Stress is an adaptive response to situations that threatens an organism and requires a flight or flight response. It is essential for the well-being of lives, although, for many emotional disorders such as depression anxiety, severe stress is considered a significant risk factor for development. The start of major depression is often linked to past life stress events, and studies show a significant link between the beginning of the major depression and life-changing events in the last three months. Sometimes previous stress happens much earlier; like in adult lives, early life stress can lead to emotional depression. So, stress can cause long-term changes in the body and lead to emotional disorders. Extreme or long-term stress, specifically in early life, is a high-risk environmental factor leading to various mental disorders like depression. Explaining the stress-related transcriptional responses underlying molecular processes is necessary to understand the process of stress-related mental disorder development.
Many studies have shown that early life stress can lead to long-term changes in behavior and neurological changes.
According to Methyl Life Pro “Depression (MDD) is a major health problem and the leading cause of disability around the globe, with a 16% lifetime prevalence.” Due to the complexity of MDD, its pathology is not yet clear. Many studies have shown that early life stress can lead to long-term changes in behavior and neurological changes. Although many theories suggest that early life stress may affect the behavior and emotions of an adult, in the long run, the underlying neurological mechanisms are not clear. Because the MDD etiology involves interaction between the environment and genes, epigenetics is important for predicting utility and treatment monitoring. Stressful life experiences can modify these risk genes through DNA methylation and microRNAs regulation and have lasting effects on the expression of these genes, which will lead to brain structure and function changes.
According to the National Institute of Health “epigenetic differences may affect the response of treatment. Although the epigenetic mechanism of antidepressant drugs is not fully understood. In the absence of DNA sequence modifications, DNA methylation can lead to heritable phenotypic changes.” Environmental pressure can cause changes in Methylation and have evolutionary consequences, even in the absence of sequential variability. However, it is largely unknown to what extent environmentally stimulated methylation mutations are transferred to offspring and whether the observed methylation mutations are independent or the result of genetic mutations in individuals. Genetically identical apomictic dandelion plants were exposed to different environmental stresses, and apomictic offspring were raised in a common non-stress environment.
Experts used a methylation-sensitive amplified fragment length polymorphism marker to screen for genome-wide methylation mutations stimulated with stress treatment and to assess the inheritance of stimulated mutations. Different stresses, especially the chemical incorporation of herbs and pathogen defense, induced significant Methylation mutation throughout the genome. Many modifications were transferred to offspring. Stress made some epigenetic differences between treatment and control and elevated epigenetic variation between plants within the treatment. These results show that methylation changes due to stress are common and mostly inherited. Sequence-free, autonomous methylation mutation generated readily. It indicates the epigenetic heredity potential to play an independent role in the evolutionary process that dominates the genetic inheritance system.
Stress levels cause variation to Methylation as stressful life events can modify risk genes through DNA methylation and microRNAs regulation and have lasting effects on the expression of risk genes, leading to changes in brain structure and its functions.