tag:theconversation.com,2011:/us/topics/nature-v-nurture-1586/articlesNature v nurture – The Conversation2019-04-17T08:24:39Ztag:theconversation.com,2011:article/1148512019-04-17T08:24:39Z2019-04-17T08:24:39ZHow the social lives of animals should form part of our conservation culture<figure><img src="https://images.theconversation.com/files/268587/original/file-20190410-2918-1tyh44h.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/line-elephants-family-walking-along-pasture-571055761?src=elfPQdcgPvf1eRUzTpvN3w-2-90">Shutterstock</a></span></figcaption></figure><p>Shared knowledge is an important currency for humans. It shapes everything from what we eat and how we dress, to how we raise our children. Some things we learn individually, some things we learn socially – from our parents, peers, teachers and the media. But how is shared information important for other species? </p>
<p><a href="https://www.nature.com/scitable/topicpage/gregor-mendel-a-private-scientist-6618227">Mendel’s pea breeding experiments</a> and the <a href="https://www.sciencehistory.org/historical-profile/james-watson-francis-crick-maurice-wilkins-and-rosalind-franklin">discovery of DNA</a> were huge steps in the revelation that there are physical “packets of information”, in the form of genes, passing between generations. This has been instrumental in our understanding of the evolution of biodiversity, and how organisms are shaped by their environment. </p>
<p>However, in addition to this physical transmission through DNA, there are other sources of information available in the natural world. Social information can operate both within and between different generations, and is vital in shaping how animals response to their ever changing world. </p>
<p>I have <a href="https://theconversation.com/the-social-life-of-sea-mammals-is-key-to-their-survival-61834">previously argued </a> that social knowledge is important for whales and dolphins. Research also shows that social learning is widespread across a wide variety of wildlife, from birds to elephants, from fish to meerkats. </p>
<p>Birds can learn <a href="https://www.sciencedaily.com/releases/2014/12/141203142536.htm">foraging techniques</a> from each other (such as opening the foil caps of milk bottles to extract the cream). Bottlenose dolphins <a href="https://www.newscientist.com/article/dn7475-dolphins-teach-their-children-to-use-sponges/">have been observed</a> learning from their mothers how to use sponges to help protect their jaws while foraging on the sea bed for fish.</p>
<p>Southern right whales <a href="https://www.abc.net.au/news/2015-11-18/southern-right-whale-migration-is-cultural-and-not-instinct/6950858">share migration routes</a> between critical feeding and breeding habitats. <a href="https://www.washingtonpost.com/national/health-science/what-elephants-can-teach-us-about-the-importance-of-female-leadership/2014/01/27/32db3f5e-7eeb-11e3-95c6-0a7aa80874bc_story.html?utm_term=.2a66b76b36c6">African elephants learn</a> from older matriarchs the location of watering holes, and how safe it is to interact with different social groups.</p>
<p>Evidence for social learning can be seen in the depths of the oceans, in deserts and on mountain tops. It is an important mechanism across the natural world, helping organisms adapt to changes in their environment. These adaptations often occur much more swiftly than in the slower process of natural selection, which brings about incremental change between generations.</p>
<h2>Learning the ropes</h2>
<p>Social learning is a rich seam of exploration for behavioural ecologists and conservation biologists. And because it can result in discrete units within a population which use that knowledge, it can help to inform us about focusing conservation efforts. </p>
<p>For example, understanding more about the mechanisms of social learning may be invaluable for the reintroduction of some captive-bred migratory bird species. It could help negotiate solutions in areas of human-wildlife conflict, such as when elephants or apes help themselves to human crops.</p>
<p>One of the results of social learning – not itself an endpoint, but an ongoing process – is animal culture. But what is animal culture? With our own inherited cultural perspective, it is understandable that animal culture is sometimes a challenging concept for us to grasp. </p>
<p>It is not the many and different ways in which other species are integrated into human culture (although that is interesting in itself). Animal culture can be defined as “information or behaviour, shared within a community, which is acquired from members of the same species through some form of social learning”. </p>
<p>The idea that other species have rich social lives, which includes some socially learned, collective ways of behaving that differentiate social groups, seems like a significant philosophical leap. But <a href="https://www.sciencemag.org/news/2013/04/strongest-evidence-animal-culture-seen-monkeys-and-whales">the evidence</a> is now unequivocal that humans are not alone in having distinct cultures.</p>
<p>The revelation of animal cultures raises a number of both ethical and scientific questions. But from a practical perspective, what does the existence of animal culture mean for our efforts to conserve the natural world? </p>
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<p>To better understand the relationship between animal sociality and conservation, the <a href="https://www.cms.int/en">Convention on the Conservation of Migratory Species of Wild Animals</a>, a treaty under the aegis of the <a href="https://www.unenvironment.org/?_ga=2.90981906.984352511.1554990950-1876702170.1554990950">United Nations Environment Programme</a>, has been spearheading work to explore how best to use the emerging science in this field to optimise conservation efforts. Its efforts so far are described in a <a href="http://science.sciencemag.org/content/363/6431/1032">recent article</a> in Science.</p>
<p>Beginning a serious dialogue on animal culture represents a paradigm shift in our understanding of what exactly biodiversity is. In addition to genes, specific kinds of behaviour are also an important aspect of the rich diversity of our planet.</p>
<p>In order to work towards conserving genetic diversity, we must now also work towards maintaining animal cultural diversity across different ecosystems. This is the challenge that lies ahead for global environmental agreements – a culture of conservation that respects the cultures of the natural world.</p><img src="https://counter.theconversation.com/content/114851/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Philippa Brakes receives funding from Whale and Dolphin Conservation (WDC)</span></em></p>Humans aren’t the only animals to learn survival tricks from each other.Philippa Brakes, Post-grad Researcher, University of ExeterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1044992018-11-05T13:28:43Z2018-11-05T13:28:43ZBlueprint by Robert Plomin: latest intelligence genetics book could be a gift for far-right<figure><img src="https://images.theconversation.com/files/243649/original/file-20181102-83651-1izpvui.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">shutterstock</span></span></figcaption></figure><p>In the prologue of his new book <a href="https://www.amazon.co.uk/Blueprint-How-DNA-Makes-Who/dp/0241282071">Blueprint</a>, psychologist Robert Plomin explains that he has been waiting 30 years to write this. In part, he says, his “cowardice” in the face of the personally and professionally “dangerous” nature of his work on genetics put him off until now. </p>
<p>The book’s central theme is laid out from the very start. DNA can “tell your fortune from the moment of your birth, it is completely reliable and unbiased”. Plomin then takes the reader through his scientific research into twins and the human genome, and argues that genetics bring huge implications for parents and public policy alike.</p>
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<p>DNA is the major systemic force, the blueprint, that makes us who we are. The implications for our lives – for parenting, education and society – are enormous. </p>
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<p>On the science, Plomin has previously expressed his support for Richard Herrnstein and Charles Murray’s racial premises in their notorious 1994 book, <a href="https://www.amazon.co.uk/Bell-Curve-Intelligence-Structure-Paperbacks/dp/0684824299">The Bell Curve: Intelligence and Class Structure in American Life</a>. The Bell Curve is highly controversial because it claims black Americans are on average significantly less intelligent than white – and suggests that genetics plays a major role in this.</p>
<p>Plomin was a leading signatory of <a href="http://www.intelligence.martinsewell.com/Gottfredson1997.pdf">The Mainstream Science on Intelligence</a>, a statement issued by a group of academic researchers in support of The Bell Curve’s racial “science” and originally published in the Wall Street Journal in December 1994. Below is an extract:</p>
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<p>The bell curve for whites is centred roughly around IQ 100; the bell curve for American blacks roughly around 85 … Heritability estimates range from 0.4 to 0.8 … indicating genetics plays a bigger role than environment in creating IQ differences.</p>
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<p>This is a view about genetics, race and intelligence <a href="https://www.theguardian.com/education/2014/feb/18/psychologist-robert-plomin-says-genes-crucial-education">Plomin has not expressly disavowed</a>. And based upon this “scientific” view of race, Herrnstein and Murray make specific policy proposals in their book, such as a radically reduced welfare state and the end of affirmative action.</p>
<p>Plomin, on the other hand, does not mention race at all in Blueprint – as with his recent book which looked at the role of genetics in education <a href="https://www.wiley.com/en-gb/G+is+for+Genes%3A+The+Impact+of+Genetics+on+Education+and+Achievement-p-9781118482780">G is for Genes</a>. This seems an extraordinary omission given the explosive implications of a scientific theory underpinned by an assumption of racial difference in intelligence. </p>
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<figcaption><span class="caption">Robert Plomin on Blueprint (book trailer).</span></figcaption>
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<p>Plomin also insists in Blueprint that “no specific policy implications follow from finding that inherited DNA differences are by far the most important source of individual differences”. But policy at present is based entirely upon environmental factors, like social need or the type of school a child attends. A shift to allocating public resources according to people’s DNA would have the most profound policy implications imaginable. </p>
<h2>Personalising education</h2>
<p>Indeed, in G is for genes, Plomin and co-author Kathryn Asbury argue that a child’s education should be “personalised” through the use of preschool DNA testing and followed by regular IQ testing. In Blueprint, Plomin explains that “if all you know about people is their DNA, you can indeed predict their school achievement”.</p>
<p>But if Plomin’s science as laid out in the statements he has made – including his support for the one published in the Wall Street Journal – is correct, education led by DNA and IQ testing would surely be racialised. This would mean most black children would receive a “personalised” education aimed at learners of below average intelligence – who can be expected to make only modest academic achievements due to their genes. This in itself seems worthy of mention in a book which has taken 30 years to write. </p>
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Read more:
<a href="https://theconversation.com/the-iq-test-wars-why-screening-for-intelligence-is-still-so-controversial-81428">The IQ test wars: why screening for intelligence is still so controversial</a>
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<p>David Gillborn, a professor of critical race studies as Birmingham University, <a href="https://www.tandfonline.com/doi/abs/10.1080/02680939.2016.1139189?src=recsys&journalCode=tedp20">noted</a> that in a 2015 <a href="https://www.bbc.co.uk/sounds/play/b06j1qts">BBC interview</a>, Plomin himself described his approach to the racial implications of his work as “softly, softly”. This was because, he said, reporting on his views on racial difference “is a distraction to my research”.</p>
<p>In Blueprint, Plomin’s account of <a href="https://www.kcl.ac.uk/ioppn/depts/sgdp-centre/research/twinsearlydevelopmentstudy(teds).aspx">his renowned longitudinal study</a> of twins – since he arrived in the UK from the US in 1994 – is fascinating. His account of <a href="https://www.ebi.ac.uk/training/online/course/gwas-catalog-exploring-snp-trait-associations/why-do-we-need-gwas-catalog/what-are-genome">Genome Wide Association Studies (GWASs)</a>, based on vast data banks, and <a href="https://ghr.nlm.nih.gov/primer/genomicresearch/snp">Single Nucleotide Polymorphisms</a> – tiny snippets of genetic information which together create our human traits – is gripping. </p>
