The Alan Sondheim Mail Archive


---------- Forwarded message ----------
Date: Mon, 09 Nov 2009 23:37:43 -0000
From: rk_stonjek <stonjek@ozemail.com.au>
Reply-To: evolutionary-psychology@yahoogroups.com
To: evolutionary-psychology@yahoogroups.com
Subject: [evol-psych] News: Early stress alters epigenome

Early stress alters  epigenome Posted by Jef Akst [Entry posted at 8th
November 2009 06:00 PM GMT]       Scientists have figured out how stress
experienced early in  life can cause long-lasting changes in physiology
and behavior -- via  epigenetics.

     Image: Max-Planck Institute of
Psychiatry,  MunichSpecifically, early stress  appears to induce
epigenetic changes in a specific regulatory region of the  genome,
affecting the expression of a hormone important in controlling mood and
cognition into adulthood, according to a study published online today
(November  8) in Nature Neuroscience.

This is the first study to depict a  molecular mechanism by which
"stress early in life can cause effects that remain  later in life,"
said epigeneticist Moshe Szyf of McGill University in Montreal.  "This
can explain a lot of things that happen to us as humans and our behavior
later in life."

Stress endured early in life can influence the quality  of physical and
mental health in adulthood, such as by causing hormonal  alterations
associated with mood and cognitive disorders. But until now,  scientists
did not understand the mechanism by which early life experiences can
produce such long-lasting effects.

According to a common hypothesis, the  environment affects mental health
by causing alterations to the physical  properties of the genome that
influence gene expression -- the epigenome.  Indeed, research suggests
that DNA methylation, one of the most intensely  studied forms of
epigenetics, may explain why maternal care has a long-term  influence on
behavior and hormones in rats.

To explore whether DNA  methylation is behind the changes associated
with stress experienced early in  life, molecular biologists Chris
Murgatroyd and Dietmar Spengler of the Max  Planck Institute of
Psychiatry in Germany and colleagues examined the  methylation patterns
of mice that were separated from their mothers for three  hours a day
for the first ten days of their lives. Specifically, the researchers
looked for differences in the gene that encodes arginine vasopressin
(AVP), a  hormone associated with mood and cognitive behaviors. The AVP
receptor is also a  promising therapeutic target for stress-related
disorders.

From 6 weeks  of age all the way up to 1 year, mice that experienced
early stress -- and  showed the predicted behavioral and hormonal
differences -- also displayed  significantly lower levels of methylation
in the regulatory region of the  Avp gene in the brain. This
hypomethylation was specific to a subset of  neurons in the hypothalamic
paraventricular nucleus -- a brain area involved in  regulating hormones
linked to stress. These mice also had higher levels of  Avp mRNA,
suggesting that lower methylation levels do indeed affect  hormone
levels.

"Essentially the genome memorizes that [early life]  stress," said Szyf,
who was not involved in the study. "Stress changes  methylation, and
that stays the whole life."

The researchers further  determined that the decreases in methylation in
stressed mice result from the  inactivation of a protein known as MeCP2,
which is involved in the initial  recruitment of proteins that methylate
the DNA.

The concept that social  states in early life can affect health in later
life is "a completely  revolutionary idea," Szyf said. This paper
provides a "detailed" molecular  mechanism by which this can occur, and
"gives substance" to this theory.

Understanding the molecular details underlying this phenomenon is
essential to developing potential therapies for mental disorders that
stem from  early adverse experiences, Murgatroyd added. "This has given
us new insight in  how to possibly develop drugs for [these illnesses]."

Treatments for  reversing the effects of early life stress should begin
as early as possible,  Spengler said. Reversing the inactivation of
MeCP2 might be possible, but "once  [methylation] is laid down, you
cannot erase [it]," he said. "This is a mark  that is very stable."
Treatments given later in life, then, must find ways to  ameliorate the
phenotype, such as by blocking AVP receptors in animals with  higher AVP
levels, he added.


Related stories:    * Epigenetic suicide  note
<http://www.the-scientist.com/2009/08/1/18/1/>
[August 2009]
     * An epigenetic  inheritance
<http://www.the-scientist.com/blog/display/55342/>
[19th January 2009]
     * Epigenetics:  Genome, Meet Your Environment
<http://www.the-scientist.com/article/display/14798/>
[5th July  2004]
    Source: TheScientist
http://www.the-scientist.com/blog/display/56139/
<http://www.the-scientist.com/blog/display/56139/>    Posted by
Robert Karl Stonjek

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