Early experiences in childhood can alter gene expression – Harvard study (PART 2)

 PART 2
Over the past 50 years, extensive research has demonstrated that the healthy development of all organs, including the brain, depends on how much and when certain genes are expressed. When scientists say that genes are “expressed,” they are referring to whether they are turned on or off—essentially whether and when genes are activated to do certain tasks. Research has shown that there are many non-inherited environmental factors and experiences that have the power to chemically mark genes and control their functions.
These influences create a new genetic landscape, which scientists call the epigenome.  Some of these experiences lead to chemical modifications that change the expression of genes temporarily, while increasing numbers have been discovered that leave chemical signatures that result in an enduring change in gene expression.
Early prenatal or postnatal experiences and exposures influence long-term outcomes by chemically altering the structure of genes. Known as epigenetic modification (from the Greek root epi, meaning upon or over), these chemical signatures are written on top of the gene without actually altering the genetic code itself.21
Instead, the signatures attract or repel other chemicals that help the genes produce the proteins that are the building blocks our brains and bodies need to develop. Research tells us that some genes can only be modified epigenetically during certain periods of development, defined as critical periods of modification, while other genes are open to alterations throughout life. 2,3,22,23,24,25 
In short, early experiences cause epigenetic adaptations in the brain that influence whether, when, and how genes build the capacity for future skills to develop.
Some of our genes provide instructions for how our bodies respond to stress, and research has shown that these genes are clearly subject to epigenetic modification. For example, research in animals has shown that stressful experiences to which the pregnant mother is exposed, or to which the offspring is exposed soon after birth, can produce epigenetic changes that chemically modify the receptor in the brain that controls the stress hormone cortisol and, therefore, determines the body’s response to threat (the fight-or-flight response).
Healthy stress responses are characterized by an elevation in blood cortisol followed by a return to baseline to avoid a highly activated state for a prolonged period of time. If young children or pregnant mothers experience toxic stress—as a result of serious adversity (such as chronic neglect, abuse, or exposure to violence) in the absence of protective relationships—persistent epigenetic changes can result. These modifications have been shown to cause prolonged stress responses, which can be likened to revving a car engine for long periods of time. Excessive stress has been correlated with changes in brain architecture and chemistry as well as animal behaviors that resemble anxiety and depression in humans.35,36,37,38,39,40
Human studies have found connections between highly stressful experiences in children and increased risk for later mental illnesses, including generalized anxiety disorder and major depressive disorder.41,42,43
Atypical stress responses over a lifetime can also result in increased risk for physical ailments, such as asthma, hypertension, heart disease and diabetes.