“We are transient beings, in a world of constantly changing culture. At home in the fields of Art and Science, seemingly capable of magnificent abstractions, humans have an intense need to externalize their insights. Music is an art and a highly transmissible cultural product, but we still have an incomplete understanding of how our musical experience shapes and is vividly retained within our brain, and how it affects our behavior. However, the developing field of social epigenetics is now helping us to describe how communication and emotion, prime hallmarks of music, can be linked to a transmissible, biochemical change.”
—Toward an Epigenetic View of Our Musical Mind
Epigenetic changes shed light on biological mechanism of autism
Scientists from King’s College London have identified patterns of epigenetic changes involved in autism spectrum disorder (ASD) by studying genetically identical twins who differ in autism traits.
The study, published in Molecular Psychiatry, is the largest of its kind and may shed light on the biological mechanism by which environmental influences regulate the activity of certain genes and in turn contribute to the development of ASD and related behaviour traits.
ASD affects approximately 1 in 100 people in the UK and involves a spectrum of disorders which manifest themselves differently in different people. People with ASD have varying levels of impairment across three common areas: deficits in social interactions and understanding, repetitive behaviour and interests, and impairments in language and communication development.
Evidence from twin studies shows there is a strong genetic component to ASD and previous studies suggest that genes that direct brain development may be involved in the disorder. In approximately 70% of cases, when one identical twin has ASD, so does the other. However, in 30% of cases, identical twins differ for ASD. Because identical twins share the same genetic code, this suggests non-genetic, or epigenetic, factors may be involved.
Epigenetic changes affect the expression or activity of genes without changing the underlying DNA sequence – they are believed to be one mechanism by which the environment can interact with the genome. Importantly, epigenetic changes are potentially reversible and may therefore provide targets for the development of new therapies.
The researchers studied an epigenetic mechanism called DNA methylation. DNA methylation acts to block the genetic sequences that drive gene expression, silencing gene activity. They examined DNA methylation at over 27,000 sites across the genome using samples taken from 50 identical twin pairs (100 individuals) from the UK Medical Research Council (MRC) funded Twins Early Development Study (TEDS): 34 pairs who differed for ASD or autism related behaviour traits, 5 pairs where both twins have ASD, and 11 healthy twin pairs.
Dr Chloe Wong, first author of the study from King’s College London’s Institute of Psychiatry, says: “We’ve identified distinctive patterns of DNA methylation associated with both autism diagnosis and related behaviour traits, and increasing severity of symptoms. Our findings give us an insight into the biological mechanism mediating the interaction between gene and environment in autism spectrum disorder.”
DNA methylation at some genetic sites was consistently altered for all individuals with ASD, and differences at other sites were specific to certain symptom groups. The number of DNA methylation sites across the genome was also linked to the severity of autism symptoms suggesting a quantitative relationship between the two. Additionally, some of the differences in DNA methylation markers were located in genetic regions that previous research has associated with early brain development and ASD.
Professor Jonathan Mill, lead author of the paper from King’s College London’s Institute of Psychiatry and the University of Exeter, says: “Research into the intersection between genetic and environmental influences is crucial because risky environmental conditions can sometimes be avoided or changed. Epigenetic changes are potentially reversible, so our next step is to embark on larger studies to see whether we can identify key epigenetic changes common to the majority of people with autism to help us develop possible therapeutic interventions.”
Dr Alycia Halladay, Senior Director of Environmental and Clinical Sciences from Autism Speaks who funded the research, says: “This is the first large-scale study to take a whole genome approach to studying epigenetic influences in twins who are genetically identical but have different symptoms. These findings open the door to future discoveries in the role of epigenetics – in addition to genetics – in the development of autism symptoms.”
From Father to Offspring: The Contribution of Paternal Involvement and the Role of Paternal Transmission of Psychopathology
Coming from a lab focused on mother-pup interactions and attachment during infancy, I never really considered the contribution of paternal care to offspring survival and development. Needless to say, I myself am guilty of minimizing the role and contribution of paternal behavior on offspring development. Much to my (pleasant) surprise, I found that there is much relevant work being done in this underrepresented area of neuroscience.
So why is the study of paternal care and related behaviors important? Let’s start off by pointing out that, much like maternal care, paternal behaviors strongly influence the emotional and social development of their offspring as well as increasing survival rate. In addition, think about this: in human culture, who is more likely to leave a household? Fathers leave the family nucleus more frequently than mothers and they are also more likely to become abusive. It should then be no surprise that the children of these fathers grow up under stressful conditions and have a higher susceptibility for developing abnormal psychosocial outcomes. In order to gain insight into the neural substrates and circuits underlying paternal behaviors, scientists are employing a vast number of animal models (i.e. birds, fish, marmosets, hamsters, voles, mice) and studying different elements of paternal care behaviors. Although the use of model organisms to study complex interactions (that are in turn influenced by society and culture), such as those pertaining to human paternal care that encompass more abstract behaviors like planning, provisioning through financial means and perceptual warmth, they provide important clues into the different mechanisms and operating factors related to the spectrum of paternal behaviors.
