This is the fourth in our conversation on past trauma. Last week, we looked at the brain in a state of siege, which is what happens when we are raised in highly stressful environments, such as poverty and abuse. Through a series of complex biological processes, our brain cells get worn down to the point where they can no longer handle the next stressful event. Eventually, whole brain systems are compromised, resulting in the underperforming thinking parts of the brain failing to modulate the overwhelmed reactive parts of the brain.
The outcome is fairly predictable: Anxiety, depression, mania, psychosis, behavioral problems. Essentially, the biology of trauma and chronic stress is the biology of mental illness, of a battered brain no longer capable of coping with its environment.
“Okay” says Tabby, responding to last week’s post, “that still doesn't explain why multiple siblings, within the same household, raised in the same environment do not ALL have ‘overly sensitized’ systems.”
Some siblings growing up in the same environment, she goes on to say, turn out just fine while others struggle. What gives?
In essence, what Tabby is asking is why some brains are more biologically resilient than others, why some individuals can “snap out of it” while others cave in. Let’s look at the resiliency/vulnerability issue from three different and overlapping perspectives: Genetics, epigenetics, and development. All three involve environment in the equation.
In 2002-2003, researchers from the NIMH and other centers published a series of eye-opening studies that - in response to stressful situations - linked certain gene variations to heightened responses in certain parts in the brain and in turn to emotions and behaviors such as fear and depression and aggressive behavior. For instance, one study - cited many times in my posts here on HealthCentral - found that those with the “short allele” to a certain gene had a far greater tendency to depression when exposed to a recent series of stressful events. (Caspi et al, "Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene," Science, July 18, 2003.)
The “short-allele” people, in essence, represented a population that was genetically vulnerable to mental stress and thus prone to depression. The “long-allele” people, by contrast, proved resilient.
This makes obvious sense when we think of our various vulnerabilities and resiliencies regarding all manner of physical stresses, such as to pain, allergens, certain types of food, bacteria and viruses, and on and on and on. But wait, the picture gets more complicated ...
The gene studies from ten years ago forcefully demonstrated that mental illness involves a complex dynamic between genes and our environment. Our genes may predispose us to depression or bipolar, for instance, but grow up in the right environment, free from trauma and abuse or resilient to stress, and perhaps these genes never get switched on.
Epigenetics is a very new field that investigates how these genes get switched on. A Pubmed search I conducted in late 2003 revealed but two study articles related to epigenetics and bipolar disorder. In early 2011, my search came up with 87 articles. Years ago, epigenetics was regarded as a sort of sideshow to genetics. Now, according to a 2010 Time Magazine article, Why Your DNA Isn't Your Destiny, it is emerging as the main event. Says the article:
More recently, however, researchers have begun to realize that epigenetics could also help explain certain scientific mysteries that traditional genetics never could: for instance, why one member of a pair of identical twins can develop bipolar disorder or asthma even though the other is fine.
As I explain it in an article on mcmanweb:
Only two percent of our DNA - via RNA - codes for proteins. Until very recently, the rest was considered "junk," the byproduct of millions of years of evolution. Now scientists are discovering that some of this junk DNA switches on RNA that may do the work of proteins and interact with other genetic material.
This is accomplished through the chemical process of methylation. Other processes such as histone acetylation have also been implicated.
Wait, the best is yet to come ...
Development, in the context of this piece, refers to anything that affects the maturation of the brain, from in utero to adulthood - to even across generations.
During the winter of 1944-45, in what is referred to as the “Dutch Winter Hunger,” the occupying Nazis cut off food supplies to the urban civilian population in the Netherlands, resulting in some 22,000 deaths. Those exposed to the starvation conditions as fetuses turned out as adults to have higher rates of obesity and susceptibility to a range of illnesses (including schizophrenia). In turn, their offspring are also experiencing higher rates of obesity and bad health.
You guessed it, epigenetics is involved. The genes may remain the same from generation to generation, but they are switched on and off differently.
The Time magazine article cites a study of recurrent feast-famine conditions in a remote northern Swedish population. According to the article, “the data suggested that a single winter of overeating as a youngster could initiate a biological chain of events that would lead one's grandchildren to die decades earlier than their peers did.”
What to Make of All This
In addition to Tabby’s query about why two siblings raised in the same conditions can turn out entirely different, she also poses this question:
Is it the relative on one of the lower branches of our root system, who was a blazing nut or tumbling in the dirt laden streets back in the 1900s sodden drunk or whatnot that is still causing us those of us in particular TODAY to seem to "fail" and "falter"?
Let’s refine Tabby’s question a bit:
Could the effects of some unknown traumatic event that a great grandparent of ours experienced a century ago somehow be biologically transmitted in a way that makes you or me - today - more prone to bipolar than your brother or sister?
The short answer, Tabby, appears to be “yes.”
Boggles the mind, doesn’t it?
Published On: June 23, 2012
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