<p>Yet in the end with Blueprint, there exists a risk that readers end up impressed by Plomin’s account of his science without being aware of the <a href="https://www.spectator.co.uk/2018/10/heredity-is-only-half-the-story/">racial and social implications of his theory</a>. And in the context of a resurgent right wing across the world <a href="https://theconversation.com/how-the-alt-right-uses-milk-to-promote-white-supremacy-94854">looking for “scientific” reasons to elevate race in public policy</a>, this seems profoundly irresponsible. </p>
<p>Maybe Plomin thought this was the right way to tackle the more difficult history associated with his work. But <a href="https://www.theguardian.com/news/2018/mar/02/the-unwelcome-revival-of-race-science">scientific racism</a> has never gone away. And ultimately, by avoiding the issue, his latest book could well attract unwanted attention from the wrong type of readers.</p>
<p><em>Robert Plomin was approached and declined to comment.</em></p><img src="https://counter.theconversation.com/content/104499/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Eric Joyce does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Genetic research on human behaviour has long been linked with eugenics and continues to attract interest from far-right groups.Eric Joyce, Doctoral Candidate in Education, University of BathLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/908522018-01-31T19:04:43Z2018-01-31T19:04:43ZKids’ learning and health is shaped by genes they don’t inherit, as well as genes they do<figure><img src="https://images.theconversation.com/files/204124/original/file-20180130-38198-yodzcu.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">There's fresh evidence to inject into the old 'nature versus nurture' debate. </span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/dannywilson/478740385/in/photolist-JiEQz-JiEPv-B7QUv-4i66py-WgWWbC-dZK4M-fC7Nc-VWAi81-c2Fxdo-no4azq-P33jf-P33hd-nCuWLu-WkfBXD-fAMmUv-ggGe1-6rNMb8-35PBhZ-5adAjG-9b7Knw-9YcZuu-ejZv31-2TH3i-eqXVCh-WkfyDK-4Z6ZtR-6Aet1c-P38uA-jiRbd-4KrqjW-Nj6ck-bQryRk-nXsM1J-6WZ1Fv-4Uf8Xy-88ipMh-R25cH-eqXVFo-P33eJ-Brq1K-niAES8-67Pe5e-JiERg-74XieZ-88tW1W-pwQRPx-9ywAMt-qc9BQT-9D6oBS-qtqNEx">dannywilson/flickr </a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span></figcaption></figure><p>It’s a hoary old debate: how much do our genes define how we grow and learn, and how much is due to the environment? A <a href="https://www.ncbi.nlm.nih.gov/pubmed/29371463">new study</a> by Kong and colleagues shows that parents’ genes, even those not passed on to children, have major effects on kids’ health and educational attainment. </p>
<p>Although this discovery has been reported by some as “<a href="https://www.nytimes.com/2018/01/25/science/children-parents-genes-education.html">headspinning</a>”, to me it is not too surprising. </p>
<p>We already know parents contribute genes that directly influence development, and that the child’s environment determines how these genes have an effect. </p>
<p>But a crucial part of this environment is the parents. To me, this new study highlights the importance of parental genes in shaping how we are raised. </p>
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Read more:
<a href="https://theconversation.com/not-just-about-sex-throughout-our-bodies-thousands-of-genes-act-differently-in-men-and-women-86613">Not just about sex: throughout our bodies, thousands of genes act differently in men and women</a>
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<h2>Genes and human development</h2>
<p>We know from many studies that most aspects of human growth and development are strongly influenced by the genetic make-up of the child. For instance, comparing identical and non-identical twins shows <a href="https://doi.org/10.1016/j.tine.2015.06.001">big genetic components</a> for such physical differences as height and weight, as well as for many behaviours, including learning ability.</p>
<p>But we also know all of these traits are strongly influenced by the environment. For instance, height can be stunted by poor nutrition, and learning ability limited by poverty.</p>
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<img alt="" src="https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/204143/original/file-20180131-38229-1hcagz0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">The development of these triplets will be shaped by their genes and their environment.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/portrait-newborn-triplets-lying-bed-629762906">from www.shutterstock.com</a></span>
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<p>Hundreds – probably thousands – of our 20,000 genes contribute to these qualities. For each gene, different variants (called “alleles”) may produce differences – large or small – in how children develop.</p>
<p>The way to identify these genes is to compare the genetic make-up of many people and see what alleles correlate – that is, show a statistically relevant match-up – with particular traits. This used to be tough when we were working one gene at a time, using clumsy ways to identify alleles by their DNA sequence or by the proteins they make. </p>
<p>Now that DNA sequencing is cheap, scientists can look at the whole genome of thousands of children, and their parents, and identify sequence differences all over the genome. This technique, called genome-wide association study (GWAS), has identified many human genes involved in <a href="https://www.nature.com/scitable/nated/topicpage/finding-genes-for-common-diseases-using-gwas-132732965">normal development and human diseases</a>. </p>
<p>For example, we know from a study of 100,000 people that 74 regions of the genome are associated with “<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751588/">educational attainment</a>” (the number of years spent studying). </p>
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Read more:
<a href="https://theconversation.com/no-epigenetics-and-environmental-responsiveness-dont-undermine-darwinian-evolution-65647">No, epigenetics and environmental responsiveness don’t undermine Darwinian evolution</a>
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<h2>Gene effects at a distance</h2>
<p>A child receives one copy (allele) of each gene via an egg from the mother, and another allele of each gene via a sperm from the father. Because mothers and fathers are likely to have slight sequence differences in most of their genes, it is easy (for a computer, that is) to identify for each gene which allele came from mum and which from dad.</p>
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<img alt="" src="https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=440&fit=crop&dpr=1 600w, https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=440&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=440&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=553&fit=crop&dpr=1 754w, https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=553&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/204179/original/file-20180131-38226-16gs0o8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=553&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Each sperm and egg carries one allele (variant) of each gene.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/sperm-fertilize-ovum-3d-illustration-791567170?src=pKX695GE8cqyQED_D8WF1A-1-99">from www.shutterstock.com</a></span>
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<p>It is also easy to do the opposite: tell which of the mother’s or father’s two alleles was transmitted to the child, and which allele did not make it into that particular contributing egg or sperm.</p>
<p>Most GWAS studies analyse only those parental alleles that were transmitted to the child. The new study deliberately looks at the parental alleles that were not transmitted. </p>
<p>The study traced genes in 21,637 men and women in Iceland, where genome data are available for the whole population. They looked in one or both parents to figure out which alleles of genes were transmitted to each subject, and discover which weren’t.</p>
<p>Then they correlated the non-transmitted parental alleles to aspects of education and health in their children. They found, overall, that non-transmitted alleles added up to major effect on the educational attainment of the child, nearly a third of the direct effect of the children’s own genes. Non-transmitted alleles had the same effect won educational attainment whether they were in mothers or fathers.</p>
<p>It was similar for components of growth and health: height, weight, body mass index, use of glucose and fat metabolism in the body, and even the number of cigarettes smoked. Again, the non-transmitted parental alleles (especially the mother’s) were found to have a major effect, even though they didn’t end up in the children. </p>
<h2>The nature of nurture</h2>
<p>So why am I not surprised by this new finding?</p>
<p>We have known for a long time that the genetic make-up of the mother may have a strong effect on the development of her offspring. “<a href="http://onlinelibrary.wiley.com/doi/10.1111/evo.12905/full">Maternal effect genes</a>” have been <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666680/">studied for decades</a> in domestic animals, even fish and fruit flies. </p>
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Read more:
<a href="https://theconversation.com/x-y-and-the-genetics-of-sex-professor-jenny-graves-awarded-the-prime-ministers-prize-for-science-2017-85740">X, Y and the genetics of sex: Professor Jenny Graves awarded the Prime Minister's Prize for Science 2017</a>
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<p>In humans and other mammals, such genes influence health and nutritional status of the mother during pregnancy, and the supply and make-up of her milk. This has big effects on the growth and development of the fetus and the infant. So it is not surprising that, in this study, the mothers’ non-transmitted alleles have a greater effect on their children’s health than those from the father. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=398&fit=crop&dpr=1 600w, https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=398&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=398&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=500&fit=crop&dpr=1 754w, https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=500&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/204128/original/file-20180131-38213-1z032b2.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=500&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Genes that determine the amount and quality of breastmilk influence child development.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/close-mother-breast-feeding-her-newborn-1009131850?src=wbRzYqxyslzPniRBXHyVFA-1-7">from www.shutterstock.com</a></span>
</figcaption>
</figure>
<p>But how would the father’s non-transmitted genes work? And how would parental genes affect the ultimate education attainment of their child?</p>
<p>The transmission of influence must be via the parents’ parenting behaviour, which is itself partly genetically determined. The priorities that parents place on reading, sport, use of alcohol and cigarettes are all shaped by genes, and create a home environment that influences children for better or for worse. </p>
<p>This work emphasises that parents are critical components of their child’s environment. Their contribution to their children’s welfare is not only directly through the alleles they pass on, but also indirectly through their own genetic make-up that influences who they are and how they raise their children. </p>
<p>Kong calls this “genetic nurture”. But I wonder if his work has inadvertently started to identify genes that contribute to “good parenting”?</p><img src="https://counter.theconversation.com/content/90852/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Jenny Graves receives funding from the Australian Research Council </span></em></p>A new paper describes the idea of “genetic nurture”, where parents’ genes, even those not passed on to their child, have major effects on kids’ health and educational attainment.Jenny Graves, Distinguished Professor of Genetics, La Trobe UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/828932017-10-16T00:32:32Z2017-10-16T00:32:32ZHealth Check: why are some people afraid of heights?<figure><img src="https://images.theconversation.com/files/187302/original/file-20170925-18346-uw6a4o.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Don't look down ... do we develop a fear of heights because of past bad experiences or are some of us just born that way?</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/download/confirm/290697971?src=YJxbHep_7vz3gssROneh-Q-1-5&size=medium_jpg">from www.shutterstock.com</a></span></figcaption></figure><p>If you’ve ever felt your heart race as you looked down from the top of a tall ladder, you’re not alone. But for some people, their distress is far more serious. Simply thinking about climbing a ladder can lead to intense fear and anxiety.</p>
