Behavioral epigenetics
[4] Behavioral epigenetics attempts to provide a framework for understanding how the expression of genes is influenced by experiences and the environment[5] to produce individual differences in behaviour,[6] cognition,[2] personality,[7] and mental health.
Nurturing behaviours from the mother rat were found to stimulate activation of stress signalling pathways that remove methyl groups from DNA.
Studies in rodents have found that the environment exerts an influence on epigenetic changes related to cognition, in terms of learning and memory;[4] environmental enrichment correlated with increased histone acetylation, and verification by administering histone deacetylase inhibitors induced sprouting of dendrites, an increased number of synapses, and reinstated learning behaviour and access to long-term memories.
[1][36] Research has also linked learning and long-term memory formation to reversible epigenetic changes in the hippocampus and cortex in animals with normal-functioning, non-damaged brains.
[1][37] In human studies, post-mortem brains from patients with Alzheimer's dementia show high levels of histone de-acetylase.
Within the prenatal times it is evident that through changes of DNA methylation, that maternal and pre-maternal distress have been connected to modifications in the fetal HPA axis.
Linkage of the impacts of childhood trauma in connection with epigenetic and anxiety, in that there is a change in DNA methylation process, increasing the chances of neuroendocrine damage to likely occur.
In relation, the neuroendocrine damage induces the state of depression, making it mentally unstable for a person to possibly perform their daily activities.
The Brain-derived neurotropic factor (BDNF) is known to change its state because of epigenetic mechanisms and contributes to the alters within the development process necessary for the brain of us individuals.
[44][45][46] Studies in rats have shown correlations between maternal care in terms of the parental licking of offspring and epigenetic changes.
[44] A high level of licking results in a long-term reduction in stress response as measured behaviorally and biochemically in elements of the hypothalamic-pituitary-adrenal axis (HPA).
[44] The opposite is found in offspring that experienced low levels of licking, and when pups are switched, the epigenetic changes are reversed.
[44] In humans, a small clinical research study showed the relationship between prenatal exposure to maternal mood and genetic expression resulting in increased reactivity to stress in offspring.
[54] Even short-term substance abuse can produce long-lasting epigenetic changes in the brain of rodents,[54] via DNA methylation and histone modification.
[19] Epigenetic modifications have been observed in studies on rodents involving ethanol, nicotine, cocaine, amphetamine, methamphetamine and opiates.
[4] Specifically, these epigenetic changes modify gene expression, which in turn increases the vulnerability of an individual to engage in repeated substance overdose in the future.
In turn, increased substance abuse results in even greater epigenetic changes in various components of a rodent's reward system[54] (e.g., in the nucleus accumbens[57]).
These include: repetitive habits that increase the risk of disease, and personal and social problems; need for immediate gratification; high rates of relapse following treatment; and, the feeling of loss of control.
At puberty, sex hormones may exert epigenetic changes (via DNA methylation) on gene expression, thus accounting for higher rates of eating disorders in men as compared to women [citation needed].
Epigenetic changes affecting a greater number of genes have been detected in men with schizophrenia as compared to women with the illness.
[67] Epigenetic dysfunction in human male sperm cells, affecting numerous genes, have been shown to increase with age.
Animals exposed to ambient air from steel mills and highways show drastic epigenetic changes that persist after removal from the exposure.
[67] Schizophrenia studies provide evidence that the nature versus nurture debate in the field of psychopathology should be re-evaluated to accommodate the concept that genes and the environment work in tandem.
As such, many other environmental factors (e.g., nutritional deficiencies and cannabis use) have been proposed to increase the susceptibility of psychotic disorders like schizophrenia via epigenetics.
[69] One study found hypomethylation of a gene promoter of a prefrontal lobe enzyme (i.e., membrane-bound catechol-O-methyl transferase, or COMT) in post-mortem brain samples from individuals with bipolar disorder.
[73] Much of the work in animal models has focused on the indirect downregulation of brain derived neurotrophic factor (BDNF) by over-activation of the stress axis.
[74][75] Studies in various rodent models of depression, often involving induction of stress, have found direct epigenetic modulation of BDNF as well.
[1] One view notes that when animal studies do not consider how the subcellular and cellular components, organs and the entire individual interact with the influences of the environment, results are too reductive to explain behaviour.
[1] However, the ultimate goal is to find patterns of epigenetic changes that can be targeted to treat mental illness, and reverse the effects of childhood stressors, for example.
If such treatable patterns eventually become well-established, the inability to access brains in living humans to identify them poses an obstacle to pharmacological treatment.
