"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, Munich
Specifically, 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 heath
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."

JE:-
So, can genes be _validly_ regarded as independently selectable from the
epigenes which control them? If so, how exactly? If not, what does this
mean with special regard to the Hamiltonian Neo Darwinian model of
Darwinism in which independent in fitness "selfish genes" have been
allowed to provide altruistic in fitness fertile organism phenotypes
which were and remain prohibited by Darwinian theory as a falsification?

Regards,

John Edser

Independent Researcher

ed...@ozemail.com.au