<p>These are the roughly <a href="https://link.springer.com/article/10.1007%2Fs00406-014-0548-y">one in 15 people</a> who have a fear of heights (<a href="https://psychcentral.com/encyclopedia/acrophobia/">acrophobia</a>) at some point in their lives.</p>
<p>So, what leads some people to feel anxious even thinking about climbing the ladder? And others happily climb up onto the roof?</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/explainer-what-are-phobias-9667">Explainer: what are phobias?</a>
</strong>
</em>
</p>
<hr>
<h2>What is acrophobia?</h2>
<p>About <a href="https://link.springer.com/article/10.1007/s00415-012-6685-1">one in three people</a> say they experience some discomfort or distress when exposed to heights. But not all of these have acrophobia. The term <a href="https://psychcentral.com/encyclopedia/acrophobia/">acrophobia</a> is reserved for people with extreme, irrational and persistent fears of heights and situations associated with them.</p>
<p>It’s one of the so-called <a href="https://www.beyondblue.org.au/the-facts/anxiety/types-of-anxiety/specific-phobias">natural environment phobias</a>, which also include a fear of thunder and lightning (astraphobia) or water (aquaphobia).</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/fear-of-death-underlies-most-of-our-phobias-57057">Fear of death underlies most of our phobias</a>
</strong>
</em>
</p>
<hr>
<p>People with acrophobia <a href="https://www.sydneyphobiaclinic.com.au/programmes/acrophobia/">often avoid situations</a> where they will be exposed to heights. However, this is not always possible.</p>
<p>When faced with heights or anticipating them, their <a href="https://backyardbrains.com/experiments/Sympathetic_Nervous_System">sympathetic nervous system</a> is aroused, as if preparing the body for an emergency. This arousal helps either approach or escape from a threat (commonly known as the <a href="https://www.britannica.com/topic/fight-or-flight-response">fight-or-flight response</a>).</p>
<p>They may experience <a href="http://www.nhs.uk/conditions/vertigo/Pages/Introduction.aspx">vertigo</a> (a moving or spinning sensation), increased heart rate, shortness of breath, sweating, <a href="http://www.sciencedirect.com/science/article/pii/S0005796709000229">anxiety</a>, shaking or trembling, and <a href="https://theconversation.com/explainer-why-do-we-get-butterflies-in-our-stomachs-72232">nausea or an upset stomach</a>.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/explainer-why-do-we-get-butterflies-in-our-stomachs-72232">Explainer: why do we get butterflies in our stomachs?</a>
</strong>
</em>
</p>
<hr>
<p>A fight-or-flight response can be <a href="https://link.springer.com/chapter/10.1007/978-0-387-72577-2_12">adaptive</a> in dangerous situations, because it can help us respond to dangerous situations. </p>
<p>But in people with acrophobia, this response can occur when <a href="https://www.scientificamerican.com/article/why-do-we-panic/">no danger is present</a>. For instance, some people are extremely distressed when thinking about heights. </p>
<p>There are <a href="http://dx.doi.org/10.1037/a0017759">two main perspectives</a> about how acrophobia develops. Broadly, fears and phobias are either innate (evolutionary perspective) or learned (behaviourist perspective). </p>
<h2>Are we born with a fear of heights?</h2>
<p>According to the <a href="http://www.iep.utm.edu/evol-psy/">evolutionary psychology perspective</a>, fears and phobias are innate. That is, people can experience a fear of heights <a href="http://www.sciencedirect.com/science/article/pii/S0005796797100377">without direct (or indirect) contact</a> with heights. Instead, acrophobia is somehow hardwired so people have this fear before they <a href="http://www.sciencedirect.com/science/article/pii/000579679390093A">first come into contact</a> with heights.</p>
<p>Evolutionary psychologists suggest people who are afraid of heights are more likely to escape from this potentially dangerous situation or avoid it altogether. By doing this, they are then more likely to survive and later reproduce, allowing them to pass on their genes. Researchers suggest that as a result, this fear has been passed down from generation to generation. </p>
<p>But this mechanism cannot account for all phobias. Innate phobias must reflect objects or situations that have presented a <a href="http://www.sciencedirect.com/science/article/pii/S0005796701000456">long-term threat to human survival</a>. Avoiding the object or situation must also increase opportunities for reproduction. </p>
<p>While the evolutionary perspective may explain phobias such as a fear of heights or snakes, it has difficulty explaining phobias associated with going to the dentist or public speaking. </p>
<h2>Do we learn to be afraid of heights?</h2>
<p>According to <a href="http://www.iep.utm.edu/behavior/">behaviourists</a>, fears and phobias are learnt, most commonly due to what’s known as <a href="https://blogs.scientificamerican.com/thoughtful-animal/what-is-classical-conditioning-and-why-does-it-matter/">classical conditioning</a>.</p>
<p>To demonstrate how <a href="http://www.sciencedirect.com/science/article/pii/014664029290010L">classical conditioning of phobias</a> occurs, consider the following scenario. </p>
<p>Imagine you climbed a tree for the first time. What is your reaction to being up a tree? According to the behaviourist perspective, you’d be unlikely to be afraid. But if you then fell from the tree, you would likely experience distress and fear. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=131&fit=crop&dpr=1 600w, https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=131&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=131&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=164&fit=crop&dpr=1 754w, https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=164&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/185442/original/file-20170911-28514-1nhvy6z.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=164&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">The first time you climb a tree, it’s unlikely you’d be afraid. But if you then fell from the tree, you’d likely experience distress and fear.</span>
<span class="attribution"><span class="source">pixabay.com</span></span>
</figcaption>
</figure>
<p>A behaviourist would expect that because the experience of being up high is followed by the trauma of falling, you may then learn to associate the negative event with heights.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=134&fit=crop&dpr=1 600w, https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=134&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=134&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=168&fit=crop&dpr=1 754w, https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=168&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/185443/original/file-20170911-28478-6pnvdn.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=168&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">You learn to associate the neutral stimulus (heights) with the fear-evoking stimulus (falling). So, you feel fear and distress the next time you are faced with heights.</span>
<span class="attribution"><span class="source">pixabay.com</span></span>
</figcaption>
</figure>
<p>Because of these learnt associations between heights and trauma, behaviourists suggest people can then be afraid of heights in future encounters. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=137&fit=crop&dpr=1 600w, https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=137&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=137&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=173&fit=crop&dpr=1 754w, https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=173&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/185444/original/file-20170911-28478-1eta5b2.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=173&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Linking fear with heights means when someone encounters the original situations (heights) they show a fear response to something that they previously showed no or a neutral response to.</span>
<span class="attribution"><span class="source">pixabay.com</span></span>
</figcaption>
</figure>
<p>The behaviourist perspective also has some problems. It finds it difficult to explain why people who have never been exposed to an object or situation can report a phobia. For example there are no snakes in New Zealand, but there are people in New Zealand with <a href="https://www.mentalhealth.org.nz/get-help/a-z/resource/24/phobias">snake phobias</a>. </p>
<p>Behaviourists also suggest fears and phobias can also be learnt <a href="http://www.sciencedirect.com/science/article/pii/S0272735808000901">vicariously</a>. So behaviourists suggest it may be that some people in New Zealand may have learnt their fear of snakes by hearing stories from other people with a fear of snakes. </p>
<p>In reality, the best explanation may be a mix of both behaviourist and evolutionary perspectives.</p>
<h2>Can it be treated?</h2>
<p>In treatment, both evolutionary and behaviourist accounts draw on <a href="http://www.sciencedirect.com/science/article/pii/S0887618509000280">the behaviourist perspective of how fears and phobias are learnt</a>. </p>
<p>Systematic desensitisation (or exposure therapy) is a <a href="https://www.mja.com.au/journal/2017/206/6/systematic-review-and-meta-analysis-treatments-acrophobia">commonly used therapy</a> for various phobias, whether the fear is innate or learnt.</p>
<p>It involves <a href="https://theconversation.com/how-virtual-reality-spiders-are-helping-people-face-their-arachnophobia-73769">gradual exposure</a> to the feared object or situation in a safe and controlled environment. This is so that when coming into contact with the feared object or situation, people learn that they are not in danger and no longer experience a phobic response. </p>
<hr>
<p><em>If this article has raised concerns for you or someone you know, please contact beyondblue for <a href="https://www.beyondblue.org.au/the-facts/anxiety/types-of-anxiety/specific-phobias">more information about phobias</a> and how to treat them.</em></p><img src="https://counter.theconversation.com/content/82893/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>There are two schools of thought to explain people’s height phobias: evolutionary and behavioural.Bek Boynton, PhD Candidate, James Cook UniversityAnne Swinbourne, Senior Lecturer, Psychology, James Cook UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/614412016-09-13T12:52:44Z2016-09-13T12:52:44ZWhy isn’t there a gene for depression?<figure><img src="https://images.theconversation.com/files/131123/original/image-20160719-8014-r3r874.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Dark skies.</span> <span class="attribution"><span class="source">Shutterstock</span></span></figcaption></figure><p>Depression is sometimes categorised as a mental, rather than a <a href="http://bjp.rcpsych.org/content/178/6/490">physical illness</a> – as though somehow mental health is different from physical health. But the brain is not a magical black box inside your head. It is an organ, just like the heart or lungs, made up of cells and supplied with blood. </p>
<p>These brain cells grow and develop, making contact with other brain cells to communicate with one another. They control all of our behaviour, emotions and actions. And sometimes they go wrong, leading to illnesses like depression.</p>
<p>Depression does <a href="http://edition.cnn.com/2009/HEALTH/03/24/suicide.hereditary.families/">run in families</a>, which could mean depression is genetic, an inherited condition. But families don’t just share genes – they also experience a similar environment. So how can we separate genetic influences on depression from environmental factors?</p>
<p>Twins are a useful tool for studying the influence of genes and the environment on many diseases. They can be identical (one egg splits to form two babies) and share the exact same genetic make up, or nonidentical (two separate eggs form two babies), sharing half of the genes. By studying genetically identical twins raised together in the same family environment, we can examine whether differences in depression rates might be due to non-shared environmental factors. </p>
<p><a href="https://genepi.qimr.edu.au/contents/p/staff/CV432.pdf">Analysis</a> in 2005 of a large number of twin studies indicated that around 40% of the risk of developing depression is genetic, and the remaining 60% associated with non-shared environmental factors. It is therefore too simplistic to say diseases like depression are either genetic or environmental. Both play their part.</p>
