certainly true to be a good high jumper you have to train a lot at high jump. But you also have to be tall. And how tall you can be is limited by your personal biology. It may be that elite athletes could come from any country in the world, if only they had the specialized training to bring out the potential of their gifted citizens. But one of the myths of elite sport that many of us cherish is that anyone could be the best, if only he or she tried hard enough. That, I believe, is sadly not true.
Sporting performance is likely to be mixture of innate biological capacity, training and mental application. The opportunity to be the best, or even self-supporting professional, is likely to be open to a small minority. This drives some to take dangerous performance enhancing drugs or give up or be a spectator.
If we were concerned about human well-being, we would shift our concern from elite sport to making sport a part of culture and everyday life, like tai chi. We have become a culture of elite sportspeople, investors in sport, and unhealthy spectators. Sport should be fun, good for you, the opportunity to develop talents and social. And most of all, something which is really open to all. Elite sport is not.
A great sporting performance is a beautiful and admirable thing. But it is better to be a player than a spectator, in sport and in life.