Childhood trauma, and especially neglect, mainly before second grade and for girls, seems the basis for most adult medical problems and self-harming behaviors. So, let’s keep up on the latest research, here are some findings:
“In individuals with a genetic predisposition, trauma causes long-term changes in DNA methylation leading to a lasting dysregulation of the stress hormone system. As a result, those affected find themselves less able to cope with stressful situations throughout their lives, frequently leading to depression, post-traumatic stress disorder or anxiety disorders in adulthood.”
Epigenetic dysregulation of the glucocorticoid receptor gene is reversible
Behaviors caused by traumatic experiences in early life are reversible…positive environmental factors can correct behavioral alterations which would otherwise be transmitted to the offspring. The symptoms and their reversal are associated with epigenetic regulation of the glucocorticoid receptor gene.
The epigenetic alterations are not only found in the hippocampus of the offspring of traumatized mice, but also in the germ cells of their fathers. The scientists thus assume that alterations in DNA methylation are transmitted to the progeny through the sperm
“At the molecular level, these behavioral alterations are associated with an increased level of the glucocorticoid receptor in the hippocampus — a brain area essential for cognitive processes and that contributes to stress responses.
- This altered expression results from an epigenetic dysregulation of the gene for the receptor that binds stress hormones like cortisone.
- The activity of this gene is normally reduced by DNA methylation, an epigenetic mark that silences genes.
- Traumatic experiences lead to the removal of some of these DNA methylation marks which results in an increase in gene activity and an increased production of the glucocorticoid receptor.
…the impact of childhood trauma can be corrected by a low-stress and enriched environment in adult life. At the same time, the correction the of DNA methylation pattern prevents the symptoms from being inherited by the offspring.
” ‘epigenetic’ marks, which determine how much a gene is expressed, were altered on this gene, both in the brain and sperm of the stressed mice when adult. The altered marks were passed on to the next generation probably through the sperm, and may partly be responsible for the altered behaviour. The mineralocorticoid receptor in question binds signal messengers such as the stress hormone cortisone which initiates a signalling cascade in neurons.”
“long-term changes in immune function caused by childhood trauma could explain increased vulnerability to a range of health problems in later life…heightened inflammation across three blood biomarkers in adults who had been victims of childhood trauma. High levels of inflammation can lead to serious and potentially life-threatening conditions such as type-2 diabetes, cardiovascular disease as well as the onset of psychiatric disorders.”
As well as the association between childhood trauma and increased blood inflammation, the researchers found that different types of trauma — emotional, physical or sexual abuse — affected these biomarkers in different ways. For instance,
- physical and sexual abuse was associated with significantly increased levels of two biomarkers — tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6),
- heightened levels of c-reactive protein (CRP) appeared to be primarily related to parental absence during early child development.
‘We also found that different types of trauma are associated with different types of inflammation. While there is no clear reason for this, there are several factors which may offer some insight, including the age and length of exposure to childhood trauma and the victim’s relationship with the perpetrator. However, further research into this and the molecular mechanisms behind these associations is warranted.’
Research Group Leader Elisabeth Binder of the Max Planck Institute of Psychiatry examined the DNA of almost 2000 Afro-Americans who had been repeatedly and severely traumatised as adults or in childhood. One-third of trauma victims had become ill and was now suffering from post-traumatic stress disorder. The risk of developing post-traumatic stress disorder rose with increasing severity of abuse only in the carriers of a specific genetic variant in the FKBP5 gene. FKPB5 determines how effectively the organism can react to stress, and by this regulates the entire stress hormone system.
“…traumatic experiences can induce behavioural disorders that are passed down from one generation to the next. It is only recently that scientists have begun to understand the physiological processes underlying hereditary trauma… identifying a key component of these processes: short RNA molecules. These RNAs are synthetized from genetic information (DNA) by enzymes that read specific sections of the DNA (genes) and use them as template to produce corresponding RNAs. Other enzymes then trim these RNAs into mature forms. Cells naturally contain a large number of different short RNA molecules called microRNAs. They have regulatory functions, such as controlling how many copies of a particular protein are made.
traumatic stress alters the amount of several microRNAs in the blood, brain and sperm — while some microRNAs were produced in excess, others were lower than in the corresponding tissues or cells of control animals. These alterations resulted in misregulation of cellular processes normally controlled by these microRNAs.
After traumatic experiences, the mice behaved markedly differently: they partly lost their natural aversion to open spaces and bright light and had depressive-like behaviours. These behavioural symptoms were also transferred to the next generation via sperm, even though the offspring were not exposed to any traumatic stress themselves.
Even passed on to the third generation
The metabolism of the offspring of stressed mice was also impaired: their insulin and blood-sugar levels were lower than in the offspring of non-traumatized parents. “We were able to demonstrate for the first time that traumatic experiences affect metabolism in the long-term and that these changes are hereditary,” says Mansuy. The effects on metabolism and behaviour even persisted in the third generation.
“With the imbalance in microRNAs in sperm, we have discovered a key factor through which trauma can be passed on,”