<p>Given that depression, like cancer, is not one single illness, it is perhaps not surprising that a single gene for depression has not been found. The variety of experiences also makes it difficult to find the right patient groups to study. People with depression may experience a single episode, or repeated episodes. They may develop depression in childhood, adolescence or later in life. Symptoms can vary, and include sleep disturbance, body weight changes, loss of interest in everyday activities, feelings of guilt and worthlessness, and suicidal thoughts. </p>
<p>The psychiatric <a href="http://www.med.unc.edu/pgc/">genetics consortium group</a> is a collaboration of hundreds of international scientists from 38 countries who share data from almost a million depressed patients worldwide. It <a href="https://www.sciencedaily.com/releases/2015/01/150107122305.htm">concluded in 2015</a> that most of the genetic effects found so far in the scientific literature are not very reliable or robust. But this does not mean genes are not involved. It just means we haven’t really done the right studies yet – because depression is such a variable condition. </p>
<p>Grouping together people with different diagnoses of depression also makes it hard to identify genetic contributions. Breakthroughs in understanding cancer in the last 20 years have really come from being able to <a href="https://theconversation.com/hard-evidence-are-we-beating-cancer-20870">separate breast cancer</a> from lung cancer from prostate cancer. But this is yet another challenge in depression research where symptoms and diagnoses are relied upon rather than a blood test for <a href="https://theconversation.com/a-blood-test-alone-wont-be-enough-to-test-for-suicide-risk-17331">specific markers</a> that can tell us that one patient has the same type of depression as another patient. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=300&fit=crop&dpr=1 600w, https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=300&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=300&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=377&fit=crop&dpr=1 754w, https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=377&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/131128/original/image-20160719-8005-16n6k44.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=377&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">A DNA sequence or events?</span>
<span class="attribution"><span class="source">shutterstock</span></span>
</figcaption>
</figure>
<p>Another consortium of scientists known as <a href="http://www.well.ox.ac.uk/converge">CONVERGE</a> has had some success in identifying genes involved in depression in an ongoing research project. They published findings from a carefully defined subgroup of severely depressed Chinese women patients with recurrent major depressive disorder. Over 10,000 participants had their DNA sequenced, which revealed <a href="https://www.neuroscience.ox.ac.uk/publications/539174">small changes in two genes</a> that were linked to major depressive disorder: the LHPP gene and the SIRT1 gene. Both are involved in cellular metabolism (how cells generate energy and signals) but their potential function in depression is not yet known.</p>
<p>Then a <a href="https://www.sciencedaily.com/releases/2016/08/160801113648.htm">recent US study</a> of more than 300,000 people of European descent reported different genes being associated with depression. In contrast to the CONVERGE group, they tried to get as many people as possible to have their DNA analysed via a commercial genomics company. This resulted in a very different population being studied including people self-reporting with depression. It remains to be tested whether these latest “genes for depression” can be verified.</p>
<h2>Environmental factors</h2>
<p>Some people don’t like the idea that there are “genes for depression” because they think that means getting the illness is somehow inevitable. But this view overlooks the adaptable nature of our brains and our genes. Genes are like a set of very complex instructions which tell the cells what proteins to make, and their activity can change, helping brain cells adapt to different situations. And let’s not forget the other factor determining liability to develop depression: the environmental influences you are exposed to, <a href="http://sciencenordic.com/how-stress-can-cause-depression">such as stress</a>. </p>
<p>So is there a gene for depression? No, there isn’t. We don’t have genes for diseases, we have genes that encode proteins that serve functions in cells.
So does that mean if your DNA has the relevant change in your LHPP or SIRT1 genes that you are going to develop depression? No, it probably means you may have an increased risk to develop depression depending on the environment you experience.</p>
<p>In the same way that we think about heart disease, cancer, obesity as having multiple “susceptibility genes”, the same is probably true for depression. It is likely that there are small changes in a number of genes, each contributing a little bit to dysfunction of your brain cells, which can then lead to you developing depression. We are finding out more all the time – and that is surely an uplifting thought.</p><img src="https://counter.theconversation.com/content/61441/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sarah Bailey has received research funding from the Wellcome Trust, Medical Research Council, the Royal Society and Janssen Pharmaceutica.
Sarah Bailey is a member of council for the British Association for Psychopharmacology and serves on the Education & Training Committee/ Animal Welfare and In Vivo Pharmacology group of the British Pharmacological Society.</span></em></p>It is an illness that runs in families – but there are other factors which go beyond inheritance.Sarah Bailey, Senior Lecturer, Neuropharmacology, University of BathLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/628442016-07-26T07:56:33Z2016-07-26T07:56:33ZCan genes really predict how well you’ll do academically?<figure><img src="https://images.theconversation.com/files/131420/original/image-20160721-32606-11008mz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/s/university+graduation/search.html?page=3&thumb_size=mosaic&inline=183338696">Rawpixel.com/Shutterstock</a></span></figcaption></figure><p>Researchers at King’s College London say they are able <a href="http://doi.org/10.1038/mp.2016.107">to predict educational achievement</a> from DNA alone. Using a new type of analysis called a “genome-wide polygenic score”, or GPS, they <a href="https://theconversation.com/your-genes-can-help-predict-how-well-youll-do-in-school-heres-how-we-cracked-it-62848">analysed DNA samples from 3,497 people</a> in the ongoing <a href="https://www.teds.ac.uk/">Twins Early Development Study</a>. They found that people whose DNA had the highest GPS score performed substantially better at school. In fact, by age 16, there was a whole school-grade difference between those with the highest GPS scores and the lowest. The researchers herald their findings as a “tipping point” in the ability to use DNA – and DNA alone – in predicting educational achievement.</p>
<p>These findings will certainly generate debate, particularly about nature versus nurture. It’s a debate that forces us – often uncomfortably – to think about what makes us who we are. Are our careers, hobbies, food preferences, income levels, emotional dispositions, or even general success in life rooted in our genes (nature)? Or are we shaped more by our environment (nurture)? If it’s all down to our genes, what happens to the idea of determining our own destiny? </p>
<p>When it comes to the subject of intelligence, which today includes behavioural genetics research into “<a href="http://doi.org/10.2307/1412107">g</a> (a measure of intelligence commonly used as a variable in research in this area) and <a href="http://doi.org/10.1177/0956797612457952">cognitive ability</a>, the nature-nurture debate becomes that much more heated.</p>
<p>There is a growing body of research that suggests intelligence is a <a href="http://doi.org/10.1038/mp.2012.184">highly heritable and polygenic trait</a>, meaning that there are many genes that predict intelligence, each with a small effect size. While the connection between genetics research on educational achievement and findings on intelligence might not seem direct, studies like the one out of King’s establishes a biological connection between "g” and educational achievement. The findings mark the strongest genetic prediction for educational achievement so far, estimating up to 9% of variance in educational achievement at age 16. </p>
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<p>But <a href="http://doi.org/10.1002/hast.497">despite claims</a> that this research moves “us closer to the possibility of early intervention and personalised learning”, there are important ethical concerns to take into account. For example, who would early intervention and personalised learning reach first? Is it possible parents with money, means, awareness and access would be first to place their children in <a href="http://eu.wiley.com/WileyCDA/WileyTitle/productCd-1118482786.html">“genetically sensitive schools”</a> in the hope of getting an extra advantage? </p>
<h2>Dark past</h2>
<p>It is not a secret that the history of intelligence research, and by extension genetics research on cognitive ability or educational achievement, is <a href="http://onlinelibrary.wiley.com/doi/10.1002/hast.492/abstract">rooted in eugenics and racism</a>, and has been used to validate the existence of racial and class differences. So how does this shameful past impact the field of behavioural genetics research today? </p>
<p>Many behavioural geneticists, like Robert Plomin, the senior author on the King’s study, believe the field has moved past this dark history and that the science is objective, neutral (as neutral as any research can be) and clear. The controversies that surround this research, at least in the eyes of Plomin and others, are fuelled by <a href="http://eu.wiley.com/WileyCDA/WileyTitle/productCd-1118482786.html">media sensationalism</a>.</p>
<p>But many bioethicists and social scientists disagree with him. They argue that society values intelligence too much for this research to remain in neutral territory. Previously, the field was largely used to marginalise certain groups, particularly low-income or ethnic minority groups. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=502&fit=crop&dpr=1 754w, https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=502&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/131762/original/image-20160725-31165-8cxrvw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=502&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Will genetic studies be used to justify inequalities?</span>
<span class="attribution"><a class="source" href="http://www.shutterstock.com/dl2_lim.mhtml?src=O6dTXcYeyM4LnDU-d3gMQw-1-1&clicksrc=download_btn_inline&id=106321706&size=medium_jpg&submit_jpg=">Olesia Bilkei/Shutterstock</a></span>
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<p>For some, attributing intelligence to genetics justifies the adverse circumstances many low-income and ethnic minority groups find themselves in; it wasn’t nurture that led to the under-performance of <a href="http://www.mitpressjournals.org/doi/abs/10.1162/003465304323031049#.V5WyIDm7iko">low-income or ethnic minority students</a> in the classroom, it was nature, and nature cannot be changed. For bioethicists today, the question hanging over this branch of behavioural genetics is: who’s to say new research in this area won’t perpetuate the same social inequalities that similar work has done before? </p>
<p>Genetic research in an area once used to oppress people should openly acknowledge this past and explicitly state what its findings can and cannot prove (what many bioethicists call <a href="http://onlinelibrary.wiley.com/doi/10.1002/hast.501/abstract">“trustworthy research”</a>).</p>
<p>Stark <a href="https://www.equalitytrust.org.uk/scale-economic-inequality-uk">class</a> and <a href="http://www.independent.co.uk/news/uk/home-news/britains-hidden-racism-workplace-inequality-has-grown-in-the-last-decade-9898930.html">race</a> divides still persist in the UK and US, two countries where this branch of research is rapidly growing. While the study mentions the impact of a person’s place in society with educational achievement, it links this status back to genetics, highlighting the genetic overlap between educational achievement, g and family socioeconomic status. </p>