Examples of Paternal Behaviors in Model Animals:
- Grooming
- Thermoregulatory behaviors (crouching, huddling to provide warmth)
- Pup retrieval
- Nest building
- Food gathering
- Baby-sitting/guarding (aka protection)
Factors modulating paternal involvement/care:
- Environment: Some species that are not usually paternal will become so when faced with tough environmental conditions (i.e. facultative care). The role of photoperiod is also known to influence bheavior of the non-parental male in some species. For example, the meadow vole will begin biparental care during the colder months of the year when there is also less daylight hours.
- Prior Experience: Previous pup experiences may affect future paternal behavior. For example, repeated pup exposure is able to induce paternal behavior in virgin male rats (FYI: pup experience is able to induce maternal behavior in virgin female rats as well.
- Maternal variables: Females are also affected by some of the same factors influencing paternal care, and they can in turn modulate/regulate paternal behavior. For example, brief cohabitation with a female is able to decrease the latency of paternal behavior initiation in prairie voles. Also, mother monkeys sometimes direct threat vocalization towards the fathers when these initiate contact with infants, thus limiting their parental involvement.
The role of paternal involvement in offspring development has also gained recent popularity due to studies that have raised the possibility that epigenetic mechanisms in fathers may contribute to the transgenerational transmission of stress-induced psychopathologies. For example, major depressive disorder (MDD) is a highly heritable psychiatric disorder that is influenced by exposure to many forms of chronic stress. Moreover, stress has been suggested to contribute to MDD via epigenetic alterations that may be passed on to subsequent generations, thus increasing vulnerability to MDD.
A recent reserach study led by Eric Nestler at Mount Sinai School of Medicine employed a chronic social defeat stress paradigm in adult male mice to investigate the transgenerational transmission of stress-vulnerability. The group, who had previously demonstrated that chronic social defeat stress induces depression and anxiety-like behaviors, studied whether exposure to chronic social defeat stress causes stress-related abnormalities in the F1 (first generation) offspring of the stressed fathers. Also, they examined known biomarkers of depression (i.e. corticosterone vascular endothelial growth factor) in male and female offspring of stressed fathers. The group found that male mice bred from defeated fathers showed a robust behavioral phenotype characterized by pronounced social and neurobehavioral deficits in multiple anxiety and depression related behavioral tasks (elevated plus maze, novelty exposure, forced swim test). However, this effect was limited in females and not as robust. The male offspring of defeated fathers also showed higher levels of corticosterone and lower levels of VEGF.
In order to directly determine a role for epigenetics, the group also did something very clever and used in vitro fertilization (IVF) in addition to regular breeding. However, they failed to find marked neurobehavioral abnormalities in these IVF offspring, suggesting that the transgenerationally transmitted behavioral phenotypes likely occur through behavioral mechanisms, although a small role for epigenetics is apparent.
Sources:
Dietz and Nestler. 2011. From father to offspring: paternal transmission of depressive-like behaviors. Neuropsychopharmacology. 37 (1): 111-2.
“EPIGENETIC INFLUENCE :We are used to thinking of genes as being the controlling factor that determines what each of us is like physically, but genes are only a tiny part of our DNA. The other 97% was thought to be junk until recently, but we now realise that epigenetics – the processes that go on outside the genes – also have a major influence on our development. Some parts act to control "switches" that turn genes on and off, or program the production of other key compounds. For a long time it was a puzzle how around 20,000 genes (far fewer than some breeds of rice) were enough to specify exactly what we were like. The realisation now is that the other 97% of our DNA is equally important.”
—20 amazing facts about the human body | Science | The Observer
Epigenetics: Researchers say meditation changes genes thereby promoting good health.
newscientist.comWithin minutes of performing a relaxation exercise, changes are evident in blood samples. “We found that the more you do it, the more profound the genomic expression changes”
A fascinating article on how meditation can actually change your genes.
Thank you iterates !
Meditation Can Change Your Genes
Meditation has existed as a form of mental training for thousands of years, but it’s only recently that psychologists and neuroscientists have discovered just how much of a change it can make in our lives.
Last year UCLA researchers found that those who had a long-term practice in meditation showed structural changes in parts of the brain associated with self-regulation and emotional processing.
They looked at brain scans and saw a process known as gyrification in the insula, the part of the brain that involves self-awareness. This process of gyrification is a “folding” of layers in the brain that enhances neural processing, improving the brain’s ability to process information, make decisions, and form memories.
And now, according to a study published in Conscious Cognition, meditation can also lead to changes in the expression of our genes.
