**1. Introduction**

Absence of early life stress has great effects on both health and well-being. This particular topic focuses on the availability or quality of food sources, exposure to toxic effects, community-based events, and the presence of stressors or threats in the ecosystem. In humans, years of extensive researches have revealed some sort of correlation among variations within being exposed in early life era and long-lasting risks of psychiatric and physical illness of maturity [1].

While it is expected that the effects of exposure to chemical substances besides deprivation or stress hormones of a vital vitamin or energy supply, they might have biological impacts on human depending on the specification of the exposure and availability. Personal and social experiences carry the partly same features with biochemical, cellular, and neurobiological changes and this case is amplified with psychosocial expertise executed on animal models in the light of finding answers to these questions.

Effects of social experiences and aggravating events taken place in life leads to the experimental study which has mainly focused on types of lab rodents (usually including mice and rats), albeit several numbers of primate studies can be obtained to maintain additional data in the interest of powerful impacts of encounters taken place in the initial stages of life [2, 3]. In these designs, impact of prenatal nervousness, absence of a mother role and also disengagement variance in maternal treatment, adolescent cultural enhancement, isolation and mature cultural anxiety. When these have been investigated, results indicate that the quality of emotional stress experience or social experiences may cause neuroendocrine consequences which effects social and reproductive behavior. While it is the evidence of there is a phase of increased sensitivity to these eco-induced factors during prenatal as well as first postnatal development, there may also be plasticity that extends into adulthood and adolescence after infancy. The long-term negative impact of the first latter life events on human brain's region-specific gene expression part would be an important finding within these studies. Substantial evidence supports the existence of longterm effects on HPA axis functioning following early life stress; these effects persist into adulthood and are accompanied by lasting behavioral changes. In clinical studies, early life stress has been shown to be a strong predictor of ACTH responsiveness [4, 5]. Further analysis of the molecular mechanisms that could mediate this long-lasting effect involved in gene regulation have been led by these findings.

Epigenetic processes are effective events in changing gene expression and the long-term effects of events experienced in the early stages of life on gene expression are the subject of biologically based research [6]. Across species, it is obvious that a selection of experiences, such as the aspects of interactions experienced socially as well as being exposed to the stressors, can trigger epigenetic consequences. In addition, these progressive outcomes may be carried over descendants in certain cases, resulting in behavioral and neurobiological disturbance of the offspring and even of the grand offspring [7, 8].