<p>The possibility that this kind of research may influence attitudes towards certain ethnic minorities and the less well off is real, as is the risk that this work might be used to justify social inequality. These concerns should be admitted and addressed by behavioural geneticists. The alternative could be a <a href="http://www.tandfonline.com/doi/full/10.1080/02680939.2016.1139189">new form of eugenics</a>.</p><img src="https://counter.theconversation.com/content/62844/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Daphne Martschenko does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Research that finds links between genes and intelligence could worsen social inequality.Daphne Martschenko, PhD Candidate, University of CambridgeLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/624492016-07-15T13:55:32Z2016-07-15T13:55:32ZJust like Mama used to make? Surprising study finds family meals don’t influence food choices in later life<figure><img src="https://images.theconversation.com/files/130544/original/image-20160714-23365-1x97z92.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">Monkey Business Images/Shutterstock</span></span></figcaption></figure><p>Many of us have experienced intense cravings for dishes our mums or dads used to cook. Indeed, it would make sense that our parents’ cooking forever shapes our food preferences. But a study of 2,865 teenage twins has now found that the effects of family upbringing on people’s food preferences disappear as they start to make their own meal choices. </p>
<p>The research, <a href="http://ajcn.nutrition.org/content/early/2016/07/05/ajcn.116.133983.full.pdf+html?sid=2c44f1a8-55da-4700-8482-a31eae861456">published in the American Journal of Clinical Nutrition</a>, is hugely important. It has long been held that targeting what people eat in childhood is key to influencing adult food choices, but this research puts that belief into question.</p>
<p>The study was conducted using a powerful method, collecting the food preferences of twins aged 18 to 19 years old. Twins inevitably share many aspects of their upbringing, but as individuals they will also have their own unique environments, such as their circles of friends. This makes it possible to examine what kind of environment has the greatest impact on their choices. What is more, by including fraternal twins (who share half their genes) and identical twins (who share all of their genes), the study was able to explore the relative impact of genes, shared environment and unique environment on preferences for a range of foods. </p>
<p>In line with <a href="http://ajcn.nutrition.org/content/early/2014/01/29/ajcn.113.077867.abstract">similar studies with younger children</a>, the research found that in older teenagers (18 to 19 year olds) genes do have an impact on food preferences. The proportion of the food preferences that are attributable to genes (and shared by identical twins) is slightly different for different food groups. Preferences for vegetables tend to have a stronger genetic component than preferences for starches such as bread, rice and cereals. Overall, the study estimated that food choice is approximately equally influenced by genetic, and environmental factors. </p>
<p>However, when looking at the influence of shared and unique environments on food preference, the relative impact differed with age. In younger children, the twins’ shared environment, such as the family, had a large influence on food preferences. But for the older teenagers, it was each individual’s unique environment, such as their group of friends, that had an influence on food preferences. Shared environment – such as their family upbringing – had no detectable influence on the older group’s preference for any of the foods included in the study. </p>
<h2>Implications for public health</h2>
<p>This is a stark finding that rather goes against the notion that you can promote healthier behaviour in an adult by <a href="https://theconversation.com/mind-the-doughnut-emotional-eating-is-a-habit-that-can-start-in-childhood-58602">getting them while they are young</a>. </p>
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<img alt="" src="https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/130547/original/image-20160714-23346-1unxx5j.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Do teenagers know what they like?</span>
<span class="attribution"><span class="source">CREATISTA/Shutterstock</span></span>
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<p>But all is not lost. These data come from older teenagers, who are 18 to 19 years old, and this has a bearing on our interpretation of the findings. Both teenagers and younger children are known to be more socially responsive than adults, meaning that <a href="http://www.sciencedirect.com/science/article/pii/S0959438816300824">they are likely to alter their behaviour</a> to align with what they see others doing. Older teenagers, unlike children, are also eating with their social group rather than with their parents and family. </p>
<p>So this study may be capturing a pattern of eating that is the result of individuals aligning their preferences with a circle of friends rather than with the culture and memory of eating that their upbringing imbued them with. It is quite possible that in the following early years of adulthood, social influence becomes less important and upbringing once again impacts on food preferences.</p>
<p>It would be premature based on these findings alone to suggest there is no value in improving childhood and family diets. We know that obesity in childhood and adolescence <a href="http://www.ncbi.nlm.nih.gov/pubmed/26696565">predicts obesity in adulthood</a>, implying that early patterns of eating continue into later life. But it is also clear that there is a need to balance family-oriented public health activities with those that improve the food environment outside the home, such as lowering the cost and increasing the availability of healthier food options. As the authors themselves acknowledge, this will require stronger engagement from government in moulding the food environment that we live in.</p><img src="https://counter.theconversation.com/content/62449/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Suzanna Forwood does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Teenagers are heavily influenced by what their friends eat, to the extent that they forget about their parents’ cooking.Suzanna Forwood, Lecturer, Psychology, Anglia Ruskin UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/449612015-07-24T01:40:00Z2015-07-24T01:40:00ZEpigenetics: phenomenon or quackery?<figure><img src="https://images.theconversation.com/files/89423/original/image-20150723-22818-esqhg8.jpg?ixlib=rb-1.1.0&rect=192%2C98%2C2865%2C1818&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Family resemblance isn't only down to genes, but also to the influence of the environment on those genes.</span> <span class="attribution"><span class="source">Mitchell Joyce/Flickr</span>, <a class="license" href="http://creativecommons.org/licenses/by-nc/4.0/">CC BY-NC</a></span></figcaption></figure><p>Are you really what your mother ate, drank or got stressed about? The simple answer is “no”, but not in the way you think. </p>
<p>We are products of <a href="http://www.amazon.co.uk/Nature-via-Nurture-Genes-experience/dp/1841157465">nature via nurture</a>. Our genes and environments interact. And “environment” can be what we are experiencing now or at any time during our life. </p>
<p>An overwhelming body of evidence, from both humans and other animals, has shown that the environment we experience in the <a href="http://www.thousanddays.org/">first 1,000 days</a> of life influences our risk of chronic diseases: conditions such as heart disease, diabetes, psychiatric disorders and some cancers. </p>
<p>Changes to <a href="https://theconversation.com/explainer-what-is-epigenetics-13877">epigenetics</a> – molecules that lie literally “on top of genes” – have been implicated as <a href="https://theconversation.com/how-your-grandparents-life-could-have-changed-your-genes-19136">a possible mechanism</a> by which early environment (nurture) can leave a long-term change in the risk for chronic disease. </p>
<h2>Nature, meet nurture</h2>
<p>In a recent article in The Guardian, Adam Rutherford <a href="http://www.theguardian.com/science/2015/jul/19/epigenetics-dna--darwin-adam-rutherford">argued</a> that the term “epigenetics” is now being abused by pseudoscientists in a similar way to “quantum” and “nano”. I’d like to argue that the term has not been misused any more than most scientific terms, bar the odd <a href="http://www.epigenetics-international.com/">cosmetic product</a>, or <a href="http://www.thinkfeelcreate.com/epigenetics.html">health store</a>. </p>
<p>Although researchers sometimes disagree over the <a href="http://www.ncbi.nlm.nih.gov/pubmed/17522671">meaning</a> of the word “epigenetics”, it can be best understood through its conceptual development over time. </p>
<p>Aristotle didn’t like the prevalent idea in his day that we all grow from a microscopic version of ourselves. He coined the term “epigenesis” to describe the developmental process whereby a complex organism develops, through successive stages, from a simple start. This is essentially what we know today as developmental biology. </p>
<p>More than 70 years ago, <a href="http://www.britannica.com/biography/C-H-Waddington">Conrad Waddington</a> modified the word to “epigenetics” and <a href="http://scholar.google.com.au/scholar_url?url=http://krishikosh.egranth.ac.in/bitstream/1/21239/1/25218.pdf&hl=en&sa=X&scisig=AAGBfm28r_BFJgGQG2KjqwwaKG_RDXumWg&nossl=1&oi=scholarr&ved=0CBsQgAMoADAAahUKEwiXqvrym_DGAhWHJaYKHbnfBE0">described it</a> as “the interactions of genes with their environment, which bring the phenotype [i.e. the set of observable characteristics of an individual] into being”; my favourite definition.</p>
<p>Fast forward to 1996. A handful of notable scientists had already begun to theorise about the molecular nature of epigenetics. These ideas were summed up by Arthur Riggs and colleagues who <a href="https://cshmonographs.org/index.php/monographs/article/view/4519/3653">defined</a> epigenetics as “the study of mitotically and/or meiotically heritable changes in gene function that cannot be explained by changes in DNA sequence”.</p>
<p>Epigenetic changes would involve small molecules jumping onto our genes. They would stay there, hanging on even through cell division (mitosis), providing a long term epigenetic legacy. “Meiosis”, the cell division that results in eggs and sperm, implied that such changes could persist from one generation to the next. </p>
<p>Fast forward again to today. Most experts’ definition of epigenetics centres around these small molecules. And what have we done with these small molecules? We now have replicated at least two <a href="http://www.ncbi.nlm.nih.gov/pubmed/25229548">epigenetic biomarkers</a> of environment from the cradle to the grave: stress and smoking. </p>
<p>We have clinical biomarkers for cancer prediction, diagnosis and prognosis currently in clinical trials. And we have strong evidence that sometimes, events such as <a href="http://www.ncbi.nlm.nih.gov/pubmed/25917771">stress</a> and <a href="http://www.ncbi.nlm.nih.gov/pubmed/25769497">diet</a> in one generation can affect the health and epigenetics of the next. Such effects have also been shown in <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=23716672">humans</a>.</p>
<h2>Epigenetic legacies</h2>
<p>Is this all non-Darwinian? Certainly not; Darwin will not be turning in his grave because he <a href="https://goo.gl/VQyjqQ">assumed</a> that cells “throw off minute granules which are dispersed throughout the whole system”. These “<a href="http://darwin-online.org.uk/converted/published/1868_Variation_F877/1868_Variation_F877.2.html">gemmules</a>” would be “collected from all parts of the system to constitute the sexual elements, and their development in the next generation forms the new being”. </p>
<p>Not entirely correct, but we do already have plausible (although not proven) set of epigenetic molecules that are <a href="http://www.ncbi.nlm.nih.gov/pubmed/25416302">candidates</a> for such particles. </p>
<p>Rutherford, in his Guardian article, rightly pointed out that epigenetic legacies may not last for more than a couple of generations. This may be because that epigenetic state has evolved to responds to environments that may change every few generations. In the longer term, it has even been <a href="https://mitpress.mit.edu/books/evolution-four-dimensions">proposed</a> that epigenetic change in response to environment may be “fixed” by a genetic mutation in the same gene that has a similar effect on its function. </p>
<p>I agree with Rutherford that much more work is needed. For example, the human studies of transgenerational effects on health that he showcases have not yet been linked to any specific epigenetic changes. Personally, I would draw the line at calling these effects “epigenetic” but wouldn’t go to war with someone who did. </p>
<h2>Spot the snake oil</h2>
