How Life Experience Chemically Coats Your DNA and Shapes Your Life Our genes are embedded in the DNA of our cells. They form the blueprints for proteins which are the chemical compounds that are the building blocks for maintaining our brains, constructing our bodies and shaping our personalities. To have an effect, a gene has to be activated to create a protein – this is called ‘gene expression’. Our cells do not use every gene in our DNA. Each of our cells does contain all of our DNA and genes, but different cells use different parts of the genes. This difference in ‘expression’ is what makes a brain cell different from a heart cell. Genes can also be turned on and turned off. Researchers have discovered that a mother rat who licks and nurtures her babies actually causes a gene to turn on which helps them to be more resilient to stress and anxiety. However, if she doesn’t lick and nurture them, a (different) gene gets turned off and depression results. Within the field of genetics there is a relatively new area called epigenetics (epi in Greek means above or beyond).  Epigenetics studies the chemical switches that turn genes on or off. Researchers are now discovering that life experiences such as trauma, drug abuse and lack of affection somehow cause satellite molecules to stick to a person’s DNA. These don’t actually alter the make-up of the gene itself, but they do help to either shut down or speed up the gene’s expression. As a result, the proteins required for health and happiness can be affected. So let’s go a level deeper now so that you can marvel along with me about how very small chemical changes can have such a huge impact. I’ve found a few pictures to try and explain things more clearly so that I don’t lose you along the way! How does a gene get silenced in the first place? The answer is quite straightforward. You need to stop the ‘machinery’ that activates the gene from getting to it. If it can’t be accessed then the gene can’t be expressed. Because the DNA molecule is so long it has to be wound up into tight coils (around molecules called ‘histones’; see picture above) in order to fit it into the nucleus of each cell. In this wound up state the genes cannot be activated and used to make proteins.  In order to be expressed, that section of DNA with the gene has to be unzipped so that it can unravel and expose itself. Then the gene can be accessed to make the required protein. In epigenetics, researchers look at mechanisms that help to block or access the cell’s genes. Such mechanisms include the adding or removal of molecules to or from the DNA or histones. This is where it gets very nifty. A very small molecule such as a methyl group (CH3: a carbon atom with 3 hydrogens attached) on the DNA physically hinders the approach of the machinery that helps the gene make the protein. This silences the gene – it literally shuts it up by enclosing it! On the other hand, when an acetyl group (COCH3) sticks to a histone the shape gets expanded and this helps the gene to express itself more easily. Science is finding out more and more that these very small chemical changes happen in response to certain life experiences. Your experiences literally shape your DNA and thus affect the proteins your cells produce – and eventually your physical and mental health.   Remember the mother rat with her babies that I just mentioned above? Neuroscientist Michael Meaney from Canada found that when the un-licked and un-cared for babies were exposed to a stressful experience their stress hormone (corticosterone) shot up higher and stayed up higher for much longer than licked and cared-for babies. Meaney wondered if the differences in the two groups of rats could be traced back to some type of gene expression. He found that in the hypothalamus area of the rat brain the un-licked and un-cared for babies had more methyl groups on the corticosterone receptor gene than the cared-for baby rats. Because of the presence of the methyl groups on the gene, the protein necessary for making the corticosterone receptor was made less easily. This led to fewer corticosterone receptors in that brain region. Fewer receptors means that the brain cannot react as quickly to reduce the effects of the high levels of stress, and so the baby rat’s system stays stressed for longer. In the case of the cared-for babies, the corticosterone receptor gene is kept fairly clean of methyl groups, so the protein gets made, and these little rats could handle stressful situations much better. What then makes this piece of research work so elegant is that Meaney then did an experiment in which he added a chemical that increases the number of acetyl groups (allow easier access) but reduces the methyl groups (prevent access) on that area of the DNA. He gave this to the un-cared for baby rats. Et voilà! The receptor gene could now be accessed and the necessary proteins made. These babies were no longer anxious in the stress situation, and their stress hormone levels were similar to those of the cared-for rats. Scientists in the field of mental illness have been getting very excited about alll this. The drug companies see a potential muli-million euro opportunity too….. Think for example along the lines of a future drug that could scrub the DNA to remove any alterations that lead to schizophrenia, depression, anxiety and addictions.  A drug that could stop methyl groups being added could help to reduce the severity of post-traumatic stress disorder in rape and trauma victims as well as soldiers in war zones. Neuroscientists are already speculating that psychotherapy may have the effect of adding acetyl groups to allow easier turn-on of certain genes. This is great news for all us healers and therapists! The problem of being able to prove this lies in the problem that you need to analyse the brain of the patient – and that would mean killing the person. And that is not too ethical…. The way that scientists normally get round this is to develop an ‘animal model’ to mimic what happens in humans. However, at the moment being able to develop an effective ‘talk therapy model’ for a rat is proving difficult!!! But I am sure that the researchers will eventually think of something very clever ;=) And of course, when this happens, I shall definitely let you know. References I. C. G. Weaver, N. Cervoni, F. A. Champagne, A. C. D'Alessio, S. Sharma, J. R. Seckl, S. Dymov, M. Szyf and M. J. Meaney. Epigenetic programming by maternal behavior. Nature Neuroscience, volume  7, pages 847-854 (2004). I. C. G. Weaver, J. Diorio, J. R. Seckl, M. Szyf, M. J. Meaney. Early Environmental Regulation of Hippocampal Glucocorticoid Receptor Gene Expression: Characterization of Intracellular Mediators and Potential Genomic Target Sites. Annals of the New York Academy of Sciences, volume 1024, pages 182-212 (2004). M. Rutter. Genes and Behavior: Nature-Nurture Interplay. Blackwell Publishing (2006). C. D. Allis, T. Jenuwein, D. Reinberg and M.-L. Caparros. Epigenetics. Cold Spring Harbor Laboratory Press (2007). E. S. Higgins. The New Genetics of Mental Illness. Scientific American Mind, vollume 19, number 3, pages 41-47. B. Lipton. The Biology of Belief: Unleashing the Power of Consciousness, Matter and Miracles (2005).