even greater epigenetic changes in various components of a rodent's reward system (e.g., in the nucleus accumbens). hence, a cycle emerges whereby changes in areas of the reward system contribute to the long-lasting neural and behavioural changes associated with the increased likelihood of addiction, the maintenance of addiction and relapse. in humans, alcohol consumption has been shown to produce epigenetic changes that contribute to the increased craving of alcohol. as such, epigenetic modifications may play a part in the progression from the controlled intake to the loss of control of alcohol consumption. these alterations may be long-term, as is evidenced in smokers who still possess nicotine-related epigenetic changes ten years after cessation. therefore, epigenetic modifications may account for some of the behavioural changes generally associated with addiction. 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. evidence for relevant epigenetic changes came from human studies involving alcohol, nicotine, and opiate abuse. evidence for epigenetic changes stemming from amphetamine and cocaine abuse derives from animal studies. in animals, drug-related epigenetic changes in fathers have also been shown to negatively affect offspring in terms of poorer spatial working memory, decreased attention and decreased cerebral volume. imprecise dna repair can leave epigenetic scars dna damage is increased in the brain of rodents by administration of the addictive substances cocaine, methamphetamine, alcohol and tobacco smoke. when such dna damages are repaired, imprecise dna repair may lead to persistent alterations such as methylation of dna or the acetylation or methylation of histones at the sites of repair. these alterations may be epigenetic scars in the chromatin that contribute to the persistent epigenetic changes found in addiction. eating disorders and obesity further information: δfosb epigenetic changes may help to facilitate the development and maintenance of eating disorders via influences in the early environment and throughout the life-span. pre-natal epigenetic changes due to maternal stress, behaviour and diet may later predispose offspring to persistent, increased anxiety and anxiety disorders. these anxiety issues can precipitate the onset of eating disorders and obesity, and persist even after recovery from the eating disorders. epigenetic differences accumulating over the life-span may account for the incongruent differences in eating disorders observed in monozygotic twins. 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 . overall, epigenetics contribute to persistent, unregulated self-control behaviours related to the urge to binge. schizophrenia further information: epigenetics of schizophrenia epigenetic changes including hypomethylation of glutamatergic genes (i.e., nmda-receptor-subunit gene nr3b and the promoter of the ampa-receptor-subunit gene gria2) in the post-mortem brains of people with schizophrenia are associated with increased levels of the neurotransmitter glutamate. since glutamate is the most prevalent, fast, excitatory neurotransmitter, increased levels may result in the psychotic episodes related to schizophrenia. epigenetic changes affecting a greater number of genes have been detected in men with schizophrenia as compared to women with the illness. population studies have established a strong association linking schizophrenia in children born to older fathers. specifically, children born to fathers over the age of 35 years are up to three times more likely to develop schizophrenia. epigenetic dysfunction in human male sperm cells, affecting numerous genes, have been shown to increase with age. this provides a possible explanation for increased rates of the disease in men. to this end, toxins (e.g., air pollutants) have been shown to increase epigenetic differentiation. animals exposed to ambient air from steel mills and highways show drastic epigenetic changes that persist after removal from the exposure. therefore, similar epigenetic changes in older human fathers are likely. 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. bipolar disorder evidence for epigenetic modifications for bipolar disorder is unclear. 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. comt is an enzyme that metabolizes dopamine in the synapse. these findings suggest that the hypomethylation of the promoter results in over-expression of the enzyme. in turn, this results in increased degradation of dopamine levels in the brain. these findings provide evidence that epigenetic modification in the prefrontal lobe is a risk factor for bipolar disorder. however, a second study found no epigenetic differences in post-mortem brains from bipolar individuals. major depressive disorder the causes of major depressive disorder (mdd) are poorly understood from a neuroscience perspective. the epigenetic changes leading to changes in glucocorticoid receptor expression and its effect on the hpa stress system discussed above, have also been applied to attempts to understand mdd. 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. studies in various rodent models of depression, often involving induction of stress, have found direct epigenetic modulation of bdnf as well. psychopathy epigenetics may be relevant to aspects of psychopathic behaviour through methylation and histone modification. these processes are heritable but can also be influenced by environmental factors such as smoking and abuse. epigenetics may be one of the mechanisms through which the environment can impact the expression of the genome. studies have also linked methylation of genes associated with nicotine and alcohol dependence in women, adhd, and drug abuse. it is probable that epigenetic regulation as well as methylation profiling will play an increasingly important role in the study of the play between the environment and genetics of psychopaths. suicide a study of the brains of 24 who died by suicide, 12 of whom had a history of child abuse and 12 who did not, found decreased levels of glucocorticoid receptor in victims of child abuse and associated epigenetic changes. social insects several studies have indicated dna cytosine methylation linked to the social behavior of insects, such as honeybees and ants. in honeybees, when nurse bee switched from her in-hive tasks to out foraging, cytosine methylation marks are changing. when a forager bee was reversed to do nurse duties, the cytosine methylation marks were also reversed. knocking down the dnmt3 in the larvae changed the worker to queen-like phenotype. queen and worker are two distinguish castes with different morphology, behavior, and physiology. studies in dnmt3 silencing also indicated dna methylation may regulate gene alternative splicing and pre-mrna maturation. limitations and future direction many researchers contribute information to the human epigenome consortium. the aim of future research is to reprogram epigenetic changes to help with addiction, mental illness, age related changes, memory decline, and other issues. however, the sheer volume of consortium-based data makes analysis difficult. most studies also focus on one gene. in actuality, many genes and interactions between them likely contribute to individual differences in personality, behaviour and health. as social scientists often work with many variables, determining the number of affected genes also poses methodological challenges. more collaboration between medical researchers, geneticists and social scientists has been advocated to increase knowledge in this field of study. limited access to human brain tissue poses a challenge to conducting human research. not yet knowing if epigenetic changes in the blood and (non-brain) tissues parallel modifications in the brain, places even greater reliance on brain research. although some epigenetic studies have translated findings from animals to humans, a some researchers caution about the extrapolation of animal studies to humans. 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. some researchers note that epigenetic perspectives will likely be incorporated into pharmacological treatments. others caution that more research is necessary as drugs are known to modify the activity of multiple genes and may, therefore, cause serious side effects. 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. future research may also focus on epigenetic changes that mediate the impact of psychotherapy on personality and behaviour. most epigenetic research is correlational; it merely establishes associations. more experimental research is necessary to help establish causation. lack of resources has also limited the number of intergenerational studies. therefore, advancing longitudinal and multigenerational, experience-dependent studies will be critical to further understanding the role of epigenetics in psychology.