<p>Epigenetics fascinates us all. Yes, we’d love to know whether diet, exercise and meditation really changed our genes. But to turn a handful of promising studies into a mountain of evidence or to fail to replicate such findings, will take time. </p>
<p>And we must never lose sight of genetics. After all, in around one fifth of genes studied, genetic sequence is a much stronger influence on epigenetic state than environment, and epigenetics and genetics <a href="http://www.cell.com/ajhg/abstract/S0002-9297%2815%2900200-1?elsca1=etoc&elsca2=email&elsca3=0002-9297_20150702_97_1_&elsca4=Cell%20Press">combined</a> are better able to explain disorders such as obesity.</p>
<p>And finally, can we begrudge the odd snake-oil salesman borrowing a technical term like “epigenetics? <a href="http://scienceblogs.com/insolence/2013/02/11/epigenetics-you-keep-using-that-word-i-do-not-think-it-means-what-you-think-it-means/">Maybe</a>, but a quick search of Google shows that reports of true scientific articles on epigenetics far outnumber those with a pseudoscience flavour. I credit the public with sufficient intelligence to sort most of the wheat from the chaff. </p>
<p>Let the (informed) debate begin.</p><img src="https://counter.theconversation.com/content/44961/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Jeffrey Craig receives funding from the Australian National Health and Medical Research Council and the Financial Markets Foundation For Children. He is affiliated with the Australian Epigenetic Alliance and the International Society for the Developmental Origins of Health and Disease.</span></em></p>Epigenetics is increasingly used as a buzzword to sell pseudoscientific products, but the truth of epigenetics is even more interesting – and complex – than the quacks claim.Jeffrey Craig, Principal Research Fellow, Murdoch Children's Research InstituteLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/325352014-10-06T20:59:38Z2014-10-06T20:59:38ZHow genes can influence children’s exam results<figure><img src="https://images.theconversation.com/files/60893/original/gdf63fft-1412588535.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">What role do genes have to play? </span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/pic-124057036/stock-photo-students-sitting-a-test-in-an-exam-hall-in-college.html?src=OsP4UyDjDaXk2r46Lb628w-1-25">Student test by wavebreakmedia/Shutterstock</a></span></figcaption></figure><p>The idea that children can inherit the ability to get good results at school can spark heated debate. But, put simply, all this means is that children differ in how easy and enjoyable they find learning and that these differences are to a large extent explained by differences in their genes, rather than differences between schools or teachers. </p>
<p>We know from previous research that educational achievement in <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1540-5834.2007.00439.x/abstract;jsessionid=2308C55109442D150D9FE8873B72AC13.f04t03">primary</a>, <a href="http://www.tweelingenregister.org/nederlands/verslaggeving/NTR_publicaties/Bartels_TR_2002.pdf">middle school</a> years and at the <a href="http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0080341">end of compulsory education</a> is highly heritable. Heritability is a population statistic – it doesn’t tell us anything about a single individual. It describes the extent to which differences between children can be put down to DNA differences, on average, in a particular population at a particular time.</p>
<h2>Twins’ exam results</h2>
<p>Our new <a href="http://www.pnas.org/cgi/doi/10.1073/pnas.1408777111">study</a>, published in the journal Proceedings of the National Academy of Sciences, focused on the UK-wide standardised exam results at age 16, the General Certificate of Secondary Education (GCSE). We obtained exam grades from over 13,000 identical and non-identical twins from the <a href="http://www.teds.ac.uk/">Twins Early Development Study</a> who were also assessed on nine broad psychological domains, including intelligence, educational self-belief, personality, behaviour problems, and well-being.</p>
<p>Identical twins share 100% of their genes, whereas non-identical twins, just like any siblings, share on average only half of the genes that vary between people. If overall, identical twins are more alike than non-identical twins on a particular trait, then this implies there is a genetic influence. </p>
<p>Our study showed that the mean results in the GCSE core subjects of English, mathematics and science is more heritable (62%) than the nine other psychological domains (35–58%) we looked at. </p>
<p>This means that differences in how well children perform at exams are to a large extent explained by the difference in their DNA. Importantly, it does not mean that genetics explain 62% of a single child’s school achievement. </p>
<h2>Not just intelligence</h2>
<p>When we analysed different traits, we found that educational achievement is <a href="https://theconversation.com/twins-show-success-at-school-is-not-just-down-to-genes-22373">correlated with many characteristics of children</a>, not just intelligence. Our results indicate that these correlations are largely mediated by genetic factors. To the extent that children’s traits predict educational achievement, they do so largely for genetic reasons. </p>
<p>Although intelligence accounts for more of the heritability of GCSE results than any other single domain, the joint contribution of children’s self-belief, behaviour problems, personality, well-being, and their perceptions of school environment, collectively account for about as much GCSE heritability as intelligence. Together with intelligence, these domains account for 75% of the heritability of GCSE performance. </p>
<h2>Indicator of equality</h2>
<p>The children in this study were all taught the national curriculum, so to some extent received a similar education. As children’s learning experiences become more similar, they begin to explain the similarities between them rather than the differences between them. As a result of these diminished environmental differences, the relative genetic influences increase. So in a way, high heritability is an indicator of equality. </p>
<p>For example, despite high heritability, with sufficient educational effort, nearly all children could reach minimal levels of literacy and numeracy. This is an explicit goal of education in Finland. Success in achieving that goal would reduce differences in children’s educational achievement, which could change heritability. Hypothetically, if all environmental effects on individual differences (such as educational inequality) were to be minimalised, then the heritability estimate for educational achievement would be 100%. </p>
<h2>Personalised learning</h2>
<p>So what to make of this? Genes are important, not just in educational achievement or intelligence, but in a whole raft of other traits which contribute to how easy and enjoyable children find learning. Education is more than what happens passively to a child. Children are active participants in selecting, modifying, and creating experiences that are matched to their genetic predispositions. In genetics, this is <a href="http://eu.wiley.com/WileyCDA/WileyTitle/productCd-1118482786,subjectCd-ED05.html">known as “gene-environment correlation”</a>. </p>
<p>At the practical level, our findings add support for the trend in education toward personalised learning rather than a one-size fits all model. None of this means that schools, parents or teachers aren’t important. Of course they are – and each has an important role in helping children achieve the best of their potential.</p>
<hr>
<p><em>Next read: <a href="https://theconversation.com/better-at-reading-than-maths-dont-blame-it-all-on-your-genes-28947">Better at reading than maths? Don’t blame it all on your genes </a></em></p><img src="https://counter.theconversation.com/content/32535/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Eva Krapohl receives funding from the Medical Research Council Studentship.</span></em></p><p class="fine-print"><em><span>Kaili Rimfeld receives funding from the Medical Research Council Studentship. </span></em></p>The idea that children can inherit the ability to get good results at school can spark heated debate. But, put simply, all this means is that children differ in how easy and enjoyable they find learning…Eva Krapohl, Phd Student, Institute of Psychiatry, Psychology & Neuroscience, King's College LondonKaili Rimfeld, PhD Student, Institute of Psychiatry, Psychology & Neuroscience, King's College LondonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/302312014-08-22T05:15:29Z2014-08-22T05:15:29ZWhy nurture is just as important as nature for understanding genetics<figure><img src="https://images.theconversation.com/files/57095/original/wh3c94g8-1408635458.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Same but different.</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/e3000/6885969828/sizes/l/in/photolist-buuoVJ-aG3uWT-6rZ1J8-fu5mW5-buRCMg-8TPNmQ-dgBVzd-j9dANX-c6ydqj-cG8oQs-5espjz-8TS9WQ-5VmxLu-5X12LB-8VCZGy-5thEEA-kvZWzp-9WDRP4-ceGuFh-bXk35v-8TPMMu-cqxQyo-8GVibC-9FtuzH-5KJ5HF-c6yUTE-c6zT83-c6A5Nm-c6yuzQ-Rx1LD-8D4Uhu-hDaqXa-hCZuF3-hD7A6Y-byj6Bn-cG98PA-cG8U17-cG9Yz7-5MkcR1-66ps6e-4DNDc4-54SvtV-bs3nZz-c6A4ps-c6ze3C-7CayPj-4J641F-66dpUo-dsH9E9-aAmkij-8YHhSB/">e³°°° </a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>We live in the <a href="http://www.theguardian.com/commentisfree/2014/aug/03/genetic-research-britain-leads-the-way">age of the genome</a>. Hardly a week goes by without a story about how genes influence our health or behaviour. There has been recent excitement around new advances in <a href="https://theconversation.com/hundreds-of-genes-and-link-to-immune-system-found-in-largest-genetic-schizophrenia-study-29531">the genetics of schizophrenia</a>, and genetic overlap <a href="http://www.nature.com/ncomms/2014/140708/ncomms5204/full/ncomms5204.html">between reading and maths</a>. In the UK, the government is also pushing forward plans <a href="http://news.sciencemag.org/biology/2014/08/u-k-s-100000-genomes-project-gets-300-million-finish-job-2017">to map 100,000 genomes</a> that will be matched to clinical data to drive “genomic medicine as part of routine care” in the NHS.</p>
<p>But genetic variation is only half the story. Environmental influences are important too, and we now know that <a href="http://www.nature.com/mp/journal/v17/n9/full/mp201268a.html">our environments can interact</a> with our genetic makeup, in ways that can be good and bad for our health. </p>
<p>One of the most striking findings from genetics research is that <a href="http://journal.frontiersin.org/Journal/10.3389/fgene.2014.00006/abstract">the influence of genes isn’t fixed</a>. Even though our DNA sequence remains the same, the impact our genes have on us can alter with age and with the different environments we experience. Epigenetics, where the environment <a href="https://theconversation.com/how-your-grandparents-life-could-have-changed-your-genes-19136">can change the expression</a> of a gene without changing DNA, is only a small part of a whole field of science looking at changes in heritability due to interactions between genes and environment. </p>
<p>For example, we know that the importance of <a href="http://onlinelibrary.wiley.com/doi/10.1038/oby.2008.434/abstract">genetic influences for body weight increases as we get older</a>. Genetic variation accounts for 48% of the differences between people in early childhood but by adolescence this rises to 78%. These estimated figures, from a study of thousands of twins in the <a href="http://www.teds.ac.uk">Twins Early Development Study</a>, have now <a href="http://onlinelibrary.wiley.com/doi/10.1002/oby.20756/full">been confirmed</a> using analyses of DNA.</p>
<p>In fact, we see <a href="http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8492271&fileId=S1832427400007994">increasing heritability</a> with age for many other human characteristics, <a href="http://www.nature.com/mp/journal/v15/n11/abs/mp200955a.html">such as IQ</a>, where the importance of genes increases from 41% in early childhood up to 66% by young adulthood.</p>
<h2>Drawing out genetic potential</h2>
<p>One of the main mechanisms behind the increasing role of genetics as we get older is choice: we have more control over <a href="http://cdp.sagepub.com/content/22/5/349.short">what we’re exposed to</a>. We can choose whether to have a doughnut for lunch, whether to visit the library, or whether to cycle to work. These environments don’t just happen to us. To some extent we control, select and create our experiences and exposures. And because our genes <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091813/">can influence these choices</a> too, we find ourselves in places and situations that in a sense draw out our genetic potential. </p>
<p>Our recent work tells us that the importance of genes and environments on childhood behaviour varies depending on where we grow up, shown <a href="http://sgdp.iop.kcl.ac.uk/davis/teds/geocoding/">in a series of UK maps</a> of genetic and environmental influences for 45 childhood traits. For example, environmental influences were more important for disruptive classroom behaviour in London, compared to the rest of the UK. </p>
<p>The challenge now is to try and understand what in the environment can create these geographically distributed effects, because for this analysis at least, we know that genetic differences cannot explain these differing patterns. </p>
<p>The interplay between nature and nurture means that identifying which genes and which environments are having an effect is difficult; turning an already complex system, that links DNA with human behaviour, into a network of genetic and environmental pathways and intersections. But if we’re to understand the mechanisms behind these effects, and to develop ways of preventing disease or promoting better outcomes or behaviours we’ll have to get to grips with it. </p>
<p>One of the simpler examples is <a href="http://www.mayoclinic.org/diseases-conditions/phenylketonuria/basics/definition/con-20026275">phenylketonuria</a>, a disease where a defective variant of a gene means patients are not able to break down the protein phenylalanine, which builds up to toxic levels that affect brain development. Only by understanding the interaction between the gene and the presence of this protein in our diets were researchers able to identify an effective treatment for a genetic disease: <a href="http://www.nhs.uk/conditions/phenylketonuria/Pages/Introduction.aspx">removing this protein</a> from what affected children eat. </p>
<p>The diet is difficult to stick to, but it shows that it is sometimes possible to overcome genetic disease by changing the environment. More complex disorders that are influenced by many genes and many environments will of course need more complex interventions, and will probably have complicated mechanisms for us to unravel. But focusing on genetics alone means we will not fully understand these systems or processes. </p>
<p>Identifying which genes influence disease is important, but it’s just the first step. As we invest more in genetic research, we need to keep context in mind too. We should invest just as heavily in new methods for tracking and analysing behaviour, environments and health outcomes to the same degree of detail as we are now studying DNA. And that includes <a href="https://theconversation.com/lack-of-trust-not-privacy-underpins-fears-about-care-data-22971">remaining open-minded</a> about initiatives such as the NHS’s <a href="http://www.england.nhs.uk/2014/01/15/geraint-lewis/">care.data</a>, which would allow researchers access to more detailed information about our health outcomes.</p>
<p>The past 15 years have seen unprecedented and unexpected advances in genetic science. We should not underestimate the parallel advances we will make by understanding environmental influences and the way they interact with our genetic makeup. Nature and nurture are both important. We must be just as ambitious about understanding nurture as we are about understanding nature, because only by joining the two will we see the full picture.</p><img src="https://counter.theconversation.com/content/30231/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Claire Haworth has received funding from the UK MRC, ESRC and the British Academy.</span></em></p>We live in the age of the genome. Hardly a week goes by without a story about how genes influence our health or behaviour. There has been recent excitement around new advances in the genetics of schizophrenia…Claire Haworth, Reader in Behavioural Genetics, University of WarwickLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/289472014-07-14T05:07:20Z2014-07-14T05:07:20ZBetter at reading than maths? Don’t blame it all on your genes<figure><img src="https://images.theconversation.com/files/53626/original/8xf2sq8v-1405076039.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Many of the genes for maths and reading overlap. </span> <span class="attribution"><a class="source" href="http://www.shutterstock.com/pic.mhtml?id=123441943&src=nJFIF-zLUgF3lijbyuh8eA-1-32">Businessman via alphaspirit/Shutterstock</a></span></figcaption></figure><p>I disliked and feared maths for most of my school career and dropped it as soon as I possibly could. My mother recalls me crying as a five-year-old because: “I can’t do the people-on-the-bus sums”. If the bus has 12 passengers and three get off, how many are left? English, by contrast, was a breeze. At seven, I stood on a chair with a microphone and read my version of Sleeping Beauty aloud to the entire school. Reading and writing already ranked high among my passions.</p>
<p>Mine isn’t an unfamiliar tale. Many people label themselves as “not a maths person” or “not much of a reader”, often while they are still children. And yet, in a <a href="http://www.nature.com/ncomms/2014/140708/ncomms5204/full/ncomms5204.html">recent study published in Nature Communications</a>, scientists showed that around half of the genes that affect how well 12-year-olds in the UK perform in maths also affect how good they are at reading. And they showed this in a new and important way.</p>
<p>For the first time ever, this study – led by UCL’s Oliver Davis, Chris Spencer at Oxford and Robert Plomin at King’s College London – was able to estimate genetic influences on learning abilities using DNA alone. The implications of this for future genetically sensitive research in the behavioural and social sciences are highly significant. It is certainly much easier to get hold of DNA than it is to get hold of a results from a large <a href="https://theconversation.com/explainer-what-is-twin-research-26468">twin sample</a> – another good way of researching this area.</p>
<h2>Overlapping genes for maths and reading</h2>
<p>The researchers analysed millions of DNA variations from almost 3,000 people and found that more than half of the differences between how well 12-year-olds performed in reading and maths could be explained by differences in their genes. But they also found that reading and maths are correlated partly for genetic reasons: many genes appear to operate in both domains.</p>
<p>These results are not in themselves new. Twin studies <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7610.2009.02114.x/full">have previously reached</a> very similar conclusions. However, the fact that such findings have now been confirmed by a genome-wide association study – where many common genetic variants are explored for association with a particular trait – is a very significant development. </p>
<p>It is interesting that in spite of using DNA data no particular genes emerged as significant influences on reading or maths. Instead, the researchers found collections of subtle DNA variations. </p>
<p>This ties in with <a href="http://www.nature.com/mp/journal/v16/n10/abs/mp201185a.html">other research</a> that has led to an understanding that many genes of small effect combine to influence complex traits and that the effects are mostly too small to pick up reliably, even with large samples. With genes it seems we’re more likely to find teams than star players.</p>
<p>The research supports the <a href="http://psycnet.apa.org/psycinfo/2005-08334-006">Generalist Genes Hypothesis</a>, the idea that genes are generalists and environments are specialists. Twin studies have found a great deal of evidence that important environments are likely to be specific to particular traits or learning outcomes. For example, a good English teacher might have a slightly different profile to a good maths teacher. The two subjects might benefit from different approaches to homework or different classroom organisation. They may, in short, need to offer different ways of drawing out genetic potential.</p>
<h2>Environment still hugely important</h2>
<p>What we have here is compelling evidence that genes influence maths and reading abilities and that at least half of the genes influencing one ability also influence the other. So, in that case, how can it be that some kids are so much better at reading than maths, and vice versa? </p>
<p>The first answer is simply that genes do not determine behaviour. Genes offer probabilities rather than prophecies. They represent “what is” rather than “what could be”. Even if you have the capacity to do well in a subject this does not automatically translate to high achievement. Motivation, confidence and interest all have a role to play too. </p>
<p>The second answer is that the genetic overlap between the two skill-sets is not 100%. Although there is evidence for shared genetic effects across reading and maths there is evidence of some genetic specificity too. </p>
<p>Most importantly, this new study highlights the role of the environment. It would appear that our life experiences have a particularly important part to play in making some people better at one subject than the other. This may happen through a variety of mechanisms including sparking an interest, inspiring future aspirations or nurturing appetites as well as aptitudes. Both genes and experiences influence the choices young people make about further education and careers and cannot be considered in isolation from each other.</p>
<p>The UK government has been pushing recently to <a href="http://news.tes.co.uk/b/news/2014/06/30/government-names-schools-which-will-integrate-shanghai-maths-methods-in-england.aspx">improve national mathematics performance</a>, and bring them up to levels seen in East Asia. Shared genetic influence on reading and maths suggests that if average maths performance lags behind average reading performance then this should, from a biological point of view, be possible. </p>
<p>The key to achieving this, however, lies in our environment rather than in our DNA. We need a better understanding of which aspects of the maths learning environment promote traits such as self-efficacy, interest and effort as well as achievement – and which don’t. We also need to understand that the same approach will not work for everyone. Drawing out individual potential requires at least a degree of personalisation.</p>
<p>And, just for the record, yes I can do the “people-on-the-bus” sums now.</p><img src="https://counter.theconversation.com/content/28947/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Kathryn Asbury does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>I disliked and feared maths for most of my school career and dropped it as soon as I possibly could. My mother recalls me crying as a five-year-old because: “I can’t do the people-on-the-bus sums”. If…Kathryn Asbury, Lecturer, Psychology in Education, University of YorkLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/213342013-12-22T20:32:51Z2013-12-22T20:32:51ZExplainer: what is heritability?<figure><img src="https://images.theconversation.com/files/38065/original/zb2hwgps-1387324039.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Heritability: how much do your genes impact your traits?</span> <span class="attribution"><span class="source">Jenn Durfey</span></span></figcaption></figure><p><a href="http://www.medicalnewstoday.com/articles/265284.php">Schizophrenia</a>, <a href="http://www.ncbi.nlm.nih.gov/pubmed/12742871">depression</a>, <a href="http://arxiv.org/abs/1303.6227">bipolar disorder</a> and <a href="http://www.biomedcentral.com/content/pdf/1866-1955-5-11.pdf">autism</a> have all had recent attention for being “genetically caused”. </p>
<p>In scientific research being genetically caused usually corresponds to having a high estimated heritability. </p>
<p>But what exactly is heritability? What does it mean when researchers and journalists label traits like these as genetic?</p>
<h2>The nature-nurture debate</h2>
<p>The <a href="https://theconversation.com/nature-v-nurture-score-one-all-3697">nature-nurture debate</a> historically referred to the disagreement between whether traits are caused by ones biology (nature) or the environment (nurture). </p>
<p>These days, disagreements centre on <em>how much</em> nature or nurture contributes. Nature – now usually referring to genes – may be <em>more</em> of a <a href="https://theconversation.com/insight-for-better-understanding-schizophrenias-genetic-basis-6988">cause of schizophrenia</a>, even though both genes and environment contribute. </p>
<p>Geneticists quantify the proportion that genes contribute using a <a href="http://en.wikipedia.org/wiki/Heritability">heritability estimate</a>, represented as h². When traits are claimed to be genetic, this usually means that they have a high heritability estimate.</p>
<h2>Making sense of heritability</h2>
<p>Heritability estimates have a value between 0 and 1. These values are sometimes represented as percentages, for instance “depression is 70% heritable” would correspond to an h² of 0.7. </p>
<p>However this does not mean that 70% of an individual’s depression is genetic, with the environment making up the other 30%. It also does not mean that 70% of depressed individuals are so because of their genes. </p>
<p>To make sense of this, imagine that we found that height was 80% heritable. It seems obvious that this could not mean that only 80% of people have their height genetically influenced. It also strange to think that my particular height of 165cm can be broken down in to 132cm of genetically caused growth and 33cm of environmentally caused growth.</p>
<p>The interplay of genes and environment for individual traits is recognised by geneticists, and cannot be broken down in to percentage values. </p>
<p>For my Labrador Bob to have brown fur, he needs to have particular genes to code for the brown pigment expressed in his coat. He also needs an environment in which to develop, in order to be able to grow fur at all.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=399&fit=crop&dpr=1 600w, https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=399&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=399&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=501&fit=crop&dpr=1 754w, https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=501&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/38066/original/h26tj6qn-1387324141.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=501&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The colour of Labrador fur is highly heritable.</span>
<span class="attribution"><span class="source">AlyssssylA</span></span>
</figcaption>
</figure>
<p>In an individual case, it does not make sense to say how much is genetically or environmentally caused. It does not make sense to talk about “how genetic” my blond hair, your short stature, or Bobs brown fur is. </p>
<p>This is why heritability estimates can only be applied to populations.</p>
<h2>Causes of trait variation</h2>
<p>So what do these numbers refer to? </p>
<p>Heritability concerns how much variation in traits is caused by variation in genes. </p>
<p>If we looked a population of people and measured their height we are likely find variation between them – some short, some tall, and some in-between. Heritability tells us if this variation occurs because people have different genes or because they live in different environments.</p>
<p>In the Labrador case – it seems that dogs with particular genes are golden, while others with different genes are black or brown. Thus there is variation in genes between the three coloured groups. </p>
<p>If we looked at the environments in which they were raised, you would find that no matter what environment these dogs are raised in, their coat colour is not affected.</p>
<p>So, Labrador coat colour variation is caused by variation in the genes, and is highly heritable. As changes in the environment have no effect at all, the heritability would be 100%, or h² = 1.</p>
<p>Human skin colour however, has a lower heritability estimate. </p>
<p>Although we know that some variation in colour can be explained by differences in genes, we also know that variation in the environment – such as sun exposure, can affect the colour of peoples’ skin. </p>
<p>So variation in skin colour is caused partially by variation in genes and partially by variation in environment.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/38064/original/h5ds5y65-1387323965.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Skin colour is influenced by genes as well as the environment, like being out in the sun.</span>
<span class="attribution"><span class="source">mikebaird</span></span>
</figcaption>
</figure>
<h2>Some strange consequences of heritability</h2>
<p>As heritability is a measure of the causes of variation in traits, things which we ordinarily think of as having a genetic basis can turn out to have low heritability. </p>
<p>For instance “walking on two legs” is a human trait which does not vary much. When it does vary, this is usually due to environmental variations, such as accidents where people lose the function of one or both legs. </p>
<p>As a consequence, “walking on two legs” has an h² close to 0. This does not mean that genes are not necessary for humans to walk on two legs. What it means is that variation in this trait is caused by primarily non-genetic factors.</p>
<p>Another strange consequence of heritability is that the estimate depends upon which population you examine. </p>
<p>For example the heritability of hair colour in a Chinese population would be quite low, yet in Australia would be quite high. This is because in China there is little “natural” variation in hair colour – variation that is genetically caused. As such, any large variations are usually due to environmental factors, such as artificial dyes.</p>
<p>So while heritability does measure the causal impact of genes, it does so in a very specific and limited way.</p><img src="https://counter.theconversation.com/content/21334/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Kate Lynch receives funding from Macquarie University. </span></em></p>Schizophrenia, depression, bipolar disorder and autism have all had recent attention for being “genetically caused”. In scientific research being genetically caused usually corresponds to having a high…Kate Lynch, Doctoral Student in Philosophy of Biology / Genetics, Macquarie UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/36972011-10-04T19:37:41Z2011-10-04T19:37:41ZNature v nurture: score one all<figure><img src="https://images.theconversation.com/files/4096/original/5127452921_b0b84a05e8_b.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Psychologists have debated whether our interests are a result of nature or nurture for more than 100 years.</span> <span class="attribution"><span class="source"> pbkwee/Flickr</span></span></figcaption></figure><p>So, you’ve got your father’s blonde hair and you were raised in a cricket-mad household and you like cricket. But is it your genes or your childhood that’s responsible for your love of cricket or your thrill-seeking, or your obsession with spicy food? </p>
<p>Is it nature or is it nurture?</p>
<p>Everyone knows about the nature versus nurture debate – are we the products of the environment we grow up in, or are we the products of the genes we’re born with? </p>
<p>It’s one of the oldest questions in psychology, and it’s been intensely debated for more than a hundred years.</p>
<p>But current social research combined with the modern gene sequencing methods are reporting a third, more nuanced possibility: could the answer be both – nature <em>and</em> nurture?</p>
<h2>Degrees of susceptibility</h2>
<p>This third option is called the <a href="http://evolution.binghamton.edu/evos/wp-content/uploads/2008/11/BelskySusceptibility.pdf">“differential susceptibility hypothesis”</a> and it proposes that people can be sensitive or insensitive to the environment they grow up in depending on their genes. </p>
<figure class="align-left ">
<img alt="" src="https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=716&fit=crop&dpr=1 600w, https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=716&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=716&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=899&fit=crop&dpr=1 754w, https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=899&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/4097/original/unhappy.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=899&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Environmental sensitivity may depend on genetic make-up.</span>
<span class="attribution"><span class="source">treehouse1977/Flickr</span></span>
</figcaption>
</figure>
<p>It’s an intriguing idea – we all know people who are extraordinarily affected by bad circumstances, and others in similar circumstances who are affected very little.</p>
<p>But so far, the differential susceptibility hypothesis has not been very well researched. </p>
<p>This is because investigations have to start with very particular genes, and very particular questions about how these genes interact with environmental circumstances.</p>
<p>But a study published today in <a href="http://www.nature.com/tp/index.html">Translational Psychiatry</a> has managed, against the odds, to do precisely that. </p>
<p>The study looks at variants in the improbably-named 5-HTTLPR – that is, different types of gene that make the protein which recycles serotonin in the brain. </p>
<p>Serotonin is the substance in the brain most involved with mood disorders, such as depression or anxiety.</p>
<p>Generally, there are two variants of this gene, “short” and “long”. People who have two of the short version have <a href="http://www.ncbi.nlm.nih.gov/pubmed/15867106">previously shown associations</a> with a higher incidence of a variety of mood disorders, slower responses to antidepressant medication and a variety of different sensitivities in their mental health. </p>
<p>But, as might be expected, this is hugely complicated. Other <a href="http://www.nature.com/ejhg/journal/v12/n5/full/5201149a.html">studies have showed no association</a> between the prevalence of this gene and any problems with affective disorders. </p>
<p>So, what’s going on?</p>
<h2>The long and short of it</h2>
<p>In this study, three different groups of children had the nature of their 5-HTTLPR gene type determined and were examined on a standardised scale of positive affect – how frequently they report being interested, energetic, excited, lively, and so on.</p>
<p>In the first group, the parents rated themselves on a scale designed to measure positive parenting. In the second group, the children brought a parent into the laboratory, researchers observed the parent /child pair interacting, and rated the parent’s positivity. And in the third group, the children themselves were asked to rate their parents’ emotional warmth.</p>
<figure class="align-right ">
<img alt="" src="https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=818&fit=crop&dpr=1 600w, https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=818&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=818&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1028&fit=crop&dpr=1 754w, https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1028&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/4098/original/happy.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1028&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Our degree of happiness and sadness may depend on both nature and nurture.</span>
<span class="attribution"><span class="source">Stenly Lam</span></span>
</figcaption>
</figure>
<p>In all three scenarios, the results were the same – children with the short gene version showed a sensitivity to their emotional environment, and children with the long version didn’t. </p>
<p>That means children with the short gene pair who received less positive parenting reported less positive affect. </p>
<p>It also means that children in the same group (short gene) who received a positive and supportive environment reported more positive affect.</p>
<p>The sensitive (short gene) children were happier in the positive environment and sadder in the negative one.</p>
<p>They were sensitive to both positive and negative environments, while those in the long gene group were insensitive to both kinds of environments. </p>
<h2>Inherited vulnerability</h2>
<p>Scientists have long discussed the idea of a genetic vulnerability – a series of circumstances where genes and environment can interact badly, producing unwanted health outcomes, usually during childhood.</p>
<p>But this is one of the first good pieces of evidence for something more substantial again – a gene variation that seems to represent the presence of an overall sensitivity, not just a particular vulnerability.</p>
<p>Still, the evidence is just an association. The next step, of course, is to investigate this experimentally – to find a group of “short gene” children who are at risk, help their parents provide a more positive parenting style, and try to record an improvement in the children over time. (Obviously, there are ethical issues with researching the hypothesis other way around.)</p>
<p>Studies, such as this one, attempting to translate direct genetic evidence into “real world” outcomes are becoming increasingly more common as our ability to ask questions about genetic variations becomes more sophisticated.</p>
<p>The eventual outcome of this line of work may be better ways of taking care of people in the population who have specific vulnerabilities and whom we can identify before they develop problems. But it might be a while yet before we find a “spicy food” gene.</p><img src="https://counter.theconversation.com/content/3697/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>James Heathers does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>So, you’ve got your father’s blonde hair and you were raised in a cricket-mad household and you like cricket. But is it your genes or your childhood that’s responsible for your love of cricket or your…James Heathers, PhD Candidate in Applied Physiology, University of SydneyLicensed as Creative Commons – attribution, no derivatives.